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[PMID]:28465331
[Au] Autor:Ohuchi H; Negishi J; Hayama Y; Miyazaki A; Shiraishi I; Ichikawa H
[Ad] Endereço:Department of Pediatric Cardiology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
[Ti] Título:Renal resistive index reflects Fontan pathophysiology and predicts mortality.
[So] Source:Heart;103(20):1631-1637, 2017 10.
[Is] ISSN:1468-201X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The renal resistive index (RRI) reflects non-renal pathophysiology, such as great artery stiffness, haemodynamics and even end-organ damage in patients with hypertension. This study was conducted to clarify the clinical significance of the RRI in Fontan pathophysiology. METHODS: We measured the RRI in 280 consecutive Fontan patients and 36 healthy controls. RESULTS: The patients exhibited a higher RRI than the controls (0.71±0.07 vs 0.60±0.04, p<0.0001). A high central venous pressure, low arterial pressure, greater pulse pressure and low arterial oxygen saturation (SaO ) independently predicted a high RRI (p<0.05-0.0001). The RRI was inversely correlated with the peak oxygen uptake (PVO ) and 24-hour creatine clearance, and was positively correlated with the plasma levels of brain natriuretic peptide (BNP) (p<0.0001 for all). The high RRI was also associated with liver dysfunction and postprandial hyperglycaemia during the oral glucose tolerance test (p<0.001). During the follow-up period, 18 patients died. Age, RRI, SaO , BNP, use of diuretics and antiarrhythmic drugs, and PVO predicted mortality. When PVO was excluded, RRI (HR: 1.13; 95% CI: 1.04 to 1.23; p<0.01) or RRI ≥0.81 (HR: 12.0; 95% CI: 3.4 to 50; p<0.0001) independently predicted mortality. CONCLUSIONS: The RRI reflected heart failure severity, hepatorenal function and glucose intolerance, and predicted all-cause mortality in Fontan patients. Therefore, the RRI may be a useful marker of Fontan-associated multiorgan pathophysiology.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/fisiopatologia
Rim/fisiopatologia
Circulação Renal/fisiologia
Resistência Vascular/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Criança
Pré-Escolar
Feminino
Técnica de Fontan
Insuficiência Cardíaca/diagnóstico por imagem
Insuficiência Cardíaca/cirurgia
Seres Humanos
Rim/irrigação sanguínea
Rim/diagnóstico por imagem
Masculino
Ultrassonografia Doppler em Cores
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1136/heartjnl-2016-310812


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[PMID]:27771702
[Au] Autor:Chade AR; Hall JE
[Ad] Endereço:Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Miss., USA.
[Ti] Título:Role of the Renal Microcirculation in Progression of Chronic Kidney Injury in Obesity.
[So] Source:Am J Nephrol;44(5):354-367, 2016.
[Is] ISSN:1421-9670
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Obesity is largely responsible for the growing incidence and prevalence of diabetes, cardiovascular and renal diseases. Current strategies to prevent and treat obesity and its consequences have been insufficient to reverse the ongoing trends. Lifestyle modification or pharmacological therapies often produce modest weight loss which is not sustained and recurrence of obesity is frequently observed, leading to progression of target organ damage in many obese subjects. Therefore, research efforts have focused not only on the factors that regulate energy balance, but also on understanding mechanisms of target organ injury in obesity. Summary and Key Message: Microvascular (MV) disease plays a pivotal role in progressive kidney injury from different etiologies such as hypertension, diabetes, and atherosclerosis, which are all important consequences of chronic obesity. The MV networks are anatomical units that are closely adapted to specific functions of nutrition and removal of waste in every organ. Damage of the small vessels in several tissues and organs has been reported in obesity and may increase cardio-renal risk. However, the mechanisms by which obesity and its attendant cardiovascular and metabolic consequences interact to cause renal MV injury and chronic kidney disease are still unclear, although substantial progress has been made in recent years. This review addresses potential mechanisms and consequences of obesity-induced renal MV injury as well as current treatments that may provide protection of the renal microcirculation and slow progressive kidney injury in obesity.
