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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical features, surgical management, and long term follow up of 32 patients from Iran with idiopathic portal hypertension are reported. Many features of the disease are similar to those reported from India and Japan. The unsuspected finding was a 46% history of marked pica of clay (geophagia) in a subset of 26 patients. In addition, 81% of our patients had a prolonged prothrombin time, despite otherwise normal to minimally abnormal liver function tests. Liver biopsies revealed intrahepatic periportal fibrosis with subintimal thickening of terminal branches, and in many specimens a striking peri-ductular fibrosis was seen in the adjacent bile ducts. The spleen was very large with a dilated artery (external diameter: 11 mm to 15 mm). Portal venous pressure (PVP) was measured intra-operatively before and after clamping the splenic artery (SA). Clamping the SA consistently caused a decreased in PVP which ranged from 2.0 to 18.2 cm water with the mean +/- SEM of 9.7 +/- 1.5 cm water (p < 0.001, paired t-test). It was equivalent to 32.3 +/- 3.6% decrease in PVP. Fifteen selected patients (Group I) were managed with splenectomy with excellent short and long term results. The selection criteria for splenectomy included a decrease in PVP to < 24 cm of water after clamping the SA. Three patients from this group were re-examined 10 to 12 years following splenectomy. Cirrhosis had not developed, but the minimal abnormalities in the liver function tests had persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:"Endemic" idiopathic portal hypertension: report on 32 patients with non-cirrhotic portal fibrosis. 129 Feb 52

In the present study alpha 1-adrenergic receptors have been investigated in liver parenchyma, obtained at the resection of prehepatic portal hypertension children without parenchymal affection (control group, n = 7) and the resection of children in parenchymal affection (group of cirrhosis, n = 8). It has been shown, that the binding of alpha 1-adrenergic antagonist 3H-prasozin (3H-PRZ) in liver parenchyma membranes of both control and cirrhosis groups is saturable and shows a high affinity. The Scatchard analysis of the binding data indicated that the binding site is characterized by Kd and Bmax of 0.6 +/- 0.12 nM, 92.8 +/- 8.0 fmol/mg, respectively, for the control group; and 1.5 +/- 0.4 nM, 254.1 +/- 28.4 fmol/mg, respectively, for the group of cirrhosis; (mean +/- SEM). It has been found that the number of binding sites of 3H-PRZ significantly increases in cirrhosis liver parenchyma in comparison with the control group. The results obtained suggest that alpha 1-adrenergic receptors play an important role in cirrhosis formation in children, showing liver parenchyma affection severity and its regenerative properties.
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PMID:[Alpha 1-adrenergic receptors in the liver parenchyma of children: the changes in cirrhosis]. 133 25

The susceptibility of the gastric mucosa to injury by topical sodium taurocholate (40 mmol/l) in hydrochloric acid (150 mmol/l) was studied in prehepatic and cirrhotic rat models of portal hypertension. Portal venous pressure was increased in rats who had undergone partial portal vein ligation compared with rats that had undergone sham operation on days 3, 7, and 28 after operation (20.6 (0.9), 14.8 (0.8), and 11.3 (0.5) mm Hg v 7.3 (0.7), 7.3 (0.6), and 8.2 (0.2) mmHg respectively (mean (SEM)). At day 3 gastric mucosal injuries were increased in rats with partial portal vein ligation compared with sham operated rats (55.3 (9.4) vs 22.3 (10.5) mm2, p = 0.006), but at the later time intervals there was no significant difference in injuries between the two groups. In rats with carbon tetrachloride induced hepatic cirrhosis, portal pressure was increased (15.6 (1.0) v 6.7 (0.6) mmHg), but again there was no significant difference in mucosal injuries relative to control animals. We conclude that gastric mucosal defence mechanisms are impaired in acute but not chronic experimental portal hypertension.
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PMID:Taurocholate induced gastric mucosal injuries in experimental portal hypertension. 154 11

Previous studies have shown that portal venous pressure increases in patients with cirrhosis after a protein meal. Since this increase may be mediated by an increase in hepatic blood flow or postsinusoidal hepatic vascular resistance, the present study was designed to examine the precise relation between the postprandial changes in these three variables in patients with cirrhosis and portal hypertension. Estimated hepatic blood flow (EHBF; indocyanine green clearance), portosystemic gradient (PSG; wedged free hepatic venous pressure), and postsinusoidal hepatic vascular resistance (PSR = PSG/EHBF) were measured simultaneously before and at 10 minute intervals after a high protein meal, containing 80 g protein, 40 g carbohydrate and 12 g fat (600 kcal) in nine patients (seven alcoholic, two non-alcoholic) with cirrhosis and portal hypertension. After the meal, the portosystemic gradient increased by 33% from mean (SEM) 15.6 (0.9) mm Hg to 20.7 (1.3) mm Hg, (p less than 0.01; Wilcoxon signed ranks test) within 30 minutes. Coincident with this increase in portosystemic gradient, estimated hepatic blood flow increased by 69.2% from 20.1 (1.7) ml/min/kg to 33.9 (2.5) ml/min/kg (p = 0.01), peak values occurring at 25 minutes, at which time the postsinusoidal hepatic vascular resistance had decreased by 31% from 1.10 (0.1) 10(-2) mm Hg/ml/min to 0.8 (0.5) 10(-2) mm Hg/ml/min (p = 0.01). These results suggest that the postprandial increase in portal venous pressure in patients with cirrhosis is mediated by an increase in hepatic blood flow and modified by a simultaneous decrease in postsinusoidal resistance.
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PMID:Postprandial changes in portal haemodynamics in patients with cirrhosis. 156 56

