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[PMID]:29366758
[Au] Autor:Yuhong L; Tana W; Zhengzhong B; Feng T; Qin G; Yingzhong Y; Wei G; Yaping W; Langelier C; Rondina MT; Ge RL
[Ad] Endereço:Research Center for High Altitude Medicine, Qinghai University, Xining 810001, China; Department of Respiratory Medicine, The Affiliated Hospital of Qinghai University, Xining 810001, China.
[Ti] Título:Transcriptomic profiling reveals gene expression kinetics in patients with hypoxia and high altitude pulmonary edema.
[So] Source:Gene;651:200-205, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: High altitude pulmonary edema (HAPE) is a life threatening condition occurring in otherwise healthy individuals who rapidly ascend to high altitude. However, the molecular mechanisms of its pathophysiology are not well understood. The objective of this study is to evaluate differential gene expression in patients with HAPE during acute illness and subsequent recovery. METHODS: Twenty-one individuals who ascended to an altitude of 3780 m were studied, including 12 patients who developed HAPE and 9 matched controls without HAPE. Whole-blood samples were collected during acute illness and subsequent recovery for analysis of the expression of hypoxia-related genes, and physiologic and laboratory parameters, including mean pulmonary arterial pressure (mPAP), heart rate, blood pressure, and arterial oxygen saturation (SpO ), were also measured. RESULTS: Compared with control subjects, numerous hypoxia-related genes were up-regulated in patients with acute HAPE. Gene network analyses suggested that HIF-1α played a central role in acute HAPE by affecting a variety of hypoxia-related genes, including BNIP3L, VEGFA, ANGPTL4 and EGLN1. Transcriptomic profiling revealed the expression of most HAPE-induced genes was restored to a normal level during the recovery phase except some key hypoxia response factors, such asBNIP3L, EGR1, MMP9 and VEGF, which remained persistently elevated. CONCLUSIONS: Differential expression analysis of hypoxia-related genes revealed distinct molecular signatures of HAPE during acute and recovery phases. This study may help us to better understand HAPE pathogenesis and putative targets for further investigation and therapeutic intervention.
[Mh] Termos MeSH primário: Doença da Altitude/genética
Hipertensão Pulmonar/genética
Edema Pulmonar/genética
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/etiologia
Lesão Pulmonar Aguda/genética
Adulto
Estudos de Casos e Controles
Estudos de Coortes
Perfilação da Expressão Gênica
Seres Humanos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


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[PMID]:29374925
[Au] Autor:Liu W; Chai JK
[Ad] Endereço:Burn Institute, the First Affiliated Hospital of PLA General Hospital, Beijing 100048, China.
[Ti] Título:[Influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with burn-blast combined injuries].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):32-39, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with severe burn-blast combined injuries. One hundred and ninety-two Sprague-Dawley rats were divided into pure burn-blast combined injury group, ulinastatin+ burn-blast combined injury group, and sham injury group according to the random number table, with 64 rats in each group. Two groups of rats with combined burn-blast injuries were inflicted with moderate blast injuries with the newly self-made explosive device. Then the rats were inflicted with 25% total body surface area full-thickness scald (hereinafter referred to as burn) on the back by immersing in 94 ℃ hot water for 12 s. Rats in sham injury group were sham injured on the back by immersing in 37 ℃ warm water for 12 s. Immediately after injury, rats in the three groups were intraperitoneally injected with Ringer's lactate solution (40 mL/kg), meanwhile rats in ulinastatin+ burn-blast combined injury group were intraperitoneally injected with ulinastatin (4×10(4)U/kg), once every 12 hours, until post injury hour (PIH) 72. Before injury, at PIH 3, 6, 12, 24, 48, 72, and on post injury day (PID) 7, 8 rats in each group were selected to harvest abdominal aortic blood samples to detect plasma levels of activated partial thromboplastin time (APTT), prothrombin time (PT), fibrinogen, D-dimer, antithrombin â…¢ (AT-â…¢), and α2-antiplasmin (α2-AP). At PIH 24, three rats in each group which were used in detection of coagulation parameters were sacrificed to observe lung injury. At PIH 72, three rats in each group were sacrificed for histopathological observation