[Mh] Termos MeSH primário: Microcirculação
Obesidade/complicações
Circulação Renal
Insuficiência Renal Crônica/etiologia
[Mh] Termos MeSH secundário: Tecido Adiposo/fisiologia
Animais
Seres Humanos
Inflamação/complicações
Microvasos/patologia
Microvasos/fisiopatologia
Neovascularização Patológica
Obesidade/fisiopatologia
Insuficiência Renal Crônica/patologia
Insuficiência Renal Crônica/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28768662
[Au] Autor:Ahmad A; Daneva Z; Li G; Dempsey SK; Li N; Poklis JL; Lichtman A; Li PL; Ritter JK
[Ad] Endereço:Department of Pharmacology and Toxicology, Virginia Commonwealth University School of Medicine, Richmond, Virginia.
[Ti] Título:Stimulation of diuresis and natriuresis by renomedullary infusion of a dual inhibitor of fatty acid amide hydrolase and monoacylglycerol lipase.
[So] Source:Am J Physiol Renal Physiol;313(5):F1068-F1076, 2017 Nov 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The renal medulla, considered critical for the regulation of salt and water balance and long-term blood pressure control, is enriched in anandamide and two of its major metabolizing enzymes, cyclooxygenase-2 (COX-2) and fatty acid amide hydrolase (FAAH). Infusion of anandamide (15, 30, and 60 nmol·min ·kg ) into the renal medulla of C57BL/6J mice stimulated diuresis and salt excretion in a COX-2- but not COX-1-dependent manner. To determine whether endogenous endocannabinoids in the renal medulla can elicit similar effects, the effects of intramedullary isopropyl dodecyl fluorophosphate (IDFP), which inhibits the two major endocannabinoid hydrolases, were studied. IDFP treatment increased the urine formation rate and sodium excretion in a COX-2- but not COX-1-dependent manner. Neither anandamide nor IDFP affected the glomerular filtration rate. Neither systemic (0.625 mg·kg ·30 min iv) nor intramedullary (15 nmol·min ·kg ·30 min ) IDFP pretreatment before intramedullary anandamide (15-30 nmol·min ·kg ) strictly blocked effects of anandamide, suggesting that hydrolysis of anandamide was not necessary for its diuretic effect. Intramedullary IDFP had no effect on renal blood flow but stimulated renal medullary blood flow. The effects of IDFP on urine flow rate and medullary blood flow were FAAH-dependent as demonstrated using FAAH knockout mice. Analysis of mouse urinary PGE concentrations by HPLC-electrospray ionization tandem mass spectrometry showed that IDFP treatment decreased urinary PGE These data are consistent with a role of FAAH and endogenous anandamide acting through a COX-2-dependent metabolite to regulate diuresis and salt excretion in the mouse kidney.
[Mh] Termos MeSH primário: Amidoidrolases/antagonistas & inibidores
Diurese
Inibidores Enzimáticos/farmacologia
Monoacilglicerol Lipases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Amidoidrolases/metabolismo
Animais
Ácidos Araquidônicos/metabolismo
Ciclo-Oxigenase 2/metabolismo
Diurese/efeitos dos fármacos
Endocanabinoides/metabolismo
Medula Renal/efeitos dos fármacos
Medula Renal/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monoacilglicerol Lipases/metabolismo
Natriurese/efeitos dos fármacos
Natriurese/fisiologia
Alcamidas Poli-Insaturadas/metabolismo
Circulação Renal/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Enzyme Inhibitors); 0 (Polyunsaturated Alkamides); EC 1.14.99.- (Ptgs2 protein, mouse); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.1.1.23 (Monoacylglycerol Lipases); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (fatty-acid amide hydrolase); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00196.2017


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[PMID]:28724607
[Au] Autor:Thomson SC; Kashkouli A; Liu ZZ; Singh P
[Ad] Endereço:Department of Medicine, University of California and VA San Diego Healthcare System, San Diego, California; and.
