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[PMID]: 29524703
[Au] Autor:Liu JKC
[Ad] Address:Department of Neuro-Oncology, Moffitt Cancer Center. Electronic address: james.liu@moffitt.org.
[Ti] Title:Neurological Deterioration Due to Brain Sag Following Bilateral Craniotomy for Subdural Hematoma Evacuation.
[So] Source:World Neurosurg;, 2018 Mar 07.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Intracranial hypotension from cerebrospinal fluid hypovolemia resulting in cerebral herniation is a rare but known complication that can occur following neurosurgical procedures, usually encountered in correlation with perioperative placement of a lumbar subarachnoid drain. Decrease in CSF volume resulting in loss of buoyancy results in downward herniation of the brain without contributing mass effect, causing a phenomenon known as 'brain sag.' Unreported previously is brain sag occurring without concomitant occult CSF leak or lumbar drainage. CASE DESCRIPTION: This case report describes a patient who underwent bilateral craniotomies for subacute on chronic subdural hematomas with successful decompression, but suffered from an acute neurological deterioration secondary to brain sag. Despite an initial improvement in neurological exam, he subsequently exhibited a progressive neurologic deterioration with evidence of cerebral herniation on neuroimaging, without evidence of continued mass effect on the brain parenchyma. After a diagnosis of 'brain sag' was determined based on imaging criteria, the patient was placed in a flat position which resulted in a rapid improvement in neurological exam without any further intervention. CONCLUSIONS: This case is unique from previous reports of intracranial hypotension following craniotomy in that the symptoms were completely reversed with positioning alone, without any evidence of active or occult CSF drainage. This report emphasizes that the diagnosis of brain sag should be taken into consideration when there is an unknown reason for neurologic decline after craniotomy, particularly bilateral craniotomies, if the imaging indicates herniation with imaging findings consistent with intracranial hypotension, without evidence of overlying mass effect.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 59250 MEDLINE  
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[PMID]: 29508455
[Au] Autor:Palma JA; Kaufmann H
[Ad] Address:Department of Neurology, Dysautonomia Center, New York University School of Medicine, New York, New York, USA.
[Ti] Title:Treatment of autonomic dysfunction in Parkinson disease and other synucleinopathies.
[So] Source:Mov Disord;33(3):372-390, 2018 Mar.
[Is] ISSN:1531-8257
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dysfunction of the autonomic nervous system afflicts most patients with Parkinson disease and other synucleinopathies such as dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure, reducing quality of life and increasing mortality. For example, gastrointestinal dysfunction can lead to impaired drug pharmacodynamics causing a worsening in motor symptoms, and neurogenic orthostatic hypotension can cause syncope, falls, and fractures. When recognized, autonomic problems can be treated, sometimes successfully. Discontinuation of potentially causative/aggravating drugs, patient education, and nonpharmacological approaches are useful and should be tried first. Pathophysiology-based pharmacological treatments that have shown efficacy in controlled trials of patients with synucleinopathies have been approved in many countries and are key to an effective management. Here, we review the treatment of autonomic dysfunction in patients with Parkinson disease and other synucleinopathies, summarize the nonpharmacological and current pharmacological therapeutic strategies including recently approved drugs, and provide practical advice and management algorithms for clinicians, with focus on neurogenic orthostatic hypotension, supine hypertension, dysphagia, sialorrhea, gastroparesis, constipation, neurogenic overactive bladder, underactive bladder, and sexual dysfunction. © 2018 International Parkinson and Movement Disorder Society.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1002/mds.27344

  3 / 59250 MEDLINE  
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[PMID]: 29477026
[Au] Autor:Khan K; Saeed S; Ramcharan A; Gray S
[Ad] Address:Department of Surgery, Harlem Hospital Columbia University Medical Center, New York, NY, USA. Electronic address: khank1@nychhc.org.
[Ti] Title:A case series of closed head trauma with pituitary stalk disruption resulting in hypopituitarism.
[So] Source:Int J Surg Case Rep;43:69-71, 2018 Feb 09.