of lung. Data were processed with analysis of variance of factorial design and least-significant difference test. (1) Compared with those of rats in sham injury group, APTT of rats in pure burn-blast combined injury group significantly prolonged at PIH 72 and on PID 7 ( <0.05 or <0.01). PT significantly prolonged at PIH 3 and 72 and significantly shortened at PIH 6 ( <0.05 or <0.01) . Fibrinogen level significantly increased from PIH 12 to PID 7 ( <0.01). AT-â…¢ level significantly decreased at PIH 6 and 12 ( <0.01), and α2-AP level significantly decreased at PIH 6 and significantly increased from PIH 24 to 72 ( <0.01). Compared with those of rats in pure burn-blast combined injury group, APTT of rats in ulinastatin+ burn-blast combined injury group significantly prolonged at PIH 3 and 6 ( <0.01) while PT significantly shortened at PIH 3, 12, and 72 ( <0.05 or <0.01). Fibrinogen level significantly decreased at PIH 6 and 12 and significantly increased at PIH 72 ( <0.05 or <0.01). AT-â…¢ level significantly increased at PIH 3, 12, 48, and 72 ( <0.05 or <0.01), and α2-AP level significantly decreased from PIH 12 to 72 ( <0.05 or <0.01). D-dimer level of rats in sham injury group, pure burn-blast combined injury group, and ulinastatin+ burn-blast combined injury group were respectively (0.084±0.013), (0.115±0.015), (0.158±0.022), (0.099±0.011), (0.099±0.012), (0.089±0.011), (0.124±0.014), and (0.116±0.018) µg/mL, (0.064±0.033), (0.114±0.016), (0.135±0.009), (0.060±0.008), (0.104±0.010), (0.124±0.020), (0.180±0.036), and (0.201±0.032) µg/mL, (0.074±0.013), (0.084±0.035), (0.101±0.050), (0.091±0.046), (0.096±0.034), (0.044±0.019), (0.106±0.049), and (0.118±0.047) µg/mL. Compared with that of rats in sham injury group, D-dimer level significantly decreased at PIH 6 and 12 and significantly increased from PIH 48 to PID 7 ( <0.05 or <0.01). Compared with that of rats in pure burn-blast combined injury group, D-dimer level of rats in ulinastatin+ burn-blast combined injury group significantly decreased at PIH 3, 48, and 72, and on PID 7 ( <0.05 or <0.01). (2) At PIH 24, there was a large amount of light red effusion in the thoracic cavity, and both lung lobes were hyperemic and edematous with a small amount of blood clots in the left and middle lobe of rats in pure burn-blast combined injury group. There was a small amount of yellowish effusion in the thoracic cavity of rats in ulinastatin+ burn-blast combined injury group, and the degree of hyperemic and edematous of bilateral lobes was lighter compared with rats in pure burn-blast combined injury group with no clot in the left lobe. No congestion, edema, or bleeding was observed in lungs of rats in sham injury group. (3) At PIH 72, disorganized alveolar structure, collapsed alveolar cavity, edematous and thickening pulmonary interstitium, infiltration of a large amount of inflammatory cells, obvious rupture of alveolar septum, and hyaline thrombus were observed in lungs of rats in pure burn-blast combined injury group. Significantly improved alveolar structure, less collapsed alveolar cavity, improved edematous pulmonary interstitium, less infiltration of inflammatory cells, rupture of alveolar septum, and no thrombus were observed in lungs of rats in ulinastatin+ burn-blast combined injury group. The lung tissue had a well-filled alveolar cavity with no interstitial edema or infiltration of inflammatory cells and no thrombosis in lungs of rats in sham injury group. Ulinastatin has positive therapeutic effects on acute lung injury in rats with severe burn-blast combined injuries through its good regulating effects on coagulation and fibrinolytic disorders caused by burn-blast combined injuries.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/tratamento farmacológico
Traumatismos por Explosões/complicações
Queimaduras/complicações
Glicoproteínas/farmacologia
Inibidores da Tripsina/farmacologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/complicações
Animais
Traumatismos por Explosões/sangue
Traumatismos por Explosões/patologia
Queimaduras/sangue
Queimaduras/patologia
Edema
Produtos de Degradação da Fibrina e do Fibrinogênio
Edema Pulmonar
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fibrin Fibrinogen Degradation Products); 0 (Glycoproteins); 0 (Trypsin Inhibitors); 0 (fibrin fragment D); OR3S9IF86U (urinastatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.007


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[PMID]:29374921
[Au] Autor:Xiao R; Huang YS; Lin GA; Yuan SA; Hu DS
[Ad] Endereço:Burn Center, the 159th Hospital of PLA, Zhumadian 463008, China.