[Ti] Título:Renal hemodynamic effects of glucagon-like peptide-1 agonist are mediated by nitric oxide but not prostaglandin.
[So] Source:Am J Physiol Renal Physiol;313(4):F854-F858, 2017 Oct 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The incretin hormone, glucagon-like peptide-1 (GLP-1), is known for responding to dietary fat and carbohydrate. It elicits effects on pancreas, gut, and brain to stabilize blood glucose levels. We have previously reported that the GLP-1 agonist, exenatide, vasodilates the kidney and suppresses proximal reabsorption. The present study was undertaken to determine whether the renal effects of exenatide are mediated by nitric oxide (NO) and/or prostaglandins. Inulin clearance (glomerular filtration rate, GFR) and urine flow rate (UV) were measured in anesthetized rats before and during exenatide infusion (1 nmol/h iv). Animals were pretreated with cyclooxygenase (COX) inhibitor (meclofenamate), NO synthase (NOS) inhibitor ( -monomethyl-l-arginine, l-NMMA), NO clamp (l-NMMA + sodium nitroprusside), or placebo. Effectiveness of COX inhibition was tested by measuring urinary prostaglandin E (UPGE ). Effectiveness of NOS blockade and NO clamp was determined by urinary NO degradation products (UNOx). Exenatide increased GFR, UV, UPGE , and UNOx. Pretreatment with meclofenamate reduced UPGE by 75% and reduced the effect of exenatide on UPGE by 30% but did not modify the effects of exenatide on GFR or UV. Pretreatment with l-NMMA reduced UNOx and the impact of exenatide on GFR and UV by 50%. Pretreatment by NO clamp did not prevent UNOx from increasing during exenatide but blunted the effects of exenatide on GFR and UV. In conclusion, exenatide is a potent renal vasodilator and diuretic in the rat. These effects of exenatide are insensitive to COX inhibition but are mediated, in part, by NO.
[Mh] Termos MeSH primário: Peptídeo 1 Semelhante ao Glucagon/agonistas
Óxido Nítrico/metabolismo
Peptídeos/farmacologia
Prostaglandinas/metabolismo
Circulação Renal/efeitos dos fármacos
Peçonhas/farmacologia
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptides); 0 (Prostaglandins); 0 (Venoms); 31C4KY9ESH (Nitric Oxide); 89750-14-1 (Glucagon-Like Peptide 1); 9P1872D4OL (exenatide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00258.2017


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[PMID]:28693425
[Au] Autor:Thomas R; Möllmann C; Ziebart A; Liu T; David M; Hartmann EK
[Ad] Endereço:Department of Anesthesiology, Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
[Ti] Título:Cyclic PaO oscillations assessed in the renal microcirculation: correlation with tidal volume in a porcine model of lung lavage.
[So] Source:BMC Anesthesiol;17(1):92, 2017 Jul 11.