[Is] ISSN:2210-2612
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Traumatic brain injury (TBI) is one of the main causes of morbidity and mortality in young trauma patients with resultant multi-organ effects. Hypopituitarism following TBI can be debilitating and life threatening. TBI which causes hypopituitarism may be characterized by a single head injury, such as from a motor vehicle accident, or by chronic repetitive head trauma, as seen in combative supports including boxing, kick-boxing, and football. In the majority of cases, a diagnosis of hypopituitarism can be entirely missed resulting in severe neuro-endocrine dysfunction. We present a case series of two patients diagnosed with hypopituitarism after TBI and treated appropriately with favorable outcome. CASE PRESENTATIONS: The first case is a 34 year-old male, who presented to the emergency department with blunt head trauma after a motor vehicle accident while riding his bicycle. He suffered from severe cranio-facial injuries, resulting in multifocal hemorrhagic contusions, epidural hematoma, and extensive cranio-facial fractures involving the sinuses. The patient developed persistent hypotension with a blood pressure as low as 60/40 mmHg on hospital day three. The second case is a 56 year-old male with a history of schizophrenia, who suffered traumatic brain injury after he was hit by a train. The patient sustained multiple facial fractures, pneumocephalus and C2/7 transverse processes fractures. He also had persistent hypotension, unresponsive to standard treatment. Investigation revealed a deficiency of anterior pituitary hormones resulting from pituitary axis disruption. DISCUSSION: Hypopituitarism is becoming an increasingly recognized complication following TBI, ranging from total to isolated deficiencies. Traumatic Brain Injury is a major public health problem and is one of the leading causes of disability. Understanding and recognizing pituitary dysfunction after TBI can lead to better outcomes and improved quality of life. CONCLUSION: Patients with major head injury and, in particular, those with fractures of the base of the skull, must be closely monitored for signs and symptoms of endocrine dysfunction. Appropriate dynamic pituitary-function screening should be performed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  4 / 59250 MEDLINE  
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[PMID]: 29410163
[Au] Autor:Bledsoe J; Woller S; Stevens S; Aston V; Patten R; Allen T; Horne B; Dong L; Lloyd J; Snow G; Madsen T; Elliott G
[Ad] Address:Department of Emergency Medicine, Stanford University-Intermountain Medical Center, Salt Lake City, UT. Electronic address: Joseph.bledsoe@imail.org.
[Ti] Title:Management of Low-Risk Pulmonary Embolism Patients Without Hospitalization: The Low-Risk Pulmonary Embolism Prospective Management Study.
[So] Source:Chest;, 2018 Feb 02.
[Is] ISSN:1931-3543
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The efficacy and safety of managing patients with low-risk pulmonary embolism (PE) without hospitalization requires objective data from US medical centers. We sought to determine the 90-day composite rate of recurrent symptomatic VTE, major bleeding events, and all-cause mortality among consecutive patients diagnosed with acute low-risk PE managed without inpatient hospitalization; and to measure patient satisfaction. METHODS: We performed a prospective cohort single-arm management study conducted from January 2013 to October 2016 in five EDs. We enrolled 200 consecutive adults diagnosed with objectively confirmed acute PE and assessed to have a low risk for mortality using the Pulmonary Embolism Severity Index (PESI) score (< 86), echocardiography, and whole-leg compression ultrasound (CUS). The primary intervention was observation in the ED or hospital (observation status) for > 12 to < 24 h, followed by outpatient management with Food and Drug Administration-approved therapeutic anticoagulation. Patients were excluded for a PESI ≥ 86, echocardiographic signs of right heart strain, DVT proximal to the popliteal vein, hypoxia, hypotension, hepatic or renal failure, contraindication to therapeutic anticoagulation, or another condition requiring hospital admission. The primary outcome was 90-day composite rate of all-cause mortality, recurrent symptomatic VTE, and major bleeding. RESULTS: The composite outcome occurred in one of 200 patients (90-day composite rate = 0.5%; 95% CI, 0.02%-2.36%). No patient suffered recurrent VTE or died during the 90-day follow-up period. A major bleed occurred in one patient. Patients indicated a high level of satisfaction with their care. CONCLUSIONS: Treatment of carefully selected patients with acute PE and low risk by PESI < 86, echocardiography, and CUS without inpatient hospitalization is safe and acceptable to patients. Results must be viewed with caution because of the small sample size relative to the end point and the generalizability surrounding availability of emergent echocardiography. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT02355548; URL: www.clinicaltrials.gov.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[Cl] Clinical Trial:ClinicalTrial
[St] Status:Publisher

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[PMID]: 29277639
[Au] Autor:Ekdahl KN; Davoodpour P; Ekstrand-Hammarström B; Fromell K; Hamad OA; Hong J; Bucht A; Mohlin C; Seisenbaeva GA; Kessler VG; Nilsson B
[Ad] Address:Department of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, Uppsala, Sweden; Linnæus Centre for Biomaterials Chemistry, Linnæus University, Kalmar, Sweden. Electronic address: Kristina.Nilsson_Ekdahl@igp.uu.se.