[Ti] Título:[Effects of cardiac support on delayed resuscitation in extensively burned patients with shock].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):8-13, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the effects of cardiac support on delayed resuscitation in extensively burned patients with shock. Clinical data of 62 extensively burned patients with shock on admission, admitted to the 159th Hospital of PLA (hereinafter referred to as our hospital) from January 2012 to January 2017, were retrospectively analyzed. They were divided into cardiac support group ( =35) and control group ( =27) according to the use of deslanoside and ulinastatin. All patients were treated with routine fluid resuscitation based on the formula of the Third Military Medical University till post injury hour (PIH) 48. Patients in cardiac support group were given slow intravenous injection of deslanoside which was added in 20 mL 100 g/L glucose injection with first dose of 0.4 to 0.6 mg, 0.2 to 0.4 mg per 6 to 8 h, no more than 1.6 mg daily, and slow intravenous injection of 1×10(5)U ulinastatin which was added in 100 mL 50 g/L glucose injection, once per 12 h. Other treatments of patients in the two groups followed the same conventional procedures of our hospital. The following data of the two groups of patients were collected. (1) The data of urine volume per hour within PIH 48, heart rate, mean arterial pressure (MAP), central venous pressure (CVP), blood lactic acid, base excess, hematocrit, and albumin at PIH 48 were recorded. (2) The input volumes of electrolyte, colloid within the first and second 24 hours post burn and the total fluid input volumes within PIH 48 were recorded. (3) The data of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, ß(2)-microglobulin, urea nitrogen, and creatinine at PIH 48 were recorded. (4) The complications including cardiac failure, pulmonary edema, pleural effusion, seroperitoneum, renal failure, sepsis, and death were also recorded. Data were processed with independent sample test, Fisher's exact test, Pearson chi-square test, or continuous correction chi-square test. (1) There were no statistically significant differences in urine volume within PIH 48, heart rate, MAP, CVP, hematocrit, or albumin at PIH 48 between the patients of two groups ( =0.150, 0.488, 0.805, 0.562, 1.742, 0.696, >0.05). While the levels of blood lactic acid and base excess were respectively (4.2±2.2) and (-4.3±2.0) mmol/L in patients of cardiac support group, which were significantly better than (5.9±1.7) and (-6.0±3.1) mmol/L in patients of control group ( =3.249, 2.480, <0.05 or <0.01). (2) There was no statistically significant difference in input volume of colloid within the first 24 hours post burn between the patients of two groups ( =0.642, >0.05). The input volume of electrolyte within the first 24 hours post burn, the input volumes of electrolyte and colloid within the second 24 hours post burn, and the total fluid input volume within PIH 48 of patients in cardiac support group were significantly less than those in control group ( =2.703, 4.223, 3.437, 2.515, <0.05 or <0.01). (3) The levels of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase, total bile acid, alanine aminotransferase, aspartate aminotransferase, ß(2)-microglobulin, urea nitrogen, and creatinine of patients in cardiac support group at PIH 48 were significantly lower than those in control group ( =3.066, 3.963, 3.225, 2.943, 2.431, 3.084, 4.052, 2.915, 3.353, <0.05 or <0.01). (4) The occurrences of pleural effusion and seroperitoneum and mortality of patients in cardiac support group were significantly lower than those in control group ( (2)=5.514, 6.984, 4.798, <0.05 or <0.01). There were no statistically significant differences in cardiac failure, pulmonary edema, renal failure, and sepsis between the patients of two groups [ (2)=1.314 (sepsis), >0.05]. The cardiotonic and cardiac protection treatments in delayed resuscitation of extensively burned patients with shock contribute to improving the cellular anonic metabolism, reducing the volume of fluid resuscitation, and mitigating the ischemic and hypoxic damage to organs, so as to lay foundation for decreasing further complication incidences and mortality.