[Is] ISSN:1471-2253
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oscillations of the arterial partial pressure of oxygen induced by varying shunt fractions occur during cyclic alveolar recruitment within the injured lung. Recently, these were proposed as a pathomechanism that may be relevant for remote organ injury following acute respiratory distress syndrome. This study examines the transmission of oxygen oscillations to the renal tissue and their tidal volume dependency. METHODS: Lung injury was induced by repetitive bronchoalveolar lavage in eight anaesthetized pigs. Cyclic alveolar recruitment was provoked by high tidal volume ventilation. Oscillations of the arterial partial pressure of oxygen were measured in real-time in the macrocirculation by multi-frequency phase fluorimetry and in the renal microcirculation by combined white-light spectrometry and laser-Doppler flowmetry during tidal volume down-titration. RESULTS: Significant respiratory-dependent oxygen oscillations were detected in the macrocirculation and transmitted to the renal microcirculation in a substantial extent. The amplitudes of these oscillations significantly correlate to the applied tidal volume and are minimized during down-titration. CONCLUSIONS: In a porcine model oscillations of the arterial partial pressure of oxygen are induced by cyclic alveolar recruitment and transmitted to the renal microcirculation in a tidal volume-dependent fashion. They might play a role in organ crosstalk and remote organ damage following lung injury.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/fisiopatologia
Microcirculação/fisiologia
Oxigênio/sangue
Circulação Renal/fisiologia
Volume de Ventilação Pulmonar/fisiologia
[Mh] Termos MeSH secundário: Animais
Pressão Sanguínea/fisiologia
Lavagem Broncoalveolar
Fluxometria por Laser-Doppler
Modelos Animais
Análise Espectral
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
S88TT14065 (Oxygen)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1186/s12871-017-0382-7


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[PMID]:28658254
[Au] Autor:Junot S; Keroak S; Del Castillo JRE; Ayoub JY; Paquet C; Bonnet-Garin JM; Troncy E
[Ad] Endereço:VetAgro Sup - Veterinary Campus of Lyon - University of Lyon, APCSE unit, Marcy l'Etoile, France.
[Ti] Título:Inhaled nitric oxide prevents NSAID-induced renal impairment in pseudo-normovolaemic piglets.
[So] Source:PLoS One;12(6):e0179475, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Inhaled nitric oxide (iNO) is commonly used as a treatment of pulmonary hypertension. Its action is purported to be specific to the lung, but extrapulmonary effects have been reported. The objective of this study was to evaluate if iNO could compensate the renal impairment induced by ketoprofen, a conventional non-steroidal anti-inflammatory drug (NSAID), during general anaesthesia. METHODS: Under pseudo-normovolaemic condition, thirty piglets were randomly assigned into 5 equal groups and equipped for renal and systemic parameters measurements. A first experiment was carried out to validate methods and reproduce the renal effects of iNO (40 ppm) in comparison with a placebo (100% oxygen). In a second experiment, iNO was inhaled for 120 minutes right after NSAID treatment (ketoprofen 2 mg×kg-1 IV, and 40 ppm iNO; group KiNO) and its effects were compared to ketoprofen alone (2 mg×kg-1 IV; group K) and placebo (saline; group C). RESULTS: In this model, iNO increased significantly renal blood flow measured by ultrasonic (RBFUL: +53.2±17.2%; p = 0.008) and by PAH clearance (RBFPAH:+78.6±37.6%; p = 0.004) methods, glomerular filtration rate (GFR: +72.6±32.5%; p = 0.006) and urinary output (UO: +47.4±24.2%; p = 0.01). In the second experiment, no significant temporal variation was noted for renal parameters in groups KiNO and C, whereas a significant and constant decrease was observed in the group K for RBFUL (max -19.0±7.1%), GFR (max -26.6±10.4%) and UO (max -30.3±10.5%). CLINICAL SIGNIFICANCE: Our experiments show that iNO, released from its transport forms after its inhalation, can improve renal safety of NSAIDs. This result is promising regarding the use of NSAIDs in critical conditions, but needs to receive clinical confirmation.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides
Cetoprofeno
Nefropatias/prevenção & controle
Óxido Nítrico/administração & dosagem
Circulação Renal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração por Inalação
Animais
Feminino
Taxa de Filtração Glomerular/efeitos dos fármacos
Nefropatias/induzido quimicamente
Masculino
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 31C4KY9ESH (Nitric Oxide); 90Y4QC304K (Ketoprofen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179475


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[PMID]:28632534
[Au] Autor:Rahmania L; Orbegozo D; Su F; Taccone FS; Vincent JL; De Backer D
[Ad] Endereço:From the Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium.
[Ti] Título:Administration of Tetrahydrobiopterin (BH4) Protects the Renal Microcirculation From Ischemia and Reperfusion Injury.