[Ti] Title:Contact (kallikrein/kinin) system activation in whole human blood induced by low concentrations of α-Fe O nanoparticles.
[So] Source:Nanomedicine;14(3):735-744, 2017 Dec 24.
[Is] ISSN:1549-9642
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Iron-oxide nanoparticles (NPs) generated by environmental events are likely to represent health problems. α-Fe O NPs were synthesized, characterized and tested in a model for toxicity utilizing human whole blood without added anticoagulant. MALDI-TOF of the corona was performed and activation markers for plasma cascade systems (complement, contact and coagulation systems), platelet consumption and release of growth factors, MPO, and chemokine/cytokines from blood cells were analyzed. The coronas formed on the pristine α-Fe O NPs contained contact system proteins and they induced massive activation of the contact (kinin/kallikrein) system, as well as thrombin generation, platelet activation, and release of two pro-angiogeneic growth factors: platelet-derived growth factor and vascular endothelial growth factor, whereas complement activation was unaffected. The α-Fe O NPs exhibited a noticeable toxicity, with kinin/kallikrein activation, which may be associated with hypotension and long-term angiogenesis in vivo, with implications for cancer, arteriosclerosis and pulmonary disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 59250 MEDLINE  
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[PMID]: 29180482
[Au] Autor:Pescatello LS; Schifano ED; Ash GI; Panza GA; Corso LML; Chen MH; Deshpande V; Zaleski A; Cilhoroz B; Farinatti P; Taylor BA; O'Neill RJ; Thompson PD
[Ad] Address:Department of Kinesiology, University of Connecticut, Storrs, Connecticut Linda.Pescatello@uconn.edu.
[Ti] Title:Deep-targeted sequencing of endothelial nitric oxide synthase gene exons uncovers exercise intensity and ethnicity-dependent associations with post-exercise hypotension.
[So] Source:Physiol Rep;5(22), 2017 Nov.
[Is] ISSN:2051-817X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In previous studies, we found an endothelial nitric oxide synthase gene ( ) variant rs2070744 associated with the ambulatory blood pressure (BP) response following bouts of moderate and vigorous intensity acute exercise, termed post-exercise hypotension (PEH). In a validation cohort, we sequenced exons for associations with PEH Obese (30.9 ± 3.6 kg m ) African American ( = 14) [AF] and Caucasian ( = 9) adults 42.0 ± 9.8 years with hypertension (139.8 ± 10.4/84.6 ± 6.2 mmHg) performed three random experiments: bouts of vigorous and moderate intensity cycling and control. Subjects were attached to an ambulatory BP monitor for 19 h. We performed deep-targeted exon sequencing with the Illumina TruSeq Custom Amplicon kit. Variant genotypes were coded as number of minor alleles (#MA) and selected for additional statistical analysis based upon Bonferonni or Benjamini-Yekutieli multiple testing-corrected -values under time-adjusted linear models for 19 hourly BP measurements for each subject. After vigorous intensity over 19 h, among variants passing multiple testing thresholds, as the #MA increased in rs891512 ( = 6.4E-04), rs867225 ( = 6.5E-04), rs743507 ( = 2.6E-06), and rs41483644 ( = 2.4E-04), systolic (SBP) decreased from 17.5 to 33.7 mmHg; and in rs891512 ( = 9.7E-05), rs867225 ( = 2.6E-05), rs41483644 ( = 1.6E-03), rs3730009 ( = 2.6E-04), and rs77325852 ( = 5.6E-04), diastolic BP decreased from 11.1 mmHg to 20.3 mmHg among AF only. In contrast, after moderate intensity over 19 h in rs3918164, as the #MA increased, SBP increased by 16.6 mmHg ( = 2.4E-04) among AF only. variants exhibited associations with PEH after vigorous, but not moderate intensity exercise among AF only. should be studied further for its effects on PEH in a large, ethnically diverse sample of adults with hypertension to confirm our findings.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  7 / 59250 MEDLINE  
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[PMID]: 29524326
[Au] Autor:Tanida M; Tao Z; Sun L; Song J; Yang W; Kuda Y; Kurata Y; Shibamoto T
[Ad] Address:Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan.