[Mh] Termos MeSH primário: Queimaduras
Ressuscitação
Choque
[Mh] Termos MeSH secundário: Coloides
Hidratação
Hematócrito
Seres Humanos
Edema Pulmonar
Estudos Retrospectivos
Sepse
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Colloids)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.003


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[PMID]:28450654
[Au] Autor:Setianto BY; Taufiq N; Hernawan H
[Ad] Endereço:Department of Cardiology and Vascular Medicine, Faculty of Medicine, Gadjah Mada University - Sardjito Hospital, Yogyakarta, Indonesia. Department of Internal Medicine, Faculty of Medicine, Gadjah Mada University - Sardjito Hospital, Yogyakarta, Indonesia. budyuls@gmail.com.
[Ti] Título:Left Circumflexus Coronary Artery Total Occlusion with Clinical Presentation as NSTEMI and Acute Pulmonary Oedema.
[So] Source:Acta Med Indones;49(1):52-56, 2017 Jan.
[Is] ISSN:0125-9326
[Cp] País de publicação:Indonesia
[La] Idioma:eng
[Ab] Resumo:Current guidelines for the management of patients with acute coronary syndromes (ACSs) focus on the electrocardiogram to divide patients into ST-elevation acute myocardial infarction (STEMI) or non-ST-elevation acute myocardial infarction (NSTEMI)/unstable angina (UA). Patients with STEMI in the earliest time will receive reperfusion therapy to destruct occlusive thrombus. An ST segment elevation is the 'sine qua non' for diagnosing acute total coronary occlusion causing transmural myocardial infarction. Left circumflex coronary artery (LCx) occlusion is often categorized as NSTEMI because of the absence of significant ST-elevation on the 12 lead standard electrocardiogram. An ST segment elevation is presented in fewer than 50% of patients with LCx total occlusion, such that the reperfusion therapy is delayed. We reported a 77 years old woman whom being diagnosed with NSTEMI because a 12 lead electrocardiogram showed ST segment depression in lead V2-V5. On coronary angiography, we found a total occlusion in the LCx artery as the culprit lession.
[Mh] Termos MeSH primário: Síndrome Coronariana Aguda/complicações
Infarto do Miocárdio sem Supradesnível do Segmento ST/diagnóstico
Edema Pulmonar/complicações
[Mh] Termos MeSH secundário: Idoso
Angiografia Coronária
Vasos Coronários/fisiopatologia
Eletrocardiografia Ambulatorial
Feminino
Seres Humanos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:28471119
[Au] Autor:Dai J; Chen SJ; Yang BS; Lü SM; Zhu M; Xu YF; Chen J; Cai HW; Mao W
[Ad] Endereço:Department of Cardiology, Zhejiang Provincial Hospital of Traditional Chinese Medicine, Hangzhou 310006, China.
[Ti] Título:Recurrence of non-cardiogenic pulmonary edema and sustained hypotension shock in cystic pheochromocytoma.
[So] Source:J Zhejiang Univ Sci B;18(5):449-452, 2017 May.
[Is] ISSN:1862-1783
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Pheochromocytoma is a rare neuroendocrine tumor which derives from chromaffin cells of the adrenal gland or relevant to sympathetic nerves and ganglia. The clinical features of pheochromocytoma are various. Paroxysmal episodes of serious hypertension, headache, palpitation, and diaphoresis are the typical manifestations (Bravo, 2004). Hypotension shock, pulmonary edema, and acute coronary syndrome induced by pheochromocytoma are uncommon (Malindretos et al., 2008; Batisse-Lignier et al., 2015). In this study, we present a rare case of cystic pheochromocytoma causing recurrent hypotension shock, non-cardiogenic pulmonary edema, and acute coronary syndrome, and the possible mechanisms are discussed.
