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At least 19 recordsLinked to original sources
PubMed1985

Interrelationship between type of spontaneous portal systemic shunt and portal vein pressure in patients with liver disease.

The interrelationship between the type and degree of spontaneous portal systemic shunting, and portal vein pressure was studied in 155 patients with liver disease by catheterizing the portal vein. The degree of portal vein shunting was measured in 100 patients and that of splenic vein shunting in 50 and that of total portal systemic shunting in 52, using macroaggregated radioalbumin. Increasing portal vein pressures were associated with progressively higher indices of portal vein shunt, splenic vein shunt, and total portal systemic shunt up to a certain level. Beyond this level, portal vein pressure did not increase further, and rather it decreased with further increasing degrees of splenic vein shunt and total portal systemic shunt. These results indicate that spontaneous portal systemic shunt keeps the portal vein pressure within certain limits or decreases it.

Catheterization↗
PubMed1982

[Sonographic assessment of the portal system in portal hypertension].

Three hundred and thirty-seven patients with portal hypertension and recurrent bleeding from oesophageal varices were examined by sonography. The situation was correctly elucidated in 17 out of 21 patients (81%) with pre-hepatic blocks, in 275 out of 313 cases (88%) with intra-hepatic blocks and in two out of three cases with post-hepatic blocks. The relevant findings consisted of stenoses and occlusions of the portal venous system and collaterals in pre-hepatic blocks, dilatation of the portal venous system and hepato-fugal collaterals in intra-hepatic blocks and occlusion of the hepatic veins in post-hepatic blocks. Sonography is recommended in cases of portal hypertension because of its non-invasive nature and high accuracy as the primary form of investigation. Spleno-portography should be used only if surgery is indicated.

Esophageal and Gastric Varices↗
PubMed1992

Pharmacology of portal-systemic collaterals in portal hypertensive rats: role of endothelium.

The portal-systemic collateral circulation of portal hypertensive rats was studied. The collaterals were perfused through the mesenteric vein with Krebs solution, which was allowed to escape through the jugular veins. The portal-collateral resistance can be quantitated from slopes of the pressure-flow relationships. In collaterals perfused at constant flow, both norepinephrine (NE) and 5-hydroxytryptamine (5-HT) increased the perfusion pressure. Phentolamine caused surmountable antagonism of the constrictor effects of NE, suggesting an involvement of alpha-adrenoceptors. The effects of 5-HT were competitively blocked by the 5-HT2 receptor-selective antagonist ICI 169,369. Isoproterenol dilated NE-preconstricted collaterals. The effect of isoproterenol was blocked by propranolol, demonstrating that the effect was mediated by beta-adrenoceptors. Acetylcholine (ACh) dilated NE-preconstricted collaterals. The dilatation effect of ACh was absent in collaterals in which the endothelium was removed. The competitive inhibitor of the nitric oxide synthase, N omega-nitro-L-arginine (L-NNA), increased collateral resistance and prevented the ACh-induced dilatation of the collaterals. The constrictor response to L-NNA and the blockade of the ACh-induced relaxation by both L-NNA and removal of endothelium are consistent with an involvement of nitric oxide. This experimental model can thus be used to explore the pathophysiological and the pharmacological properties of the collateral venous bed in portal hypertensive states.

Animals↗
PubMedDate not supplied

Long-term neuropsychological outcome in children undergoing portal-systemic shunts for portal vein obstruction without liver disease.

