Hemodynamic evaluation of octreotide in patients with hepatitis B-related cirrhosis

Lin, Han‐Chieh; Tsai, Yang‐Te; Lee, Fa-Yauh; Lee, Shou‐Dong; Hsia, Hsiao-Chung; Lin, Wen-Jeh; Lo, Kwang‐Juei

doi:10.1016/0016-5085(92)91117-m

Cited by 79 publications

(56 citation statements)

References 29 publications

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“…Some studies found that the acute administration of OCT decreases portal pressure 25 but most studies failed to achieve such beneficial effects. 26,27 OCT has been shown to prevent postprandial increase in portal pressure in stable cirrhotics but its practical role in BEVs is still unclear. 28 Furthermore, a previous study found that OCT injection in cirrhotic patients caused marked but transient reductions in portal pressure and azygos blood flow because of rapid development of desensitization.…”

Section: Discussionmentioning

confidence: 99%

Clinical trial: the effect of somatostatin vs. octreotide in preventing post‐endoscopic increase in hepatic venous pressure gradient in cirrhotics with bleeding varices

Vlachogiannakos

Kougioumtzian

Triantos

et al. 2007

Aliment Pharmacol Ther

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Section: Discussionmentioning

confidence: 99%

Clinical trial: the effect of somatostatin vs. octreotide in preventing post‐endoscopic increase in hepatic venous pressure gradient in cirrhotics with bleeding varices

Vlachogiannakos

Kougioumtzian

Triantos

et al. 2007

Aliment Pharmacol Ther

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“…sistance, were not affected. [7][8][9][10][11] The mechanism of action Plasma glucagon levels were decreased in portal vein-of octreotide in portal hypertension has not been docustenosed rats receiving either long-term or 1-day octreo-mented. No systemic and regional hemodynamic data tide compared with rats receiving placebo.…”

mentioning

confidence: 99%

Effects of long-term administration of octreotide in portal vein-stenosed rats

LIN

1996

Hepatology

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vein-stenosed rats without affecting the degree of mesThe hemodynamic effects of long-term administration enteric-systemic shunts. (HEPATOLOGY 1996;23:537-543.) of octreotide in portal hypertension has not been established. In addition, whether long-term octreotide treatment prevents the development of portosystemic shuntsOctreotide is a synthetic long-acting analog of sohas not yet been evaluated. Hence, the current study matostatin. 1 This drug has been shown to have potenwas undertaken to evaluate the effects of long-term ad-tial beneficial effects in the management of acute hemministration of octreotide in rats with portal vein steno-orrhage from esophageal varices. 2-4 Hemodynamic sis. Immediately after portal vein stenosis or sham oper-studies in portal hypertensive animals showed that ation, rats were given either a long-term octreotide acute intravenous infusion of octreotide resulted in a administration of 100 mg/kg or a placebo every 12 hours dose-dependent decrease in portal pressure associated by subcutaneous injection for 14 consecutive days. Systemic hemodynamics and regional blood flows, degree with increases in vascular resistances, indicating vasoof mesenteric-systemic shunts, and plasma glucagon constrictive effects of octreotide. 5 In addition, in portal concentrations were measured after the final dose of vein-stenosed rats, a 4-day course of octreotide treatoctreotide or placebo. A fifth group of portal vein-ste-ment starting at the time of portal vein stenosis amelionosed rats received hemodynamic and plasma glucagon rated vasodilatation and sodium retention. 6 However, measurements after 1-day octreotide treatment given at in cirrhotic patients, short-term administration of oc-14 days after surgery. Long-term octreotide treatment treotide markedly decreased hepatic and azygous blood modified the hyperdynamic circulation without affect-flows with minimal effect on portal pressure, and the ing the degree of mesenteric-systemic shunts, and 1-day systemic hemodynamic values, including cardiac outoctreotide treatment decreased portal tributary blood put, mean arterial pressure, and systemic vascular reflow without affecting the portal pressure, systemic hemodynamics, and degree of mesenteric-systemic shunts. sistance, were not affected. [7][8][9][10][11] The mechanism of action Plasma glucagon levels were decreased in portal vein-of octreotide in portal hypertension has not been docustenosed rats receiving either long-term or 1-day octreo-mented. No systemic and regional hemodynamic data tide compared with rats receiving placebo. In contrast, have yet been reported after long-term administration chronic octreotide treatment did not affect any of the of octreotide in portal hypertensive animals. Moreover, hemodynamic values or plasma glucagon levels in sham-whether chronic octreotide treatment prevents the deoperated rats. In conclusion, long-term administration velopment of portosystemic shunts, as shown by other of octreotide modified in part the development of portal vasoactive drugs such as ...

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“…The exact mechanisms of the hemodynamic changes in response to octreotide are partly unknown, 1 and only a transient or no effect on hepatic venous pressure gradient (HVPG) has been demonstrated. [2][3][4][5][6] Lately, a marked increase of lower esophageal sphincter pressure has been described in response to intravenous octreotide in portal hypertensive patients in addition to a sustained suppression of postprandial splanchnic hyperemia. 3,[7][8][9] These effects coincide with a reduction of plasma glucagon, 8,9 and this mechanism has been thought to be responsible for the suppression of splanchnic hyperemia.…”

mentioning

confidence: 99%

Effects of a long-acting formulation of octreotide on renal function and renal sodium handling in cirrhotic patients with portal hypertension: A randomized, double-blind, controlled trial

et al. 2001

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Octreotide has been widely used for controlling acute variceal bleeding in cirrhotic patients. The exact mechanisms of the hemodynamic changes in response to octreotide are partly unknown, 1 and only a transient or no effect on hepatic venous pressure gradient (HVPG) has been demonstrated. [2][3][4][5][6] Lately, a marked increase of lower esophageal sphincter pressure has been described in response to intravenous octreotide in portal hypertensive patients in addition to a sustained suppression of postprandial splanchnic hyperemia. 3,7-9 These effects coincide with a reduction of plasma glucagon, 8,9 and this mechanism has been thought to be responsible for the suppression of splanchnic hyperemia. However,

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Hemodynamic evaluation of octreotide in patients with hepatitis B-related cirrhosis

Cited by 79 publications

References 29 publications

Clinical trial: the effect of somatostatin vs. octreotide in preventing post‐endoscopic increase in hepatic venous pressure gradient in cirrhotics with bleeding varices

Clinical trial: the effect of somatostatin vs. octreotide in preventing post‐endoscopic increase in hepatic venous pressure gradient in cirrhotics with bleeding varices

Effects of long-term administration of octreotide in portal vein-stenosed rats

Effects of a long-acting formulation of octreotide on renal function and renal sodium handling in cirrhotic patients with portal hypertension: A randomized, double-blind, controlled trial

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