Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portal circulation in patients with chronic liver diseases was evaluated by [99mTc]pertechnetate per-rectal scintigraphy. Technetium-99m pertechnetate (10 mCi) was instilled into the upper rectum, and serial scintigrams were taken. Radioactivity curves for the liver and heart were then recorded sequentially. Through analysis of these curves, the per-rectal portal shunt index (Sl) was calculated for six healthy subjects and 228 patients, 59 with chronic hepatitis, seven with idiopathic portal hypertension, six with primary biliary cirrhosis, and 156 with cirrhosis. In the healthy subjects, the Sl was 1.9-5.2% (mean 4.1%). In hepatitis, the mean Sl was 7.1%, and in cirrhosis, 52.9%. The Sl was higher in cirrhotic patients with esophageal varices than in those without (p less than 0.001), and in cirrhotic patients with encephalopathy than in those without (p less than 0.01). For some patients with portal hypertension, portal collateral circulation could be depicted, and images of changes in the portal collateral circulation after vascular anastomosis were seen.
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PMID:Portal circulation by technetium-99m pertechnetate per-rectal portal scintigraphy. 283 55

The effects of a somatostatin analogue, SMS 201-995 on hepatic haemodynamics were studied in rats with dimethylnitrosamine-induced cirrhosis. An intravenous infusion of 1, 2 or 4 micrograms kg-1 body wt h-1 SMS 201-995 produced a rapid and sustained decrease in portal pressure, portal venous flow and liver blood flow without significantly altering arterial blood pressure or pulse. The reductions in portal pressure, portal venous flow and liver blood were accompanied by an increase in splanchnic vascular resistance. Portal venous resistance was not affected. Subcutaneous injection of 2 micrograms kg-1 body wt SMS 201-995 produced a gradual decrease in portal pressure, the maximum reduction occurring 18 min after administration. This reduction in portal pressure was sustained for a further 20 min. The results suggest that SMS 201-995 may be of value in the control of bleeding oesophageal varices. Furthermore, the prolonged duration of action of SMS 201-995 following its subcutaneous administration suggests that the analogue may be useful in the long-term management of portal hypertension in patients with cirrhosis.
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PMID:The effects of a somatostatin analogue SMS 201-995 on hepatic haemodynamics in the cirrhotic rat. 286 12

Reports on the effects of somatostatin on hepatic haemodynamics in the cirrhotic patient have provided conflicting results. Therefore, we studied the effects of different modes and rates of somatostatin administration on hepatic haemodynamics in the cirrhotic rat. Portal pressure (PP), wedged hepatic venous pressure (WHVP), portal venous flow (PVF), liver blood flow (LBF) and systemic blood pressure were measured in rats with dimethylnitrosamine-induced cirrhosis. Somatostatin was administered as a rapid injection, a continuous infusion or as a bolus dose followed by a constant infusion. One group of rats with a previously constructed portacaval shunt received a bolus dose of somatostatin followed by a constant infusion. A rapid injection of somatostatin was attended by a rapid and significant fall in all the haemodynamic parameters measured (p less than 0.01). Continuous infusion of somatostatin [4 or 8 micrograms/kg body weight (BW) h] resulted in a gradual but significant reduction in PP, WHVP, PVF and LBF (p less than 0.05), but had no effect on systemic blood pressure. A bolus dose of somatostatin (2, 4 or 8 micrograms/kg BW over 2 min) resulted in a rapid decrease in PP, WHVP, PVF and LBF (p less than 0.01), the decreases being maintained by continuous infusion. In rats with a portacaval shunt a bolus dose of somatostatin (8 micrograms/kg BW) resulted in a rapid fall in WHVP and LBF, the decrease being maintained by a continuous infusion (8 micrograms/kg BW/h).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of somatostatin on hepatic haemodynamics in the cirrhotic rat. 286 55

