The effect of non-protein liquid meals on the hepatic venous pressure gradient in patients with cirrhosis

McCormick, P. Aiden; Dick, Robert; Graffeo, M; Wagstaff, D; Madden, Angela; McIntyre, Neil; Burroughs, Andrew K.

doi:10.1016/0168-8278(90)90117-a

Cited by 53 publications

(25 citation statements)

References 10 publications

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“…14,19 On the other hand, several recent studies have shown that the increased HVPG observed in portal hypertensive cirrhotic patients is not stable, but is significantly modified by several physiological stimuli. Thus, HVPG is significantly increased after a meal, 20 which has been suggested to play a key role in promoting a progressive dilatation of the varices and bleeding, as well as in aggravating the bleeding episode and promoting early rebleeding. 21 More recently, we described a daily variation of HVPG (following a circadian rhythm) in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Effects of propranolol on the hepatic hemodynamic response to physical exercise in patients with cirrhosis

et al. 1998

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Physical exercise increases portal pressure (hepatic venous pressure gradient [HVPG]) in patients with cirrhosis.It is unknown if this deleterious effect is associated with changes in gastroesophageal collateral blood flow and if these can be prevented by propranolol administration. The aim of this study was to characterize the effects of propranolol on the splanchnic hemodynamic response to exercise in patients with cirrhosis. Twenty-three patients with cirrhosis and portal hypertension had hemodynamic measurements in baseline conditions, and during moderate cycling exercise (40 W) under double-blind propranolol or placebo administration. In patients receiving placebo, HVPG significantly increased during exercise (from 16.7 ؎ 0.9 to 19.0 ؎ 1.0 mm Hg; P F .01), hepatic blood flow (HBF) decreased (-18% ؎ 4%; P F .01), while azygos blood flow (AzBF) was unchanged (4% ؎ 12%; ns). In patients receiving propranolol, portal pressure did not increase during exercise, but decreased from 16.3 ؎ 1.0 to 12.9 ؎ 1.1 mm Hg (P F .01). The lack of increase in HVPG in response to exercise in patients receiving propranolol may be related to a more pronounced decrease in HBF, as compared with patients receiving placebo, and to a blunted increase in cardiac output (CO). Moderate physical exercise adversely influences the hepatic hemodynamics in patients with cirrhosis, causing a significant increase in portal pressure. This is effectively prevented by propranolol pretreatment. (HEPATOL-OGY 1998;28:677-682.)

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Section: Discussionmentioning

confidence: 99%

Effects of propranolol on the hepatic hemodynamic response to physical exercise in patients with cirrhosis

et al. 1998

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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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“…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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The effect of non-protein liquid meals on the hepatic venous pressure gradient in patients with cirrhosis

Cited by 53 publications

References 10 publications

Effects of propranolol on the hepatic hemodynamic response to physical exercise in patients with cirrhosis

Effects of propranolol on the hepatic hemodynamic response to physical exercise 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

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