It has been proposed that in liver cirrhosis portal hypertension causes splanchnic vasodilation and this induces blood volume expansion to maintain blood pressure. The current study was designed to explore the homeostatic response to sodium restriction, a maneuver aiming to contract blood volume, in compensated cirrhosis. Mean blood pressure, sympathetic nervous activity, and proximal sodium reabsorption were evaluated in 16 healthy control and 21 nonazotemic cirrhotic patients (11 without ascites and 10 with ascites) under two experimental conditions: after 4 days on a free sodium diet (basal condition) and after 4 days on a restricted sodium diet (40 mmol/day). No differences were observed in basal conditions in the above parameters between control and cirrhotic patients without ascites. However, cirrhotic patients with ascites showed lower basal values of mean blood pressure and higher basal levels of both plasma norepinephrine and fractional proximal sodium reabsorption than controls. Neither control nor cirrhotic patients with ascites showed significant changes in the measured parameters after sodium restriction. In contrast, in nonascitic patients, this maneuver induced an elevation in plasma norepinephrine concentration (164.4 +/- 24.6 vs. 270.1 +/- 24.9 pg/mL; mean +/- SEM; P less than 0.005) and in fractional proximal sodium reabsorption (86.4 +/- 2.1 vs. 91.8% +/- 0.5%; P less than 0.01). In addition, the nonascitic cirrhotic patients became hypotensive compared with controls (80.9 +/- 1.6 vs. 88.5 +/- 4.8 mm Hg; P less than 0.05) when subjected to the low-sodium diet. In patients without ascites, under conditions of sodium restriction, the decrease in mean arterial pressure correlated inversely with the increase in plasma norepinephrine concentration (r = -0.713; P less than 0.05), whereas the levels of plasma norepinephrine correlated directly with fractional proximal sodium reabsorption (r = 0.893; P less than 0.01). These findings suggest that ineffective circulatory volume is detected in nonascitic cirrhotic patients only under conditions of sodium restriction, but it is always present in cirrhotic patients with ascites, irrespectively of the amount of sodium in the diet. These results are compatible with the existence of fixed arterial vasodilation in cirrhosis.
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PMID:Abnormal sympathetic and renal response to sodium restriction in compensated cirrhosis. 193 7

This study's purpose was to determine whether portal hypertension adversely affects small intestinal mucosal injury. Portal hypertension was produced in male Sprague-Dawley rats by two-stage ligation of the portal vein. Sham-operated rats were used as controls. Two weeks later, intestinal injury was produced by in vivo perfusion with 5 mM chenodeoxycholic acid for 30 min. Intestinal injury was assessed by quantitative morphometry and by measuring intestinal water and mannitol absorption. Portal hypertension resulted in more injury in the distal perfused intestine as manifested by increased villus tip denudation [portal hypertensive 52.5 +/- 9.6 (SEM) vs controls 28.1 +/- 5.7 microns, P = 0.05). Additionally there was a significant decrease in the unperfused duodenal villus height in portal hypertensive rats (portal hypertensive 755 +/- 22 vs controls 848 +/- 28 microns, P less than 0.02). Portal hypertension had no significant effect on the increase in mannitol absorption or water secretion caused by chenodeoxycholic acid perfusion. This study suggests that portal hypertension alters small intestinal mucosa and increases susceptibility to injury.
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PMID:Effect of portal hypertension on in vivo bile acid-mediated small intestinal mucosal injury in the rat. 211 62