[So] Source:Anesth Analg;125(4):1253-1260, 2017 Oct.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Abdominal aortic aneurysm surgery with suprarenal cross-clamping is often associated with renal injury. Although the mechanism underlying such injury is unclear, tissue ischemia and reperfusion, which induces endothelial dysfunction and decreases the availability of tetrahydrobiopterin (BH4), may play a role. We evaluated whether BH4 administration prevents renal ischemia/reperfusion injury in an animal model of aortic cross-clamping. METHODS: Nineteen anesthetized, mechanically ventilated, and invasively monitored adult sheep were randomized into 3 groups: sham animals (n = 5) that underwent surgical preparation but no aortic clamping; an ischemia/reperfusion group (n = 7), where the aorta was clamped above the renal arteries for 1 hour, and a BH4 group (n = 7), in which animals received 20 mg/kg of BH4 followed by aortic cross-clamp for 1 hour. Animals were followed for a maximum of 6 hours after reperfusion. The renal microcirculation was evaluated at baseline (before clamping), and 1, 4, and 6 hours after reperfusion using side-stream dark field videomicroscopy. The renal lactate-to-pyruvate ratio was evaluated using microdialysis. The primary outcome was the change in proportion of small perfused vessels before and after injury. Secondary outcomes were renal tissue redox state and renal function. RESULTS: Ischemia/reperfusion injury was associated with increases in heart rate and mean arterial pressure, which were blunted by BH4 administration. From the first to the sixth hour after reperfusion, the small vessel density (estimated mean difference [EMD], 1.03; 95% confidence interval [CI], 0.41-1.64; P = .003), perfused small vessel density (EMD, 0.84; 95% CI, 0.29-1.39; P = .005), and proportion of perfused small vessels (EMD, 8.60; 95% CI, 0.85-16.30; P = .031) were altered less in the BH4 than in the ischemia/reperfusion group. The renal lactate-to-pyruvate ratios were lower in the cortex in the BH4 than in the ischemia/reperfusion group from the first to the sixth hour after reperfusion (EMD, -19.16; 95% CI, -11.06 to 33.16; P = .002) and in the medulla from the first to the fourth hour (EMD, -26.62; 95% CI, -18.32 to 38.30; P = .020; and EMD, -8.68; 95% CI, -5.96 to 12.65; P = .019). At the sixth hour, serum creatinine was lower in the BH4 than in the ischemia/reperfusion group (EMD, -3.36; 95% CI, -0.29 to 1.39; P = .026). CONCLUSIONS: In this sheep model of renal ischemia/reperfusion, BH4 pretreatment reduced renal microvascular injury and improved renal metabolism and function. Further work is needed to clarify the potential role of BH4 in ischemia/reperfusion injury.
[Mh] Termos MeSH primário: Biopterina/análogos & derivados
Isquemia/prevenção & controle
Rim/efeitos dos fármacos
Microcirculação/efeitos dos fármacos
Circulação Renal/efeitos dos fármacos
Traumatismo por Reperfusão/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Biopterina/administração & dosagem
Feminino
Isquemia/fisiopatologia
Rim/irrigação sanguínea
Rim/fisiologia
Microcirculação/fisiologia
Substâncias Protetoras/administração & dosagem
Distribuição Aleatória
Circulação Renal/fisiologia
Traumatismo por Reperfusão/fisiopatologia
Ovinos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protective Agents); 22150-76-1 (Biopterin); EGX657432I (sapropterin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000002131


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[PMID]:28617696
[Au] Autor:He X; Su F; Xie K; Taccone FS; Donadello K; Vincent JL
[Ad] Endereço:1Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles, Brussels, Belgium. 2Department of Intensive Care, Sun Yat-sen University Cancer Center, Guangzhou, China. 3Anesthesia and Intensive Care B, Department of Surgery, Dentistry, Pediatrics and Gynecology, University of Verona, AOUI-University Hospital Integrated Trust of Verona, Verona, Italy.
