Hyperglucagonemia and hyperkinetic circulation after portocaval shunt in the rat

Kravetz, David; Arderiu, M T; Bosch, J.; Fuster, Josep; Visa, J; Casamitjana, R.; Rodés, Juan

doi:10.1152/ajpgi.1987.252.2.g257

Cited by 28 publications

(25 citation statements)

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“…The hypothesis of ADH hyposecretion by PCS rats is supported by the fact that homozygous rats with hereditary diabetes in sipidus also manifest dramatic polyuria and excrete 80% less prostaglandins than con trols [12]. On the other hand, we have found plasma glucagon levels 3 times greater in PCS than in control rats [ 13], agreeing with other authors [14], Among the actions of this hormone an increase in glomerular filtration rate and diuresis can be included [15]. Thus, hyperglucagonemia of PCS rats may contrib ute to the aforementioned renal function de rangements.…”

Section: Discussionsupporting

confidence: 92%

Renal Function Derangements Induced by Portacaval Anastomosis in Normal Rats

Romeo

López‐Farré²,

Martín‐Paredero³

et al. 1991

Eur Surg Res

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The purpose of this study was to determine the renal function derangements that portacaval shunting caused in previously normal rats. Eight rats suffered a surgical portacaval shunt (PCS) and another 8 a sham operation (SHAM). Renal function was investigated by determining urinary volume, sodium, potassium, creatinine and aldosterone excretion, in basal conditions and after sodium overload. Plasma renin concentration and urinary excretion of PGE₂, 6-keto-PGF_1α and TXB₂ were also determined in basal conditions. PCS rats showed increased urinary volume, creatinine excretion and endogenous creatinine clearance, either in basal conditions or after sodium load. After the latter, PCS animals also showed sodium retention and hyperaldosteronuria. PCS caused in basal conditions a striking diminution in urinary excretion of all prostaglandins and no changes in plasma renin. In conclusion, PCS in the normal rat caused a renal dysfunction consisting of polyuria, possibly related to ADH disfunction and an inability to manage a sodium load.

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Section: Discussionsupporting

confidence: 92%

Renal Function Derangements Induced by Portacaval Anastomosis in Normal Rats

Romeo

López‐Farré²,

Martín‐Paredero³

et al. 1991

Eur Surg Res

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“…This would have advantages over the commonly used drugs for portal hypertension in which a reduction of portal pressure is commonly associated with a decrease in hepatic perfusion. 41 With an increase in PVBF by mechanical pumping, it may be envisaged that the cardiac output would increase as found with portocaval shunts, 42 worsening the abnormal systemic and splanchnic hemodynamics found in portal hypertension. However, in this study a 3-hour period of augmented portal flow produced no significant alternations in the systemic hemodynamics, including mean arterial blood pressure, heart rate, body temperature, and oxygen saturation.…”

Section: Discussionmentioning

confidence: 99%

The effect of mechanically enhancing portal venous inflow on hepatic oxygenation, microcirculation, and function in a rabbit model with extensive hepatic fibrosis

