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At least 91 records · Page 5Linked to original sources
PubMed1989

Hemodynamic effects of blood volume restitution following a hemorrhage in rats with portal hypertension due to cirrhosis of the liver: influence of the extent of portal-systemic shunting.

The present study investigated whether, in rats with portal hypertension due to cirrhosis of the liver induced by carbon tetrachloride, blood volume restitution following a hemorrhage produces an increase of portal pressure beyond control values, as observed in rats with prehepatic portal hypertension. Since carbon tetrachloride-induced cirrhosis caused mild portal-systemic shunting, in some of the cirrhotic rats (12 of 29 rats) portal-systemic shunting was enhanced by a transient (4 days) partial constriction of the portal vein, which was removed 1 week prior to the study. After baseline measurements of portal pressure and arterial pressure, 15 ml per kg of blood were withdrawn at a rate of 0.3 ml per min and reinfused 15 min later. After blood reinfusion, portal pressure and arterial pressure were measured again, and cardiac output, regional blood flows and portal-systemic shunting were determined using radioactive microspheres. Portal-systemic shunting was 78 +/- 11% of total blood flow in the cirrhotic rats that had temporary portal vein constriction, but only 5 +/- 2% (p less than 0.001) in those that did not. Blood volume restitution in low-portal-systemic shunting rats did not produce any significant modification in splanchnic or systemic hemodynamics. However, in rats with high portal-systemic shunting, blood volume restitution produced a significant increase in portal pressure (from 9.9 +/- 0.9 to 13.5 +/- 0.9 mmHg, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Noninvasive evaluation of portal-systemic shunting by glyceryl trinitrate.

Portal-systemic shunting is an important circulatory abnormality in patients with liver cirrhosis. Glyceryl trinitrate (GTN) that is normally subject to first pass elimination, may exhibit higher bioavailability in these patients. This study compares the pharmacodynamic effects of GTN after peroral and sublingual administration for noninvasive assessment of shunting. Six control subjects and 15 patients with cirrhosis were studied after oral and sublingual application of 0.5 mg of GTN. Liver cirrhosis was complicated by portal hypertension in 7 of the patients and 4 patients had surgically implanted portocaval anastomosis. Digital plethysmography, which is highly sensitive and is essentially noninvasive in nature, was used to assess and compare the pharmacodynamic effects of GTN. The following values of the ratio of areas under the pharmacodynamic effects/time curve were obtained: 0.08 +/- 0.06 in healthy subjects, 0.52 +/- 0.21 in patients with uncomplicated cirrhosis, 0.99 +/- 0.34 in patients with portal hypertension and 1.24 +/- 0.43 in patients with portal-systemic shunts. We conclude that increased bioavailability of GTN reflects portal-systemic shunting and might be used providing that the pharmacodynamic data reflect both pharmacokinetic variability and the pharmacokinetic-pharmacodynamic interrelations.

Administration, Oral↗
PubMed1985

Portal hemodynamics in chronic portal-systemic encephalopathy. Angiographic study in seven cases.

A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. All 7 patients had a large gastro-renal or spleno-renal shunt, and a large proportion of superior mesenteric venous blood was being shunted as estimated from the diameter of the portal and the collateral vein, whereas in nonencephalopathic patients in whom part of the superior mesenteric venous blood was shunting this diversion was much less (P less than 0.001). Only one of the chronic portal-systemic encephalopathic patients had esophageal varices, insignificant in size, and the incidence of esophageal varices was significantly less compared to the 12 nonencephalopathic control patients with portal hypertension who had either a gastro-renal or spleno-renal shunt (P less than 0.05). It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices.

Ammonia↗
PubMed1994

Acetylsalicylic acid in the prevention of early stenosis and occlusion of transjugular intrahepatic portal-systemic stent shunts: a controlled study.

Stenosis or occlusion of the transjugular intrahepatic portal-systemic stent shunt may be initiated by aggregation and activation of thrombocytes on the surface of the metallic stent material. To find effective prevention of this event, we conducted a controlled trial administering acetylsalicylic acid for 3 mo. Forty-four patients (8 women and 36 men) with portal hypertension were included in this study. The patients were randomized into a group receiving 100 mg acetylsalicylic acid/day (n = 21) or into a control group (n = 23). Treatment was started immediately after transjugular intrahepatic portal-systemic stent shunt. Three months after transjugular intrahepatic portal-systemic stent shunt, 15 patients in the acetylsalicylic acid group and 19 patients in the control group underwent clinical reevaluation, gastroscopy and recatheterization with determination of the portal-systemic pressure gradient. No variceal bleeding occurred in any patients. In four patients in the acetylsalicylic acid group, erosive gastritis was observed in gastroscopy in contrast to only one patient in the control group. Complete patency of the stent was noted in 10 of 15 patients in the acetylsalicylic acid group and in 14 of 19 patients in the control group. Transjugular intrahepatic portal-systemic stent shunt restenosis associated with a significant increase of the portal-systemic gradient occurred in five patients in the acetylsalicylic acid group, which required redilation in all and additional stent placement for expansion of the stented tract in two patients. In the control group, redilation was necessary in five patients with additional stent extension in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Effect of intrahepatic portal-systemic shunting on hepatic ammonia extraction in patients with cirrhosis.