Forty-two children with portal vein obstruction (cavernoma) and without liver disease had a portosystemic surgical shunt performed at different ages. All of them had severe gastrointestinal hemorrhage prior to surgery. To evaluate the long-term neurological and psychological effects of shunt procedures in children with normal liver function, they were studied up to 24 years postoperatively with psychometric testing. A comparison with two control groups as to the impact of surgery, family situation, and neonatal events was considered. Twenty-four children with portal vein obstruction who were not operated on and 19 children splenectomized for hematological reasons acted as the control groups. No differences were observed in schooling and employment. Psychometric tests were almost identical in shunted patients and in the control groups. Minimal portal systemic encephalopathy appeared to be undetectable clinically either by electroencephalogram or by venous ammonia levels. The results of psychometric tests appear to show no loss of intellectual and psychological capacity in patients operated on for portal obstruction. Only visual memory and spatiotemporal tests showed slightly worse results in those children who underwent this procedure. Further longitudinal studies are required to substantiate these findings.

Adolescent↗
PubMed1984

Portal systemic encephalopathy.

Portal systemic encephalopathy is a neuropsychiatric disorder that occurs secondary to chronic liver disease. It is a chronic and disabling disorder that must be treated concurrently with liver disease. In chronic liver disease, the regenerative capacity of the liver to produce new cells is eventually hampered and scar tissue develops. Scarring reduces blood flow through the liver. The vein most affected is the portal vein which contributes 75 percent of the blood to the liver as it evolves from tributaries off the abdominal organs. To eliminate the high pressure in the portal vein caused by the reduced blood flow, the portal vein develops collateral vessels that bypass the liver and drain directly into the inferior vena cava. When blood is not cleared, or when hepatic functioning fails, toxins accumulate in the circulation and affect the central nervous system. The neuropsychiatric manifestations that occur represent the symptoms seen in portal systemic encephalopathy. With renewed understanding of the disease and its neuropsychiatric manifestations, both clinicians and patients are able to minimize its untoward effects. This article reviews the pathogenesis, stages, diagnosis and treatment of the disease and aims at giving nurse practitioners a thorough review so they can better teach patients how to help themselves.

Anti-Bacterial Agents↗
PubMed1988

Role of intrahepatic portal-systemic shunts in the reduction of portal blood supply to liver cells in cirrhosis.

To assess the role of intrahepatic portal-systemic shunts in the reduction of portal blood supply to the liver cells in cirrhosis, we measured portal venous flow (blood flow in the portal trunk) by the pulsed Doppler flowmeter and intrahepatic portal-systemic shunt index from the counts over the lungs and liver in both the anterior and posterior projections after instillation of 99mTc-macroaggregated albumin in the portal vein, and calculated portal sinusoidal flow (blood flow into the sinusoids via the portal vein), using the equation, (sequence; see text) in 47 patients with posthepatitic cirrhosis, and measured portal venous flow in 63 healthy adults in whom portal sinusoidal flow should be comparable to portal venous flow. Portal sinusoidal flow was significantly reduced in cirrhotics with an intrahepatic portal-systemic shunt index averaging 24%, whereas portal venous flow was similar in the cirrhotics and control. There was a significant inverse correlation between intrahepatic portal-systemic shunt index and portal sinusoidal flow. When cirrhotics were divided into three stages, based on Child's grading, intrahepatic portal-systemic shunt index was significantly increased in the group order of Child's A (8 +/- 9%), Child's B (27 +/- 22%), and Child's C patients (46 +/- 19%), and portal sinusoidal flow was decreased in the same order. Portal sinusoidal flow was significantly reduced in Child's B and Child's C patients, but not in Child's A patients, compared with the control. In conclusion, intrahepatic portal-systemic shunts may play a role, at least in part, in the reduction of portal blood supply to the liver cells in patients with advanced stage of posthepatitic cirrhosis when large intrahepatic portal-systemic shunts develop.

Adult↗
PubMed1984

Chronic portal-systemic encephalopathy with normal portal vein pressure possibly due to noncirrhotic portal fibrosis.