The drugs currently under investigation in the prevention of recurrent gastrointestinal bleeding in cirrhosis are likely to decrease the portal pressure by means of a primary reduction of portal blood flow. The hemodynamic effects of beta-blocking agents and vasodilatory drugs were noninvasively measured in eight patients with cirrhosis by means of pulsed echo-doppler equipment. Portal caliber, blood velocity and flow were recorded hourly after a single dose of propranolol (40 mg p.o.) or atenolol (100 mg p.o.), and every 5 min after treatment with isosorbide dinitrate (5 mg sublingually). The drugs were administered at random with an interval of 2 days or more. The portal caliber decreased after atenolol, but did not change after propranolol and isosorbide. The blood velocity decreased by 29 +/- 2% 3 hr after propranolol, by 26 +/- 2% 3 hr after atenolol and by 31 +/- 3% 15 min after isosorbide. The portal blood flow decreased by 0.29 +/- 0.03 liters per min after propranolol, by 0.34 +/- 0.06 after atenolol and by 0.26 +/- 0.03 after isosorbide, without any difference among the various treatments. beta-blockers and vasodilatory drugs have comparable effects on portal blood flow. beta 1-selective and nonselective beta-blockers are similarly effective in keeping with the hypothesis that changes in portal blood flow are mainly due to the block of beta 1-receptors.
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PMID:Portal venous flow in response to acute beta-blocker and vasodilatatory treatment in patients with liver cirrhosis. 287 67

The intra- and early postoperative courses of 142 consecutive patients who underwent liver resections using vascular occlusions to reduce bleeding were reviewed. In 127 patients, the remnant liver parenchyma was normal, and 15 patients had liver cirrhosis. Eighty-five patients underwent major liver resections: right, extended right, or left lobectomies. Portal triad clamping (PTC) was used alone in 107 cases. Complete hepatic vascular exclusion (HVE) combining PTC and occlusion of the inferior vena cava below and above the liver was used for 35 major liver resections. These 35 patients had large or posterior liver tumors, and HVE was used to reduce the risks of massive bleeding or air embolism caused by an accidental tear of the vena cava or a hepatic vein. Duration of normothermic liver ischemia was 32.3 +/- 1.2 minutes (mean +/- SEM) and ranged from 8 to 90 minutes. Amount of blood transfusion was 5.5 +/- 0.5 (mean +/- SEM) units of packed red blood cells. There were eight operative deaths (5.6%). Overall, postoperative complications occurred in 46 patients (32%). The patients who experienced complications after surgery had received more blood transfusion than those with an uneventful postoperative course (p less than 0.001). The length of postoperative hospital stay was also correlated with the amount of blood transfused during surgery (p less than 0.001). On the other hand, there was no correlation between the durations of liver ischemia of up to 90 minutes and the lengths of postoperative hospital stay. The longest periods of ischemia were not associated with increased rates of postoperative complications, liver failures, or deaths. There was no difference in mortality or morbidity after major liver resections performed with the use of HVE as compared with major liver resections carried out with PTC alone, although the lesions were larger in the former group. It is concluded that the main priority during liver resections is to reduce operative bleeding. Vascular occlusions aim at achieving this goal and can be extended safely for up to 60 minutes.
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PMID:Vascular occlusions for liver resections. Operative management and tolerance to hepatic ischemia: 142 cases. 291 65

A comparative study of portal hemodynamics was made in 79 cirrhotics (24 cirrhotics with a large spleen greater than or equal to 500 cm3 in volume, 55 cirrhotics with a spleen less than 500 cm3 in volume), 22 patients with idiopathic portal hypertension, and 63 healthy adults who served as the control for portal and splenic venous flows. Portal and splenic venous flows were significantly increased in the group order of the cirrhosis without splenomegaly group, the cirrhosis with splenomegaly group, and idiopathic portal hypertension group. Intrahepatic shunt index was significantly greater in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly group, and it was negligible in the idiopathic portal hypertension group. Portal vein pressure was significantly elevated in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly and idiopathic portal hypertension groups. Postsinusoidal resistances were significantly greater in the two groups of cirrhosis than in the idiopathic portal hypertension group, whereas presinusoidal resistance was significantly greater in the idiopathic portal hypertension group than in the two groups with cirrhosis. It is concluded that these differences are inconsistent with the view that cirrhosis with splenomegaly comes from idiopathic portal hypertension.
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PMID:Differences in portal hemodynamics in cirrhosis and idiopathic portal hypertension. 292 62