[Ti] Title:Anaphylactic hypotension causes renal and adrenal sympathoexcitaion and induces c-fos in the hypothalamus and medulla oblongata: Anaphylaxis affects the brain and activates sympathetic nerves.
[So] Source:Exp Physiol;, 2018 Mar 10.
[Is] ISSN:1469-445X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:NEW FINDINGS: What is the central question of this study? Whether anaphylaxis affects sympathetic outflows to the brown adipose tissue (BAT) and adrenal grand is not known. Moreover, it is unknown whether anaphylaxis affects some brain areas in association with sympathetic regulation. What is the main finding and its importance? We showed that sympathoexcitatory responses to anaphylaxis regionally occurred in the kidney and adrenal grand, but not in the thermogenesis-related BAT. Further, anaphylactic hypotension also caused increase in c-fos immunoreactivity in the hypothalamic and medullary areas. Moreover, catecholaminergic neurons of the brain stem causes adrenal sympathoexcitation in a baroreceptor-independent manner. ABSTRACT: We previously reported that sympathetic nerve activity (SNA) to the kidney and the hind limb increases during anaphylactic hypotension in anesthetized rats. Based on this evidence, we examined effects of anaphylactic hypotension on SNA to the brown adipose tissue (BAT), and the adrenal gland and kidney in anesthetized rats. We demonstrated that adrenal and renal SNA, but not BAT-SNA, were stimulated. In addition, the effects of anaphylaxis on neural activities of the hypothalamic and medullary nuclei, which are candidates for relaying efferent SNA to the peripheral organs, were investigated via immunohistochemical staining of c-fos. Anaphylaxis increased c-fos expression in the neurons of the paraventricular nucleus (PVN) of the hypothalamus and in those of the nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM) of the medulla oblongata; c-fos was expressed in gamma-aminobutyric acid (GABA)-ergic neurons of the NTS and in the catecholaminergic neurons of the RVLM. In addition, c-fos expression in the rostral NTS and mid NTS during anaphylaxis were reduced by sinoaortic baroreceptor denervation, however increased c-fos expression in the caudal NTS and RVLM or adrenal sympathoexcitation were not affected by sinoaortic baroreceptor denervation. These results indicated that anaphylactic hypotension activates the hypothalamic PVN, and the medullary NTS and RVLM, independently of the baroreflex pathway. Further, it stimulated efferent SNA to the adrenal grand and kidney to restore blood pressure. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1113/EP086809

  8 / 59250 MEDLINE  
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[PMID]: 29523389
[Au] Autor:Arnold AC; Ng J; Raj SR
[Ad] Address:Department of Neural and Behavioral Sciences, Penn State College of Medicine, 500 University Drive, Mail Code H109, Hershey, PA, USA; Autonomic Dysfunction Center, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA.
[Ti] Title:Postural tachycardia syndrome - Diagnosis, physiology, and prognosis.
[So] Source:Auton Neurosci;, 2018 Feb 28.
[Is] ISSN:1872-7484
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Postural tachycardia syndrome (POTS) is a heterogeneous clinical syndrome that has gained increasing interest over the past few decades due to its increasing prevalence and clinical impact on health-related quality of life. POTS is clinically characterized by sustained excessive tachycardia upon standing that occurs in the absence of significant orthostatic hypotension and other medical conditions and or medications, and with chronic symptoms of orthostatic intolerance. POTS represents one of the most common presentations of syncope and presyncope secondary to autonomic dysfunction in emergency rooms and in cardiology, neurology, and primary care clinics. The most sensitive method to detect POTS is a detailed medical history, physical examination with orthostatic vital signs or brief tilt table test, and a resting 12-lead electrocardiogram. Additional diagnostic testing may be warranted in selected patients based on clinical signs. While the precise etiology remains unknown, the orthostatic tachycardia in POTS is thought to reflect convergence of multiple pathophysiological processes, as a final common pathway. Based on this, POTS is often described as a clinical syndrome consisting of multiple heterogeneous disorders, with several underlying pathophysiological processes proposed in the literature including partial sympathetic neuropathy, hyperadrenergic state, hypovolemia, mast cell activation, deconditioning, and immune-mediated. These clinical features often overlap, however, making it difficult to categorize individual patients. Importantly, POTS is not associated with mortality, with many patients improving to some degree over time after diagnosis and proper treatment. This review will outline the current understanding of diagnosis, pathophysiology, and prognosis in POTS.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 59250 MEDLINE  
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[PMID]: 29505505
[Au] Autor:Zhang ZG; Liu XM
[Ti] Title:A case report with shock induced by tolvaptan in an elderly patient with congestive heart failure.