et al. 1999

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Enhancing the portal venous blood flow (PVBF) has been shown to reduce portal pressure and intrahepatic vascular resistance and to improve liver function in isolated cirrhotic rodent livers in vitro. The aim of this study was to assess the short-term effect of mechanically pumping the portal inflow on hepatic microcirculation (HM), oxygenation, and function in an animal model of extensive hepatic fibrosis. New Zealand white rabbits underwent laparotomy and exposure of the liver: group 1 (n ‫؍‬ 7) were normal controls; group 2 (n ‫؍‬ 7) had hepatic fibrosis. Total hepatic blood flow (THBF) and HM was measured along with continuous monitoring of intrahepatic tissue oxygenation using near infrared spectroscopy (NIRS). Baseline hepatic hemodynamics and liver function were measured in both groups. PVBF was then increased by 50% over a 3-hour period in the hepatic fibrosis group using a miniature portal pump designed for human implantation, and the hemodynamics were monitored continuously. Liver function tests were repeated after portal pumping. In comparison with normal controls, animals with hepatic fibrosis had a higher portal pressure (13.0 ؎ 3.6 vs. 3.7 ؎ 1.4 mm Hg, P F .001, mean ؎ SD vs. controls), reduced PVBF (52.4 ؎ 24.6 vs. 96.9 ؎ 21.1 mL/min, P ‫؍‬ .003), and increased portal vascular resistance (P ‫؍‬ .001). THBF and flow in the HM was lower than in controls, and liver function tests were abnormal. After a 3-hour period of enhanced portal flow in animals with hepatic fibrosis, the portal pressure greatly reduced (13.0 ؎ 3.6 to 2.5 ؎ 1.1 mm Hg, P F .001) as did the intrahepatic portal resistance ( Current aims in the management of portal hypertension are to reduce portal venous pressure (PVP), to increase blood flow through hepatic parenchyma, 1 and to decompress esophageal and gastric varices. 2,3 Reduction of PVP minimizes the risk of bleeding from varices, the likelihood of hepatic encephalopathy and problems relating to first pass uptake of drugs. 4 Reduced portal pressure also decreases intestinal venous congestion and could increase blood flow through the hepatic parenchyma and hence increase liver function. 5 In 1991, Habib et al. 6 first introduced the concept of mechanical pumping of portal blood to enhance hepatic portal inflow. Since then, we have seen a number of publications in this field. 7-10 Cardoso et al. [7][8][9] showed that augmenting portal inflow to isolated perfused cirrhotic rat and human livers decreased intrahepatic resistance without a change in intrahepatic shunting and resulted in liver function improvement. Bernadich et al. 10 found that in rats with portal hypertension owing to portal vein stenosis, mechanical portal pumping decreased portal pressure and portal-systemic shunting without having a significant effect on systemic hemodynamics. In cirrhosis, several early studies provided evidence that it was vasoactive mediators coupled with the extensive destruction of hepatocytes and nodular regeneration that contributed to the pathogenesis of portal hypertension. [11][12][13]...

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“…The techniques used for the hemodynamic measurements have been previously described (6,7,9,14). Briefly, the rats were anesthetized with ketamine-HC1 (100 mg per kg body weight i.m.).…”

Section: Methodsmentioning

confidence: 99%

Propranolol Decreases Portal Pressure Without Changing Portocollateral Resistance in Cirrhotic Rats

et al. 1989

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Propranolol decreases portal pressure by reducing portal blood inflow. Studies in rats with prehepatic portal hypertension due to portal vein stenosis (a model with extensive portosystemic shunting) have shown that propranolol increases the portocollateral resistance, which hinders the fall in portal pressure. The present study examined the effects of propranolol on splanchnic and systemic hemodynamics in rats with portal hypertension due to cirrhosis of the liver, a model which is characterized by mild portosystemic shunting. Two groups of rats with CCl4-induced cirrhosis were studied: the propranolol group (n = 8), which received a propranolol infusion of 2 mg per 15 min, and controls (n = 9), which received a placebo (saline) infusion. Hemodynamic measurements were done using radiolabeled microspheres. Propranolol-treated rats had significantly lower cardiac output (-31%) and heart rate (-26%) than controls (p less than 0.001). Hepatic artery flow was not modified by propranolol. Propranolol caused splanchnic vasoconstriction, manifested by increased splanchnic resistance (+57%) and by a significant fall in portal blood inflow (4.8 +/- 0.4 vs. 6.3 +/- 0.5 ml per min.100 gm in controls, p less than 0.05). In contrast with rats with prehepatic portal hypertension, propranolol did not increase portal resistance in cirrhotic rats [2.0 +/- 0.2 vs. 2.0 +/- 0.1 mmHg per ml per min.100 gm body weight (not significant)]. Hence, the fall in portal pressure (-19%) was expected from the decrease in portal inflow (-24%). These results suggest that increased portal resistance in rats with prehepatic portal hypertension may represent an intrinsic effect of propranolol on the portocollateral vessels, since beta-blockade does not modify portal vascular resistance in cirrhosis.

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Hyperglucagonemia and hyperkinetic circulation after portocaval shunt in the rat

Cited by 28 publications

References 0 publications

Renal Function Derangements Induced by Portacaval Anastomosis in Normal Rats

Renal Function Derangements Induced by Portacaval Anastomosis in Normal Rats

The effect of mechanically enhancing portal venous inflow on hepatic oxygenation, microcirculation, and function in a rabbit model with extensive hepatic fibrosis

Propranolol Decreases Portal Pressure Without Changing Portocollateral Resistance in Cirrhotic Rats

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