Portal vascular resistance was measured percutaneously in 60 patients with chronic liver disease and in 5 control subjects. The portal vascular resistance (PVR) was calculated, using the following equation, from the portal blood flow (QPV), portal venous pressure (PPV), and hepatic venous pressure (PHV): PVR = (PPV - PHV)/QPV. The portal blood flow was measured using an ultrasonic Doppler duplex system, and the portal venous and hepatic venous pressures were measured using percutaneous transhepatic catheterization and venous catheterization, respectively. The wedged hepatic venous pressure was measured by occluding the hepatic venous branch using a balloon catheter. The portal vascular resistance was 0.25 +/- 0.13 mmHg X ml-1 X min X kg body weight (mean +/- SD, n = 5) in the control group, 0.64 +/- 0.29 mmHg X ml-1 X min X kg body wt (n = 13) in the chronic active hepatitis group, 1.34 +/- 0.79 mmHg X ml-1 X min X kg body wt (n = 30) in the cirrhosis group, and 0.85 +/- 0.69 mmHg X ml-1 X min X kg body wt (n = 13) in the idiopathic portal hypertension group.
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PMID:Measurement of portal vascular resistance in patients with portal hypertension. 293 45

Changes that occurred in splanchnic circulation with the progression of chronic liver disease were investigated using an ultrasonic Doppler flowmeter in healthy adults and in patients with chronic active hepatitis and liver cirrhosis in the supine position after an overnight fast. Superior mesenteric venous flow, splenic venous flow, and portal venous flow were significantly increased in patients with liver cirrhosis but not in patients with chronic active hepatitis compared with normal subjects. Portal venous flow (control value 10.5 +/- 2.3 ml/min/kg body weight) minus the sum of superior mesenteric venous flow and splenic venous flow was 0.8 +/- 2.1 ml/min/kg body weight in the control, (0.1 +/- 1.9) in chronic active hepatitis, and (-2.2 +/- 4.3) in liver cirrhosis; the difference was significant between the control and cirrhosis groups. These results indicate that in patients with liver cirrhosis a hyperdynamic state occurs in the splanchnic circulation of the intestine and spleen and that some portion of splanchnic blood flow bypasses the liver into the systemic circulation.
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PMID:Changes of splanchnic circulation with progression of chronic liver disease studied by echo-Doppler flowmetry. 295 38

48 patients with partial or complete portal vein thrombosis or tumor stenosis were examined by pulsed Doppler duplex scanning. In addition to the analysis of morphological changes, the pulsed Doppler duplex system yields functional data on the acceleration of blood flow in stenosis, flow in partial thrombosis and in differentiation between tubular cystic structures like arterial vessels, venous collaterals and dilated bile ducts. Qualitative and quantitative measurements of portal blood flow were performed in 55 cirrhotics and 15 healthy volunteers. Portal venous velocity and portal venous blood flow were significantly reduced in patients with cirrhosis. In 46 cases a hepatopetal blood flow was shown. In five cases a hepatofugal flow and in four cases a stagnant flow was found in the portal vein. Spontaneous portal systemic collaterals with hepatofugal flow were shown in 41% of cases. 11 patients with surgical portacaval shunts were examined. Patency was demonstrated in five patients where the anastomotic site was visible. Pulsed Doppler duplex sonography proved a valuable tool in the assessment of morphologic changes and revealed qualitative and quantitative data of portal venous hemodynamics.
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PMID:[Duplex sonography of the splenoportal axis]. 295 80

Changes of portal, superior mesenteric, and splenic venous flows after a meal were studied with the duplex ultrasonic Doppler flowmeter in normal subjects, in patients with chronic active hepatitis, and in those with cirrhosis for 2 h after ingestion of a liquid meal (14% protein, 56% lipid, 30% carbohydrate, 300 kcal). Portal and superior mesenteric venous flows increased significantly throughout the experiment, whereas no significant change occurred in splenic venous flow after the meal in all three groups. The extent of the increase in portal venous flow was significantly lower in patients with cirrhosis, compared with normal subjects and patients with chronic active hepatitis, whereas superior mesenteric venous flow increased to the same extent in all three groups. The sum of superior mesenteric and splenic venous flows was less than the estimated portal venous flow in both normal subjects and patients with chronic active hepatitis; however, this value was greater than the portal venous flow in patients with cirrhosis. The difference widened during postprandial mesenteric hyperemia, indicating an increase of blood flow into the portal-systemic shunts. In conclusion 1) postprandial hyperemia occurs in the intestine, but not in the spleen, to the same extent in patients with chronic active hepatitis or with cirrhosis, as in normal subjects, and 2) a considerable amount of postprandial mesenteric hyperemia bypasses the liver into the systemic circulation of patients with cirrhosis but not in patients with chronic active hepatitis and normal subjects.
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PMID:Portal hemodynamics after meal in normal subjects and in patients with chronic liver disease studied by echo-Doppler flowmeter. 295 48


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