Increased plasma ammonia levels in patients with advanced cirrhosis have been attributed to reduced conversion of enteric ammonia to urea by the diseased liver and to entry of enteric ammonia into systemic circulation by way of portal-systemic shunts. Because single-pass extraction is high for portal venous ammonia, reduction of portal blood supply to hepatocytes may have detrimental effects on the hepatic extraction of ammonia. To assess how the development of intrahepatic portal-systemic shunts alters hepatic ammonia metabolism, we determined portal and hepatic venous ammonia levels along with measurements of intrahepatic portal-systemic shunts using 99mTc-macroaggregated albumin in 46 patients with portal hypertension. Hepatic venous ammonia levels in the groups of patients with idiopathic portal hypertension, Child class A cirrhosis and Child class B or C cirrhosis were 36 +/- 17, 75 +/- 26 and 93 +/- 52 micrograms/dl, respectively, in increasing order, and portal venous ammonia extraction rates as calculated with the equation (portal venous ammonia-hepatic venous ammonia)/portal venous ammonia x 100% were decreased in the same order (77% +/- 14%, 50% +/- 21%, 40% +/- 25%, respectively). Furthermore, we noted a significant negative correlation between the intrahepatic shunt indexes as calculated by counts per minute in lungs/counts per minute in lungs and liver x 100% and the ammonia extraction rates. It was noteworthy that among Child class C patients, the ammonia extraction rates were significantly lower in patients with high intrahepatic shunt indexes than in those with low shunt indexes. These results demonstrate a significant direct relationship between hepatic ammonia extraction rates and intrahepatic shunting in cirrhosis.

Adult↗
PubMedDate not supplied

Scintigraphic documentation of systemic-portal shunting.

Two unusual cases of iliac vein thrombosis are presented. They were studied with radionuclide venography of the left lower-extremity in which one of the collateral channels was the inferior mesenteric vein and showed the entire liver and lungs simultaneously. This vein does not appear to have been clearly identified with radioisotopic techniques previously. Using the anterior projection over the lungs and liver, ratios of liver to lungs, liver to (liver + lungs), right lung to (liver + lungs) and left lungs to (liver + lungs) were calculated. In patient 1, the shunted tracer represented 82% of the total activity and in patient 2 it was 21.5%.

Collateral Circulation↗
PubMed1999

Subclinical portal-systemic encephalopathy in a child with congenital absence of the portal vein.

A 6-year-old girl with congenital absence of the portal vein (CAPV) who had persistent hyperammonemia due to a congenital portosystemic shunt is reported. The patient only exhibited mild intention tremor, without any apparent neurological manifestations of portal-systemic encephalopathy. However, magnetic resonance imaging of the head showed white matter atrophy with ventricular dilatation, which is thought to represent subclinical brain damage caused by chronic hyperammonemia. This is the first report of subclinical portal-systemic encephalopathy in a patient with CAPV. The present case suggests that the effect of a congenital portosystemic shunt on the central nervous system is serious, but can be clinically latent in children with CAPV.

Angiography↗
PubMed2005

High prevalence of spontaneous portal-systemic shunts in persistent hepatic encephalopathy: a case-control study.

Large spontaneous portal-systemic shunts have been occasionally described in patients with cirrhosis. This study was undertaken to assess the prevalence of portal-systemic shunts in patients with cirrhosis with recurrent or persistent hepatic encephalopathy (HE) as compared with patients with cirrhosis without HE. Fourteen patients with cirrhosis with recurrent or persistent HE (cases) and 14 patients with cirrhosis without previous or present signs of overt HE matching for age and degree of liver failure (controls) were studied. Each patient underwent neurological assessment and cerebral magnetic resonance (MR) imaging to exclude organic neurological pathological conditions. HE evaluation included psychometric performance (Trail-Making Test A), electroencephalogram (EEG), mental status examination and grading, arterial, venous, and partial pressure of ammonia determination. The presence of portal-systemic shunts was assessed by portal venous phase multidetector-row spiral computed tomography (CT). Large spontaneous portal-systemic shunts were detected in 10 patients with HE and in only 2 patients without HE (71% vs. 14%; chi square = 9.16; df = 1.0; P = .002). The patients with HE presented ascites (P = .002) and medium/large esophageal varices (P = .02) less frequently than the control group. In conclusion, our study suggests that large spontaneous shunts may often sustain the chronicity of HE; the presence of large shunts should be sought in patients with cirrhosis with recurrent or persistent HE.