[Ti] Título:Should Hyperoxia Be Avoided During Sepsis? An Experimental Study in Ovine Peritonitis.
[So] Source:Crit Care Med;45(10):e1060-e1067, 2017 Oct.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Optimizing oxygen delivery is an important part of the hemodynamic resuscitation of septic shock, but concerns have been raised over the potentially deleterious effects of hyperoxia. We evaluated the impact of hyperoxia on hemodynamics, the microcirculation, and cerebral and renal metabolism in an ovine model of septic shock. DESIGN: Randomized animal study. SETTING: University hospital animal research laboratory. SUBJECTS: Fourteen adult female sheep. INTERVENTIONS: After induction of fecal peritonitis, sheep were randomized to ventilation with an FIO2 of 100% (n = 7) or an FIO2 adjusted to maintain PaO2 between 90 and 120 mm Hg (n = 7, control). All animals were fluid resuscitated and observed until death. MEASUREMENTS AND MAIN RESULTS: In addition to hemodynamic measurements, we assessed the sublingual microcirculation, renal and cerebral microdialysis and microvascular perfusion, and brain tissue oxygen pressure. Hyperoxic animals initially had a higher mean arterial pressure than control animals. After onset of shock, hyperoxia blunted the decrease in stroke volume index observed in the control group. Hyperoxia was associated with a higher sublingual microcirculatory flow over time, with higher cerebral perfusion and brain tissue oxygen pressure and with a lower cerebral lactate-to-pyruvate ratio than in control animals. Hyperoxia was also associated with preserved renal microvascular perfusion, lower renal lactate-to-pyruvate ratio, and higher PaO2/FIO2 ratio. CONCLUSIONS: In this acute peritonitis model, hyperoxia induced during resuscitation provided better hemodynamics and peripheral microvascular flow and better preserved cerebral metabolism, renal function, and gas exchange. These observations are reassuring with recent concerns about excessive oxygen therapy in acute diseases.
[Mh] Termos MeSH primário: Hiperóxia/fisiopatologia
Peritonite/fisiopatologia
Respiração Artificial/métodos
Choque Séptico/terapia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Circulação Cerebrovascular/fisiologia
Feminino
Ácido Láctico/metabolismo
Microcirculação/fisiologia
Modelos Animais
Oxigênio/sangue
Troca Gasosa Pulmonar/fisiologia
Ácido Pirúvico/metabolismo
Distribuição Aleatória
Circulação Renal/fisiologia
Ovinos
Choque Séptico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
33X04XA5AT (Lactic Acid); 8558G7RUTR (Pyruvic Acid); S88TT14065 (Oxygen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0000000000002524


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[PMID]:28579560
[Au] Autor:Wei J; Song J; Jiang S; Zhang G; Wheeler D; Zhang J; Wang S; Lai EY; Wang L; Buggs J; Liu R
[Ad] Endereço:Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida.
[Ti] Título:Role of intratubular pressure during the ischemic phase in acute kidney injury.