[So] Source:Medicine (Baltimore);97(1):e8706, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Tolvaptan (TLV) is a new vasopressin type 2 receptor antagonist effective in patients with heart failure (HF). Accumulating evidences have revealed that treatment with TLV does not alter the blood pressure significantly. PATIENT CONCERNS: An 84-year-old man was diagnosed with acute exacerbation of chronic HF due to ischemic cardiomyopathy, arrhythmia, mitral and aortic regurgitation. Treatment with TLV increased the urine volume and improved the dyspnea. After 4 days use of TLV (3.75 mg QD, 7.5 mg QD, 7.5 mg QD, and 15 mg QD, respectively), decrease in blood pressure to less than 90/60 mmHg was observed continuously and the lowest blood pressure was 80/37 mmHg. He was apyretic and felt only thirsty. Central venous pressure was 12 cmH2O. DIAGNOSES: Because no other medications were changed and no signs of hypovolemic, septic, allergic, or cardiac shock were detected, we suspected an adverse reaction to TLV. INTERVENTION: Intravenous hydration was performed with 250 mL of normal saline. OUTCOMES: His blood pressure increased gradually and the statue of hypotention lasted for 14 hours. The dose of TLV was decreased to 7.5 mg/d from the next day to discharge. During this period, his blood pressure was stable at about 125/60 mmHg. LESSONS: TLV has side effect of severe hypotension that is consistent with its physiological activity. The dose should be increased gradually to achieve the desired effect, while attention should be paid to potential drug interactions.
[Mh] MeSH terms primary: Antidiuretic Hormone Receptor Antagonists/adverse effects
Benzazepines/adverse effects
Heart Failure/drug therapy
Shock/chemically induced
[Mh] MeSH terms secundary: Aged, 80 and over
Humans
Male
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Antidiuretic Hormone Receptor Antagonists); 0 (Benzazepines); 21G72T1950 (tolvaptan)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008706

  10 / 59250 MEDLINE  
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[PMID]: 29496565
[Au] Autor:Oliveira-Paula GH; Lacchini R; Pinheiro LC; Ferreira GC; Luizon MR; Garcia WNP; Garcia LV; Tanus-Santos JE
[Ad] Address:Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, SP, Brazil.
[Ti] Title:Endothelial nitric oxide synthase polymorphisms affect the changes in blood pressure and nitric oxide bioavailability induced by propofol.
[So] Source:Nitric Oxide;75:77-84, 2018 Feb 27.
[Is] ISSN:1089-8611
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Propofol anesthesia is usually accompanied by hypotension, which is at least in part related to enhanced endothelial nitric oxide synthase (NOS3)-derived NO bioavailability. We examined here whether NOS3 polymorphisms (rs2070744, 4b/4a VNTR, rs3918226 and rs1799983) and haplotypes affect the changes in blood pressure and NO bioavailability induced by propofol. Venous blood samples were collected from 168 patients at baseline and after 10 min of anesthesia with propofol 2 mg/kg administered intravenously by bolus injection. Genotypes were determined by polymerase chain reaction and haplotype frequencies were estimated. Nitrite concentrations were measured by using an ozone-based chemiluminescence assay, while NOx (nitrites + nitrates) levels were determined by using the Griess reaction. We found that CT + TT genotypes for the rs3918226 polymorphism, the ba + aa genotypes for the 4b/4a VNTR and the CTbT haplotype were associated with lower decreases in blood pressure and lower increases in nitrite levels after propofol anesthesia. On the other hand, the TCbT and CCbT haplotypes were associated with more intense decreases in blood pressure and higher increases in nitrite levels in response to propofol. Our results suggest that NOS3 polymorphisms and haplotypes influence the hypotensive responses to propofol, possibly by affecting NO bioavailability.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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