[Mh] Termos MeSH primário: Neoplasias das Glândulas Suprarrenais/complicações
Neoplasias das Glândulas Suprarrenais/diagnóstico
Feocromocitoma/complicações
Feocromocitoma/diagnóstico
Edema Pulmonar/diagnóstico
Edema Pulmonar/etiologia
Choque/etiologia
[Mh] Termos MeSH secundário: Neoplasias das Glândulas Suprarrenais/terapia
Cistos/complicações
Cistos/diagnóstico
Cistos/terapia
Diagnóstico Diferencial
Feminino
Seres Humanos
Hipotensão/diagnóstico
Hipotensão/etiologia
Hipotensão/terapia
Meia-Idade
Feocromocitoma/terapia
Edema Pulmonar/terapia
Recuperação de Função Fisiológica
Recidiva
Choque/diagnóstico
Choque/prevenção & controle
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1631/jzus.B1600411


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[PMID]:29202543
[Au] Autor:Wang XT; Liu DW; Zhang HM; Long Y; Guan XD; Qiu HB; Yu KJ; Yan J; Zhao H; Tang YQ; Ding X; Ma XC; Du W; Kang Y; Tang B; Ai YH; He HW; Chen DC; Chen H; Chai WZ; Zhou X; Cui N; Wang H; Rui X; Hu ZJ; Li JG; Xu Y; Yang Y; Ouyan B; Lin HY; Li YM; Wan XY; Yang RL; Qin YZ; Chao YG; Xie ZY; Sun RH; He ZY; Wang DF; Huang QQ; Jiang DP; Cao XY; Yu RG; Wang X; Chen XK; Wu JF; Zhang LN; Yin MG; Liu LX; Li SW; Critical Hemodynamic Theraphy Collaboration Group (CHTC Group)
[Ti] Título:[Experts consensus on the management of the right heart function in critically ill patients].
[So] Source:Zhonghua Nei Ke Za Zhi;56(12):962-973, 2017 Dec 01.
[Is] ISSN:0578-1426
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To establish the experts consensus on the right heart function management in critically ill patients. The panel of consensus was composed of 30 experts in critical care medicine who are all members of Critical Hemodynamic Therapy Collaboration Group (CHTC Group). Each statement was assessed based on the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) principle. Then the Delphi method was adopted by 52 experts to reassess all the statements. (1) Right heart function is prone to be affected in critically illness, which will result in a auto-exaggerated vicious cycle. (2) Right heart function management is a key step of the hemodynamic therapy in critically ill patients. (3) Fluid resuscitation means the process of fluid therapy through rapid adjustment of intravascular volume aiming to improve tissue perfusion. Reversed fluid resuscitation means reducing volume. (4) The right ventricle afterload should be taken into consideration when using stroke volume variation (SVV) or pulse pressure variation (PPV) to assess fluid responsiveness.(5)Volume overload alone could lead to septal displacement and damage the diastolic function of the left ventricle. (6) The Starling curve of the right ventricle is not the same as the one applied to the left ventricle,the judgement of the different states for the right ventricle is the key of volume management. (7) The alteration of right heart function has its own characteristics, volume assessment and adjustment is an important part of the treatment of right ventricular dysfunction (8) Right ventricular enlargement is the prerequisite for increased cardiac output during reversed fluid resuscitation; Nonetheless, right heart enlargement does not mandate reversed fluid resuscitation.(9)Increased pulmonary vascular resistance induced by a variety of factors could affect right heart function by obstructing the blood flow. (10) When pulmonary hypertension was detected in clinical scenario, the differentiation of critical care-related pulmonary hypertension should be a priority. (11) Attention should be paid to the change of right heart function before and after implementation of mechanical ventilation and adjustment of ventilator parameter. (12) The pulmonary arterial pressure should be monitored timingly when dealing with critical care-related pulmonary hypertension accompanied with circulatory failure.(13) The elevation of pulmonary aterial pressure should be taken into account in critical patients with acute right heart dysfunction. (14) Prone position ventilation is an important measure to reduce pulmonary vascular resistance when treating acute respiratory distress syndrome patients accompanied with acute cor pulmonale. (15) Attention should be paid to right ventricle-pulmonary artery coupling during the management of right heart function. (16) Right ventricular diastolic function is more prone to be affected in critically ill patients, the application of critical ultrasound is more conducive to quantitative assessment of right ventricular diastolic function. (17) As one of the parameters to assess the filling pressure of right heart, central venous pressure can be used to assess right heart diastolic function. (18). The early and prominent manifestation of non-focal cardiac tamponade is right ventricular diastolic