Octreotide prevents postprandial splanchnic hyperemia in patients with portal hypertension

Albillos, Agustı́n; Rossi, Irma; Iborra, Jerónimo; Lledó, José Luis; Calleja, José Luís; Barrios, C.; Garcı́a, Pilar López; Escartín, P

doi:10.1016/s0168-8278(94)80142-8

Cited by 71 publications

(36 citation statements)

References 26 publications

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“…The systemic and splanchnic response to the test meal was evaluated at 30 minutes, when maximal postprandial hyperemia and increase in HVPG has been demonstrated to occur. [17][18][19][20] HVPG was also measured at 15 minutes.…”

Section: Methodsmentioning

confidence: 99%

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

et al. 2010

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Presence of bacterial DNA in noninfected patients with cirrhosis and ascites is associated with a marked inflammatory response including activation of the inducible form of nitric oxide synthase and release of nitric oxide, similar to that observed in patients with spontaneous bacterial peritonitis. Although presence of bacterial DNA is associated with an impaired prognosis, no information is available regarding its hemodynamic consequences. Systemic and hepatic hemodynamics before and after a liquid test meal were assessed in a series of 75 noninfected patients with cirrhosis (55 with ascites). Bacterial DNA was measured by polymerase chain reaction. Bacterial DNA was detected only in patients with ascites. Clinical data and liver function were similar in ascitic patients with presence (n 5 21) or absence of bacterial DNA (n 5 34). Bacterial-DNA(1) patients had significantly lower mean arterial pressure (P 5 0.002) and systemic vascular resistance (P 5 0.03) than bacterial-DNA(2) patients. Cardiac output, cardiopulmonary pressures, hepatic venous pressure gradient (HVPG), and hepatic blood flow were similar in both groups. Thirty minutes after the test meal, in response to increased blood flow caused by postprandial hyperemia, there was a significantly greater increase in HVPG and impaired hepatic vasorelaxation in bacterial-DNA(1) as compared with bacterial-DNA(2) patients, which indicates hepatic endothelial dysfunction. Indeed, the increase in HVPG after the test meal significantly correlated with serum bacterial DNA concentration. Conclusion: Presence of bacterial DNA, a marker of bacterial translocation, is associated with aggravation of peripheral vasodilation and with worsening of intrahepatic endothelial dysfunction. (HEPATOLOGY 2010;52:2044-2052 P ortal hypertension is a serious consequence of cirrhosis that can result in life-threatening complications with increased mortality and morbidity.1 The primary factor in the pathophysiology of portal hypertension is increased intrahepatic resistance to portal-collateral blood flow. Portal hypertension is further aggravated by increased portal venous inflow, caused by splanchnic vasodilation. Moreover, insufficient nitric oxide (NO) availability in the hepatic microcirculation is considered an important factor that contributes to increase the hepatic vascular resistance. Because of this, the cirrhotic liver, unlike the normal liver, cannot vasodilate in response to a volume flow load such as that caused by meals, which results in abrupt postprandial increases in portal pressure, a concept known as intrahepatic endothelial dysfunction. [2][3][4][5]

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Section: Methodsmentioning

confidence: 99%

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

et al. 2010

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“…The systemic and splanchnic response to the test meal was evaluated at 30 minutes, when maximal postprandial hyperemia and increase in HVPG has been demonstrated to occur. [27][28][29] HVPG was also measured at 15 minutes.…”

Section: Methodsmentioning

confidence: 99%

Ascorbic acid improves the intrahepatic endothelial dysfunction of patients with cirrhosis and portal hypertension

et al. 2006

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Patients with cirrhosis show intrahepatic endothelial dysfunction, characterized by an impaired flow-dependent vasorelaxation. This alteration is responsible for the marked postprandial increase in portal pressure and is attributed to an insufficient release of nitric oxide (NO). Ascorbic acid reverts endothelial dysfunction in other vascular disorders, via the increase of NO bioavailability through the neutralization of superoxide anions, thus preventing the scavenging of NO by superoxide. This study examined whether acute ascorbic acid administration might improve endothelial dysfunction in cirrhosis. Thirty-seven portal hypertensive patients with cirrhosis had measurements of hepatic and systemic hemodynamics, ascorbic acid, and malondialdehyde (MDA). Patients were randomly allocated to receive ascorbic acid (3 g, intravenously, n ‫؍‬ 15) or placebo (n ‫؍‬ 12) followed by a liquid meal. A third group received ascorbic acid followed by a sham meal (n ‫؍‬ 10). Measurements were repeated after 30 minutes (hepatic venous pressure gradient at 15 and 30 minutes). Patients with cirrhosis had significantly lower ascorbic acid levels and higher MDA than healthy controls. Ascorbic acid significantly reduced MDA levels and markedly attenuated the postprandial increase in the hepatic venous pressure gradient (4% ؎ 7% vs. 18% ؎ 10% in placebo at 30 minutes, P < .001). Ascorbic acid followed by sham meal did not modify hepatic or systemic hemodynamics. In conclusion, patients with cirrhosis exhibited intrahepatic endothelial dysfunction, associated with decreased levels of ascorbic acid and increased levels of MDA. Ascorbic acid improved intrahepatic endothelial dysfunction, blunting the postprandial increase in portal pressure. These results encourage the performance of further studies testing antioxidants as adjunctive therapy in the treatment of portal hypertension. (HEPATOLOGY 2006;43:485-491.) P ortal hypertension is a serious consequence of cirrhosis and can result in life-threatening complications with increased mortality and morbidity. 1 Portal hypertension is determined by an increased resistance to portal-collateral blood flow and aggravated by an increased portal venous inflow, caused by splanchnic vasodilatation. 2 The primary factor in the pathophysiology of portal hypertension is increased resistance. 3 In cirrhosis, the increase in resistance occurs at the level of the hepatic microcirculation and is promoted by the morphological changes occurring in chronic liver diseases. In addition, the active contraction of different cell types that are able to constrict or relax in a reversible and graded manner in response to several stimuli promote a further increase or decrease in the intrahepatic resistance. 4 Insufficient nitric oxide (NO) production is considered a major pathogenic factor increasing intrahepatic vascular tone in cirrhosis. [5][6][7] The increased vascular tone is From the