[So] Source:Am J Physiol Renal Physiol;312(6):F1158-F1165, 2017 Jun 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute kidney injury (AKI) induced by clamping of renal vein or pedicle is more severe than clamping of artery, but the mechanism has not been clarified. In the present study, we tested our hypothesis that increased proximal tubular pressure (P ) during the ischemic phase exacerbates kidney injury and promotes the development of AKI. We induced AKI by bilateral clamping of renal arteries, pedicles, or veins for 18 min at 37°C, respectively. P during the ischemic phase was measured with micropuncture. We found that higher P was associated with more severe AKI. To determine the role of P during the ischemic phase on the development of AKI, we adjusted the P by altering renal artery pressure. We induced AKI by bilateral clamping of renal veins, and the P was changed by adjusting the renal artery pressure during the ischemic phase by constriction of aorta and mesenteric artery. When we decreased renal artery pressure from 85 ± 5 to 65 ± 8 mmHg, P decreased from 53.3 ± 2.7 to 44.7 ± 2.0 mmHg. Plasma creatinine decreased from 2.48 ± 0.23 to 1.91 ± 0.21 mg/dl at 24 h after renal ischemia. When we raised renal artery pressure to 103 ± 7 mmHg, P increased to 67.2 ± 5.1 mmHg. Plasma creatinine elevated to 3.17 ± 0.14 mg·dl·24 h after renal ischemia. Changes in KIM-1, NGAL, and histology were in the similar pattern as plasma creatinine. In summary, we found that higher P during the ischemic phase promoted the development of AKI, while lower P protected from kidney injury. P may be a potential target for treatment of AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/fisiopatologia
Pressão Arterial
Isquemia/fisiopatologia
Túbulos Renais/fisiopatologia
Artéria Renal/fisiopatologia
Circulação Renal
Veias Renais/fisiopatologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/patologia
Lesão Renal Aguda/prevenção & controle
Animais
Constrição
Creatinina/sangue
Modelos Animais de Doenças
Receptor Celular 1 do Vírus da Hepatite A/sangue
Isquemia/metabolismo
Isquemia/patologia
Isquemia/prevenção & controle
Túbulos Renais/metabolismo
Túbulos Renais/patologia
Lipocalina-2/sangue
Masculino
Camundongos Endogâmicos C57BL
Artéria Renal/cirurgia
Veias Renais/cirurgia
Índice de Gravidade de Doença
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Havcr1 protein, mouse); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Lipocalin-2); 126469-30-5 (Lcn2 protein, mouse); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00527.2016


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[PMID]:28548006
[Au] Autor:Zhang X; Sun Y; Chen Z; Jing Y; Xu M
[Ad] Endereço:1 Department of Vascular Surgery, The Clinical Medical College of Yangzhou University, Yangzhou, China.
[Ti] Título:Management of Endovascular Aortic Aneurysm Complications via Retrograde Catheterization Through the Distal Stent-Graft Landing Zone.
[So] Source:Vasc Endovascular Surg;51(6):390-393, 2017 Aug.
[Is] ISSN:1938-9116
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: A retrograde technique through the gap between the distal stent landing zone and the iliac artery wall has been applied to treat type II endoleak after endovascular aortic aneurysm repair (EVAR). In this study, we tried to investigate its efficacy in the management of type III endoleak and intraoperative accidental events. METHODS: We reported 2 complications of EVAR that were difficult to treat with conventional methods. One patient had a sustained type III endoleak after EVAR, and the right renal artery was accidentally sealed by a graft stent in the other patient during the operation. RESULTS: Both complications were managed by the retrograde technique from the distal stent landing zone. In the first case, the endoleak was easily embolized by the retrograde catheterization technique, and in the second case, a stent was implanted in the right renal artery using the retrograde technique to restore blood flow. CONCLUSION: In some EVAR cases, the technique of retrograde catheterization through the distal stent-graft landing zone is feasible, safe, and easy to perform.
[Mh] Termos MeSH primário: Implante de Prótese Vascular/efeitos adversos
Implante de Prótese Vascular/instrumentação
Prótese Vascular
Embolização Terapêutica
Endoleak/terapia
Procedimentos Endovasculares
Aneurisma Ilíaco/cirurgia
Obstrução da Artéria Renal/terapia
Stents
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Angiografia por Tomografia Computadorizada
Endoleak/diagnóstico por imagem
Endoleak/etiologia
Procedimentos Endovasculares/instrumentação
Seres Humanos
Aneurisma Ilíaco/diagnóstico por imagem
Masculino
Obstrução da Artéria Renal/diagnóstico por imagem
Obstrução da Artéria Renal/etiologia
Obstrução da Artéria Renal/fisiopatologia
Circulação Renal
Resultado do Tratamento
Grau de Desobstrução Vascular
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1177/1538574417710414



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