involvement, the elevated right atrial pressure should be noticed. (19) The effect of increased intrathoracic pressure on right heart diastolic function should be valued. (20) Ttricuspid annular plane systolic excursion (TAPSE) is an important parameter that reflects right ventricular systolic function, and it is recommended as a general indicator of critically ill patient. (21) Circulation management with right heart protection as the core strategy is the key point of the treatment of acute respiratory distress syndrome. (22) Right heart function involvement after cardiac surgery is very common and should be highly valued. (23) Right ventricular dysfunction should not be considered as a routine excuse for maintaining higher central venous pressure. (24) When left ventricular dilation, attention should be paid to the effect of left ventricle on right ventricular diastolic function. (25) The impact of left ventricular function should be excluded when the contractility of the right ventricle is decreased. (26) When the right heart load increases acutely, the shunt between the left and right heart should be monitored. (27) Attention should be paid to the increase of central venous pressure caused by right ventricular dysfunction and its influence on microcirculation blood flow. (28) When the vasoactive drugs was used to reduce the pressure of pulmonary circulation, different effects on pulmonary and systemic circulation should be evaluated. (29) Right atrial pressure is an important factor affecting venous return. Attention should be paid to the influence of the pressure composition of the right atrium on the venous return. (30) Attention should be paid to the role of the right ventricle in the acute pulmonary edema. (31) Monitoring the difference between the mean systemic filling pressure and the right atrial pressure is helpful to determine whether the infusion increases the venous return. (32) Venous return resistance is often considered to be a insignificant factor that affects venous return, but attention should be paid to the effect of the specific pathophysiological status, such as intrathoracic hypertension, intra-abdominal hypertension and so on. Consensus can promote right heart function management in critically ill patients, optimize hemodynamic therapy, and even affect prognosis.
[Mh] Termos MeSH primário: Estado Terminal
Diástole/fisiologia
Hidratação
Insuficiência Cardíaca/diagnóstico por imagem
Hemodinâmica/fisiologia
[Mh] Termos MeSH secundário: Pressão Venosa Central
Consenso
Cuidados Críticos
Insuficiência Cardíaca/etiologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Edema Pulmonar
Respiração Artificial
Síndrome do Desconforto Respiratório do Adulto
Disfunção Ventricular Direita/diagnóstico por imagem
Função Ventricular Esquerda
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1426.2017.12.017


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[PMID]:29040264
[Au] Autor:Huber W; Gruber A; Eckmann M; Elkmann F; Klein I; Lahmer T; Mayr U; Schellnegger R; Schneider J; Batres-Baires G; Fekecs L; Beitz A; Berbara H; Schmid R; Herner A
[Ad] Endereço:Medizinische Klinik und Poliklinik, Klinikum rechts der Isar der Technischen Universität München, München, Germany.
[Ti] Título:Comparison of pulmonary vascular permeability index PVPI and global ejection fraction GEF derived from jugular and femoral indicator injection using the PiCCO-2 device: A prospective observational study.
[So] Source:PLoS One;12(10):e0178372, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Transpulmonary thermodilution (TPTD) is used to derive cardiac output CO, global end-diastolic volume GEDV and extravascular lung water EVLW. To facilitate interpretation of these data, several ratios have been developed, including pulmonary vascular permeability index (defined as EVLW/(0.25*GEDV)) and global ejection fraction ((4*stroke volume)/GEDV). PVPI and GEF have been associated to the aetiology of pulmonary oedema and systolic cardiac function, respectively. Several studies demonstrated that the use of femoral venous access results in a marked overestimation of GEDV. This also falsely reduces PVPI and GEF. One of these studies suggested a correction formula for femoral venous access that markedly reduced the bias for GEDV. Consequently, the last PiCCO-algorithm requires information about the CVC, and correction for femoral access has been shown. However, two recent studies demonstrated inconsistencies of the last PiCCO algorithm using incorrected GEDV for PVPI, but corrected GEDV for GEF. Nevertheless, these studies were based on mathematical analyses of data displayed in a total of 15 patients equipped with only a femoral, but not with a jugular CVC. Therefore, this study compared PVPI_fem and GEF_fem derived from femoral TPTD to