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“…In the light of our results, we can hypothesize that other physiologic situations known to transiently increase portal pressure and/or AzBF, such as moderate physical exercise 11,12 or meals, [13][14][15][16][17][18][19][20] may cause significant increases in variceal pressure. It is of interest to note that propranolol therapy has been shown to prevent the changes in HVPG associated with moderate exercise.…”

Section: Discussionmentioning

confidence: 96%

Increasing intra-abdominal pressure increases pressure, volume, and wall tension in esophageal varices

et al. 2002

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Many daily activities cause acute elevations of intra-abdominal pressure (IAP). In portal hypertensive cirrhotic patients, increased IAP increases absolute portal pressure and azygos blood flow, suggesting that it may have detrimental consequences at the esophageal varices. The aim of this study was to investigate the effects of increased IAP on variceal pressure, size, and wall tension. Endosonography and a noninvasive endoscopic pressure gauge were used to measure variceal pressure, radius, wall tension, and volume in baseline conditions and after increasing IAP by 10 mm Hg using an inflatable girdle in 14 patients with cirrhosis and esophageal varices. Increasing IAP markedly increased variceal pressure (from 13.3 ؎ 4.2 to 17.4 ؎ 4.6 mm Hg; P ‫؍‬ .0001) and radius (from 2.9 ؎ 1.0 to 3.9 ؎ 1.1 mm; P ‫؍‬ .0001). Consequently, wall tension dramatically increased (from 38.7 ؎ 13.6 to 65.9 ؎ 23.8 mm Hg ⅐ mm, ؉78%; P ‫؍‬ .0001). Variceal volume increased significantly from 1,264 ؎ 759 to 2,025 ؎ 1,129 mm 3 (P ‫؍‬ .0001). In conclusion, in portal hypertensive cirrhotic patients, increases in IAP have deleterious effects on variceal hemodynamics, markedly increasing the volume, pressure, and wall tension of the varices. Increases in IAP may contribute to the progressive dilatation that precedes the rupture of the varices in portal hypertension. V ariceal wall tension is thought to represent the key factor determining variceal rupture. 1,2 Wall tension is the inwardly directed force that opposes the expanding force that the increased intravascular pressure and blood flow exert on the variceal wall. 1 It is calculated by Frank's modification of Laplace's law, as the transmural pressure at the varices (the difference between intravariceal and esophageal luminal pressures) times the radius of the varix, divided by the thickness of the variceal wall. 1 Several efforts have been made to obtain objective measurements of variceal wall tension. In that regard, we have previously shown that the combination of endosonography and endoscopic measurement of transmural variceal pressure allows a quantitative, objective, and reproducible estimation of variceal wall tension. 3 In addition, endosonography allows for estimation of variceal volume in the distal esophagus. 3 Elevations of intra-abdominal pressure (IAP) in cirrhotic patients have significant effects on both the systemic and the splanchnic circulation. A previous study from our laboratory showed that brief mechanical elevations of IAP increased azygos blood flow (AzBF), an index of gastroesophageal collateral blood flow, and the absolute portal pressure, estimated by the wedged hepatic venous pressure. 4 Therefore, an elevated IAP may be associated with acute increments of both variceal pressure and variceal blood flow.Moreover, Kravetz et al. 5 showed that in cirrhotic patients with ascites releasing an increased IAP by means of total volume paracentesis decreased intravariceal pressure. These effects of total volume paracentesis may be related to a significant decrease ...

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Octreotide prevents postprandial splanchnic hyperemia in patients with portal hypertension

Cited by 71 publications

References 26 publications

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

Ascorbic acid improves the intrahepatic endothelial dysfunction of patients with cirrhosis and portal hypertension

Increasing intra-abdominal pressure increases pressure, volume, and wall tension in esophageal varices

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