1. In order to study the acute effects of blood volume changes on the vascular resistance of portal-systemic collaterals (collateral vascular resistance), a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the rat. In this model, we determined the haemodynamic effects of haemorrhage (1.8 ml/100 g body weight) or intravenous infusion of a volume expander (1.8 ml/100 g body weight). Cardiac output and regional blood flows were measured by the radioactive microsphere method. 2. Haemorrhage significantly reduced arterial pressure from 108 +/- 4 to 92 +/- 4 mmHg (mean +/- SEM), cardiac output from 56 +/- 4 to 24 +/- 2 ml min-1 100 g-1 body weight, portal pressure from 15.1 +/- 1.5 to 10.0 +/- 1.4 mmHg and portal tributary blood flow from 19.9 +/- 2.3 to 8.3 +/- 1.4 ml/min. Consequently, collateral vascular resistance significantly increased from 6.6 +/- 0.9 x 10(3) to 11.1 +/- 2.0 x 10(3) kPa 1(-1) s. 3. Volume expansion reduced arterial pressure from 98 +/- 3 to 90 +/- 3 mmHg, and significantly increased cardiac output from 43 +/- 3 to 55 +/- 3 ml min-1 100 g-1 body weight, portal pressure from 13.9 +/- 0.7 to 16.5 +/- 0.8 mmHg and portal tributary blood flow from 16.4 +/- 1.3 to 28.2 +/- 3.2 ml/min. Consequently, collateral vascular resistance significantly decreased from 7.0 +/- 0.5 x 10(3) to 4.9 +/- 0.4 x 10(3) kPa l-1 s. 4. This study shows that in rats with portal hypertension, portal-systemic collateral vascular resistance is modified by alterations in blood volume.
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PMID:Effects of haemorrhage and volume expansion on portal-systemic collateral vascular resistance in conscious portal hypertensive rats. 215 48

Nitrates decrease portal pressure by decreasing portal venous inflow and resistance. We studied over 20 minutes the effect of 10 mg isosorbide dinitrate sublingual on intrasplenic pulp pressure, mean arterial pressure and heart rate, in 13 patients with cirrhotic or non-cirrhotic portal hypertension. The pulp pressure fell progressively over 20 minutes, from mean 43.6 +/- 2.4 (SEM) to 35.6 +/- 1.8 cm H2O (p less than 0.001). This was accompanied initially by a significant fall in mean arterial pressure (85.8 +/- 1.9 to 80.4 +/- 2.7 mmHg at 4 minutes; p less than 0.01) and rise in heart rate (92.5 +/- 5.0 to 102.6 +/- 5.9 per minute at 6 minutes; p less than 0.02), following which these parameters remained stable. One patient developed giddiness due to hypotension at 15 minutes. We conclude that sublingual isosorbide dinitrate decreases pulp pressure in cirrhotic and non-cirrhotic portal hypertensives, but this is initially accompanied by significant hemodynamic changes.
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PMID:Effect of sublingual isosorbide dinitrate in portal hypertension. 232 97

The effects of portal hypertension on gastric motor function were investigated using the rat staged portal vein ligation model. Gastric emptying of liquids and solids was studied separately following meals labeled with 51Cr or 99Tc by whole stomach scintillation counting. Portal hypertension was consistently established in experimental rats (splenic pulp pressure: mean +/- SEM, portal hypertension versus control, 16.8 +/- 0.7 vs 11.8 +/- 0.7 mm Hg, P less than 0.0001). Although liquids were emptied in an exponential manner and solids in a linear fashion, gastric emptying of both meals was more rapid in the experimental rats. Ten minutes after the liquid meal, more than 50% of the meal had emptied from the stomachs of portal hypertensive rats while only one third of the meal had cleared in the control group (P less than 0.02). Gastric emptying of the solid meal was significantly accelerated in experimental rats at 60 and 120 min (percent meal remaining: portal hypertension versus control, 41.9 +/- 4.0 vs 55.4 +/- 3.5 and 21.5 +/- 4.9 vs 32.6 +/- 4.3, P less than 0.05). Stomachs of portal hypertensive animals were heavier (P less than 0.009) and histologic examination revealed submucosal edema. Thus, a possible mechanism of the disrupted gastric motor function in portal hypertension is decreased gastric wall compliance secondary to edema.
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PMID:Gastric emptying of liquids and solids in the portal hypertensive rat. 234 13

The effects of portal hypertension on gut function may be mediated by venous congestion and altered circulating levels of enteric hormones and neuropeptides. We designed this study to determine the effects of chronic intestinal venous hypertension (VHT), in isolation, on gut motility and absorption. In 10 dogs, a 20- to 25-cm loop of jejunum was isolated from the fecal stream, but myoneural continuity was maintained with the proximal bowel by a seromuscular bridge. In 5 dogs, VHT was created in the loop by a fixed stenosis of its venous drainage; a sham procedure was performed in a further 5 animals. Serosal monopolar electrodes were placed in all animals. Absorptive function and myoelectrical activity were studied over a 4-week period. Venous hypertension was achieved and sustained in the VHT animals; loop vein pressures for VHT vs control in cm H2O (means +/- SEM) are: initial--29.8 +/- 1.8 vs 7.5 +/- 0.4 (P less than 0.01), and at 4 weeks--17.6 +/- 6.88 vs 7.3 +/- 0.2 (P less than 0.01). Absorption of Na+, Cl-, glucose, and water was impaired in VHT loops. Normal patterns of fasting and postprandial myoelectrical activity were preserved in the VHT animals. We conclude that chronic VHT, in the absence of portosystemic shunting, results in impaired absorption of water, glucose, and electrolytes without any change in intestinal motility.
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PMID:The effect of mesenteric venous hypertension on gut motility and absorption. 236 16


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