values derived from jugular indicator injection in 25 patients with both jugular and femoral CVCs. METHODS: 54 datasets in 25 patients were recorded. Each dataset consisted of three triplicate TPTDs using the jugular venous access as the gold standard and the femoral access with (PVPI_fem_cor) and without (PVPI_fem_uncor) information about the femoral indicator injection to evaluate, if correction for femoral GEDV pertains to PVPI_fem and GEF_fem. RESULTS: PVPI_fem_uncor was significantly lower than PVPI_jug (1.48±0.47 vs. 1.84±0.53; p<0.001). Similarly, PVPI_fem_cor was significantly lower than PVPI_jug (1.49±0.46 vs. 1.84±0.53; p<0.001). This is explained by the finding that PVPI_fem_uncor was not different to PVPI_fem_cor (1.48±0.47 vs. 1.49±0.46; n.s.). This clearly suggests that correction for femoral CVC does not pertain to PVPI. GEF_fem_uncor was significantly lower than GEF_jug (20.6±5.1% vs. 25.0±6.1%; p<0.001). By contrast, GEF_fem_cor was not different to GEF_jug (25.6±5.8% vs. 25.0±6.1%; n.s.). Furthermore, GEF_fem_cor was significantly higher than GEF_fem_uncor (25.6±5.8% vs. 20.6±5.1%; p<0.001). This finding emphasizes that an appropriate correction for femoral CVC is applied to GEF_fem_cor. The extent of the correction (25.5/20.6; 124%) for GEF and the relation of PVPI_jug/PVPI_fem_uncor (1.84/1.48; 124%) are in the same range as the ratio of GEDVI_fem_uncor/GEDVI_fem_cor (1056ml/m2/821mL/m2; 129%). This further emphasizes that GEF, but not PVPI is corrected in case of femoral indicator injection. CONCLUSIONS: Femoral indicator injection for TPTD results in significantly lower values for PVPI and GEF. While the last PiCCO algorithm appropriately corrects GEF, the correction is not applied to PVPI. Therefore, GEF-values can be used in case of femoral CVC, but PVPI-values are substantially underestimated.
[Mh] Termos MeSH primário: Permeabilidade Capilar
Débito Cardíaco
Cateterismo Venoso Central/métodos
Meios de Contraste/farmacocinética
Monitorização Fisiológica/métodos
Volume Sistólico
[Mh] Termos MeSH secundário: Idoso
Água Extravascular Pulmonar
Feminino
Veia Femoral
Coração/fisiopatologia
Seres Humanos
Injeções Intravenosas
Unidades de Terapia Intensiva
Veias Jugulares
Cirrose Hepática/diagnóstico
Cirrose Hepática/fisiopatologia
Cirrose Hepática/terapia
Pulmão/irrigação sanguínea
Pulmão/fisiopatologia
Meia-Idade
Monitorização Fisiológica/instrumentação
Estudos Prospectivos
Edema Pulmonar/diagnóstico
Edema Pulmonar/fisiopatologia
Edema Pulmonar/terapia
Síndrome do Desconforto Respiratório do Adulto/diagnóstico
Síndrome do Desconforto Respiratório do Adulto/fisiopatologia
Síndrome do Desconforto Respiratório do Adulto/terapia
Sepse/diagnóstico
Sepse/fisiopatologia
Sepse/terapia
Termodiluição/métodos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Contrast Media)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178372


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[PMID]:28941803
[Au] Autor:Xue R; Jiang J; Dong B; Tan W; Sun Y; Zhao J; Chen Y; Dong Y; Liu C
[Ad] Endereço:Department of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China; Key Laboratory on Assisted Circulation, Ministry of Health, Guangzhou, China.
[Ti] Título:DJ-1 activates autophagy in the repression of cardiac hypertrophy.
[So] Source:Arch Biochem Biophys;633:124-132, 2017 Nov 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiac hypertrophy is the risk factor of heart failure when the heart is confronted with pressure overload or neurohumoral stimuli. Autophagy, a conserved degradative pathway, is one of the important mechanisms involved in the regulation of cardiac hypertrophy. DJ-1 is a traditional anti-oxidative protein and emerging evidence suggested that DJ-1 might modulate autophagy. However, the regulation of autophagy by DJ-1 in the process of cardiac hypertrophy remains unknown. In our study, we firstly discovered that the expression of DJ-1declined in the process of pressure overload cardiac hypertrophy, and its alteration was parallel with the impairment of autophagy. Furthermore, we proved that DJ-1 knockout mice exhibited a more hypertrophied phenotype than wildtype mice in cardiac hypertrophy which indicated that DJ-1 is responsible for the repression of cardiac hypertrophy. Furthermore, DJ-1 knockout significantly exacerbated pulmonary edema due to cardiac hypertrophy. In the process of cardiac hypertrophy, DJ-1 knockout significantly impaired autophagy activation and enhanced mTORC1 and mTORC2 phosphorylation were found. Similarly, our in vitro study proved that DJ-1 overexpression ameliorated phenylephrine (PE)-induced cardiac hypertrophy and promoted autophagy activation. Taken together, DJ-1 might repress both pressure overload and PE-induced cardiac hypertrophy via the activation of autophagy.