Aged↗
PubMed1979

Brain proteins in experimental portal-systemic shunting.

Experimental portal-systemic shunting is accompanied by a reduction of the soluble brain proteins. Isoelectric focusing does not indicate any selective decrease of one particular protein or group of proteins. The reduction persists with sustained shunting. The interference with brain protein metabolism is compatible with a grossly normal behavior, alterness and locomotion.

Albumins↗
PubMed1991

Catecholamine concentrations in the hepatic portal system: effect of surgical stress upon portal levels.

The biological effects of a hormone are dependent on the concentration delivered to the target tissue. This is generally best reflected in the arterial concentration. However, the liver is unique in that it receives substantial additional blood flow from the portal venous system. This may be important in the case of the catecholamines, where extraction or spillover from the splanchnic circulation may occur. In this study we examined portal venous catecholamine concentrations in anesthetized, laparotomized rabbits. We compared the values with simultaneously sampled arterial levels to evaluate the effects of the splanchnic tissues upon a wide range of catecholamine concentrations delivered to the liver during a state of stress. Spillover of norepinephrine and extraction of epinephrine were observed in all rabbits. Mean (+/- SEM) arterial norepinephrine concentrations were elevated, 716 +/- 167 pg/ml (n = 11); mean portal concentrations were 178 +/- 37% higher (p less than 0.01), at 1,425 +/- 301 pg/ml, representing net spillover from splanchnic tissues. In addition, significant extraction of epinephrine was observed; arterial concentrations were 2,144 +/- 580 pg/ml (n = 11). Portal levels were 1,205 +/- 382 pg/ml, 38 +/- 7.45% lower than corresponding arterial concentrations (p less than 0.02). Furthermore, there was a concentration-dependent effect upon norepinephrine spillover; the highest arterial norepinephrine concentrations were associated with the lowest splanchnic spillover. This resulted in a negative correlation between the arterial norepinephrine levels and the percent increase from spillover into the portal vein (r = -0.81, p less than 0.003). We conclude that portal venous catecholamine concentrations are significantly different from arterial levels in anesthetized, laparotomized rabbits over a wide range of concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Effects of endothelin-1 on portal-systemic collaterals of common bile duct-ligated cirrhotic rats.

BACKGROUND/AIMS: Endothelin-1 (ET-1) may induce intrahepatic vasoconstriction and consequently increase portal pressure. Endothelin-1 has been shown to exert a direct vasoconstrictive effect on the collateral vessels in partially portal vein-ligated rats with a high degree of portal-systemic shunting. This study investigated the collateral vascular responses to ET-1, the receptors in mediation and the regulation of ET-1 action by nitric oxide and prostaglandin in cirrhotic rats with a relatively low degree of portal-systemic shunting. METHODS: The portal-systemic collaterals of common bile duct-ligated (BDL) cirrhotic rats were tested by in situ perfusion. The concentration-response curves of collaterals to graded concentrations of ET-1 (10(-10)-10(-7) m) with or without BQ-123 (ET(A) receptor antagonist, 2 x 10(-6) m), BQ-788 (ET(B) receptor antagonist, 10(-7) m) or both were recorded. In addition, the collateral responses to ET-1 with preincubation of N(omega)-nitro-L-arginine (NNA, 10(-4) M), indomethacin (INDO, 10(-5) M) or in combination were assessed. RESULTS: Endothelin-1 significantly increased the perfusion pressures of portal-systemic collaterals. The ET-1-induced constrictive effects were inhibited by BQ-123 or BQ-123 plus BQ-788 but not by BQ-788 alone. The inhibitory effect was greater in the combination group. Pretreatment of NNA or NNA plus INDO equivalently enhanced the response of ET-1 while pretreatment of INDO alone exerted no effect. CONCLUSION: Endothelin-1 has a direct vasoconstrictive effect on the collaterals of BDL cirrhotic rats, mainly mediated by ET(A) receptor. Endogenous nitric oxide may play an important role in modulating the effects of ET-1 in the portal-systemic collaterals of BDL cirrhotic rats.

Animals↗