Hemodynamic effects of one week of carvedilol administration on cirrhotic rats

H, Lin; Huang, Yo-Ping; Wei, Hung-Chi; Yang, Ying‐Ying; Lee, Tzung-Yan; Wang, Yingwen; Hou, Ming‐Chih; Lee, Shou‐Dong

doi:10.1007/s00535-006-1782-5

Cited by 12 publications

(8 citation statements)

References 41 publications

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“…Carvedilol may be the optimal choice for beta-blockade in patients with ESLD. It has been demonstrated to cause a reduction in portal pressure through decreased splanchnic blood flow and decreased portocollateral resistance (66,67). Carvedilol has also been shown to be superior to other beta-blocking agents in reducing the hepatic venous pressure gradient (66,68).…”

Section: Pre-operative Cardiovascular Assessment and Managementmentioning

confidence: 98%

Cardiovascular Risk Assessment of the Liver Transplant Candidate

Raval

Harinstein

Skaro

et al. 2011

Journal of the American College of Cardiology

229

174

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Liver transplantation (LT) candidates today are increasingly older, have greater medical acuity, and have more cardiovascular comorbidities than ever before. Steadily rising model for end-stage liver disease (MELD) scores at the time of transplant, resulting from high organ demand, reflect the escalating risk profiles of LT candidates. In addition to advanced age and the presence of comorbidities, there are specific cardiovascular responses in cirrhosis that can be detrimental to the LT candidate. Patients with cirrhosis requiring LT usually demonstrate increased cardiac output and a compromised ventricular response to stress, a condition termed cirrhotic cardiomyopathy. These cardiac disturbances are likely mediated by decreased beta-agonist transduction, increased circulating inflammatory mediators with cardiodepressant properties, and repolarization changes. Low systemic vascular resistance and bradycardia are also commonly seen in cirrhosis and can be aggravated by beta-blocker use. These physiologic changes all contribute to the potential for cardiovascular complications, particularly with the altered hemodynamic stresses that LT patients face in the immediate post-operative period. Post-transplant reperfusion may result in cardiac death due to a multitude of causes, including arrhythmia, acute heart failure, and myocardial infarction. Recognizing the hemodynamic challenges encountered by LT patients in the perioperative period and how these responses can be exacerbated by underlying cardiac pathology is critical in developing recommendations for the pre-operative risk assessment and management of these patients. The following provides a review of the cardiovascular challenges in LT candidates, as well as evidence-based recommendations for their evaluation and management.

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Section: Pre-operative Cardiovascular Assessment and Managementmentioning

confidence: 98%

Cardiovascular Risk Assessment of the Liver Transplant Candidate

Raval

Harinstein

Skaro

et al. 2011

Journal of the American College of Cardiology

229

174

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“…All rats were anesthetized with 100 mg/kg ketamine. PVP and Q SMA were then measured [22,23]. Additionally, blood samples were collected for liver function (ALT, AST, ALKP, cGT and total bilirubin) measurements.…”

Section: Experiments 1: Hemodynamic and Liver Function Measurementsmentioning

confidence: 99%

Effects of N-acetylcysteine administration in hepatic microcirculation of rats with biliary cirrhosis

Yang

Lee

Huang³

et al. 2008

Journal of Hepatology

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“…The effect of reduced intrahepatic resistance may have an additional portal hypotensive effect. Animal studies using bile duct ligated rats have shown that carvedilol reduces portocollateral resistance and endothelial-related vasodilatation in the splanchnic circulation because of reduced expression of eNOS [36]. The effect of carvedilol on the splanchnic circulation probably reflects a dynamic interplay between a receptor-mediated vasoconstriction and endothelial-related vasodilatation, with the net effect being splanchnic vasoconstriction.…”

Section: Introductionmentioning

confidence: 97%

“…Potentially, the beneficial effects of unopposed a receptor stimulation on the splanchnic circulation may be somewhat less with carvedilol. However, animal studies have shown that splanchnic blood flow is reduced with carvedilol [36]. This may reflect the relatively weak and incomplete a blocking actions of carvedilol on the splanchnic circulation, not enough to counteract the strong blockade of b 2 receptors.…”

Section: Introductionmentioning

confidence: 97%

The role of carvedilol in the management of portal hypertension

Tripathi

Hayes

2010

European Journal of Gastroenterology & Hepatology

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Carvedilol is a potent noncardioselective beta-blocker, with weak vasodilating properties because of alpha 1 blockade. A reduction in both intrahepatic and portocollateral resistance contribute to enhanced effects on portal pressure. There are 10 published hemodynamic studies involving 168 patients investigating the role of carvedilol in portal hypertension. A reduction in the hepatic venous pressure gradient of up to 43% (range 10-43%) has been reported, particularly after chronic administration. However, tolerability at doses greater than 12.5 mg/day was comprised because of a fall in mean arterial pressure (MAP), particularly in ascitic patients. Carvedilol was more effective than propranolol in reducing hepatic venous pressure gradient in two of three studies, albeit with a greater decrease in MAP. One study showed deterioration of pre-existing ascites with carvedilol. The addition of nitrates to propranolol was less effective than carvedilol monotherapy in another study. A large multicentre, randomized controlled trial comparing carvedilol with variceal band ligation for the prevention of variceal bleeding has been published. Carvedilol resulted in fewer episodes of bleeding, although there was no difference in survival. Carvedilol was well tolerated. Carvedilol is a promising agent, and seems to be more effective than propranolol in hemodynamic studies. The efficacy in primary prevention of variceal bleeding suggests that carvedilol has a role in the management of clinically significant portal hypertension.

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Hemodynamic effects of one week of carvedilol administration on cirrhotic rats

Abstract: Carvedilol decreased portal pressure through a reduction of splanchnic blood flow associated with a decrease in hepatocollateral resistance. Additionally, administration of carvedilol decreased endothelial-related vasodilatory activities.

Cited by 12 publications

References 41 publications

Cardiovascular Risk Assessment of the Liver Transplant Candidate

Cardiovascular Risk Assessment of the Liver Transplant Candidate

Effects of N-acetylcysteine administration in hepatic microcirculation of rats with biliary cirrhosis

The role of carvedilol in the management of portal hypertension

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