[Mh] Termos MeSH primário: Autofagia/genética
Cardiomegalia/genética
Pulmão/metabolismo
Miocárdio/metabolismo
Proteína Desglicase DJ-1/genética
Edema Pulmonar/genética
[Mh] Termos MeSH secundário: Animais
Autofagia/efeitos dos fármacos
Cardiomegalia/induzido quimicamente
Cardiomegalia/metabolismo
Cardiomegalia/patologia
Regulação da Expressão Gênica
Pulmão/patologia
Alvo Mecanístico do Complexo 1 de Rapamicina
Alvo Mecanístico do Complexo 2 de Rapamicina
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Complexos Multiproteicos/genética
Complexos Multiproteicos/metabolismo
Miocárdio/patologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Fenilefrina/efeitos adversos
Fosforilação
Cultura Primária de Células
Proteína Desglicase DJ-1/deficiência
Edema Pulmonar/induzido quimicamente
Edema Pulmonar/metabolismo
Edema Pulmonar/patologia
Ratos Sprague-Dawley
Índice de Gravidade de Doença
Serina-Treonina Quinases TOR/genética
Serina-Treonina Quinases TOR/metabolismo
Vasoconstritores/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Multiprotein Complexes); 0 (Vasoconstrictor Agents); 1WS297W6MV (Phenylephrine); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2); EC 3.1.2.- (PARK7 protein, mouse); EC 3.1.2.- (Protein Deglycase DJ-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


  9 / 15266 MEDLINE  
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[PMID]:28886777
[Au] Autor:Senthilkumaran S; Menezes RG; Jena NN; Thirumalaikolundusubramanian P
[Ad] Endereço:Department of Emergency and Critical Care, Be Well Hospital, Erode, Tamil Nadu, India.
[Ti] Título:Pulmonary Edema After Near Hanging: An Insight.
[So] Source:Air Med J;36(5):224, 2017 Sep - Oct.
[Is] ISSN:1532-6497
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Asfixia
Edema Pulmonar
[Mh] Termos MeSH secundário: Seres Humanos
Tentativa de Suicídio
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:H
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE


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[PMID]:28797399
[Au] Autor:Patil PD; Cua YM; Farver C; Perez RL; Mehta AC; Panchabhai TS
[Ad] Endereço:Department of Hospital Medicine, Medicine Institute, Cleveland Clinic, Cleveland, OH.
[Ti] Título:A 54-Year-Old Man With Anasarca, Dyspnea, and Recurrent Bilateral Pleural Effusions.
[So] Source:Chest;152(2):e39-e44, 2017 Aug.
[Is] ISSN:1931-3543
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CASE PRESENTATION: A 54-year-old African-American man presented with 2 years of progressively worsening dyspnea and anasarca. Over the past 6 months he gained 30 lbs with worsening lower extremity, abdominal wall, and scrotal edema. A recent workup for cardiac, renal, and liver disease, including two-dimensional echocardiogram, liver and renal function tests, and abdominal ultrasound, was unremarkable. He reported a 15-pack year history of smoking and quit 3 years ago. Chest radiograph at that time revealed bilateral pleural effusions that were both reportedly milky in appearance when drained by thoracenteses.
[Mh] Termos MeSH primário: Amiloidose/diagnóstico
Pneumopatias/etiologia
Doenças Pleurais/etiologia
Edema Pulmonar/diagnóstico por imagem
Edema Pulmonar/etiologia
[Mh] Termos MeSH secundário: Amiloidose/diagnóstico por imagem
Quilotórax/diagnóstico por imagem
Quilotórax/etiologia
Dispneia/etiologia
Edema/diagnóstico por imagem
Edema/etiologia
Seres Humanos
Pneumopatias/diagnóstico por imagem
Masculino
Meia-Idade
Doenças Pleurais/diagnóstico por imagem
Derrame Pleural/etiologia
Recidiva
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE



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