This is the report of a 50-year-old man with a more than 20-year history of chronic progressive portal-systemic encephalopathy. Liver tests were normal except for increased serum ammonia and indocyanine green plasma retention. The liver pathology was compatible with idiopathic portal hypertension or noncirrhotic portal fibrosis, demonstrating localized surface nodularity and portal fibrosis. Percutaneous transhepatic catheterization of the portal vein revealed near top normal portal vein pressure and a large shunt connecting the left gastric or superior mesenteric vein and the left renal vein. Presumably, the patient had portal hypertension in the past and formation of a short, large-caliber shunt between the portal system and the renal vein effectively decompressed the portal circulation.

Catheterization↗
PubMed1983

Increased plasma ammonia may inhibit cellular release of branched-chain amino acids in systemic portal encephalopathy.

Plasma amino acid patterns were determined before and after hemofiltration (HF) and hemodialysis (HD) in 6 patients with portal systemic encephalopathy (PSE) and compared with the plasma AA patterns of 16 patients with chronic renal failure (CRF) treated either by HF or HD. The branched-chain amino acids (BCAA) increased paradoxically in PSE patients during HF but not with HD. There were no differences in BCAA's with HF as compared to HD in the CRF patients. The amount of amino acids lost was the same with both treatment modalities and in both patient groups. Much of the amino acids lost were released from the intracellular space. The BCAA release was significantly higher in PSE patients during HF. No correlation was found between plasma insulin, glucagon, and cortisol levels and BCAA release. An inverse correlation was found between the amount of BCAA's released from the intracellular space and the plasma ammonia levels. It is suggested that a selective cellular transport mechanism for BCAA exists which is inhibited by high plasma ammonia levels in PSE.

Adult↗
PubMed1991

Early chronic administration of propranolol reduces the severity of portal hypertension and portal-systemic shunts in conscious portal vein stenosed rats.

We investigated the effects of early chronic administration of propranolol on systemic and splanchnic hemodynamic changes, and the development of portal-systemic shunts in conscious, unrestrained, portal vein stenosed rats. Compared to rats receiving placebo, early chronic propranolol (75 mg kg-1 day-1) administration to rats begun 3 days before portal vein stenosis and then continued for 10 consecutive days, resulted in a significant decrease in both portal pressure (11.8 +/- 1.5 mmHg) and portal-systemic shunts (48 +/- 18%) which were measured 2 to 3 h after the final dose of propranolol (15.2 +/- 1.5 mmHg and 84 +/- 5%, respectively). These beneficial effects were also observed 18 to 24 h after the final dose of chronic propranolol. In rats given propranolol continuously for 5 days starting 5 days after portal vein stenosis, portal pressure (11.8 +/- 1.2 mmHg) was significantly lower than in the placebo group but portal-systemic shunts (76 +/- 14%) were not significantly different. In rats receiving a single dose of propranolol (75 mg/kg) 10 days after portal vein stenosis and measured 2 to 3 h after propranolol administration, portal pressure (12.8 +/- 1.0 mmHg) was significantly lower than in the placebo group. Portal-systemic shunts (72 +/- 17%), however, showed no significant difference from the placebo group. Similar values in portal pressure (13.3 +/- 1.2 mmHg) and portal-systemic shunts (83 +/- 21%) were also observed in rats 18 to 24 h after a single dose of propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Two cases of portal-systemic shunts demonstrated by portal venography performed by operative cannulation of ileocolic vein.

Two cases of portal-systemic shunt were presented. A 70 year-old cirrhotic female, who was suffered from mental confusion, underwent portal venography which demonstrated a large varicose vein connecting the inferior mesenteric vein with the left renal vein. The mean portal pressure was 15 cm saline. There were no esophagogastric varices. A 47 year-old cirrhotic female, who was admitted for evaluation of liver dysfunction found incidentally, underwent portal venography which revealed a dilated coronary vein connecting to the left renal vein. The portal pressure was 23 cm saline. There was no evidence of esophageal varices. Portal venography was performed through the ileocolic vein in both cases. In general, bleeding varices may develop most commonly in coronary-azygous system and less frequently in the territory of the superior and inferior mesenteric veins. On the contrary, retroperitoneal portal-systemic shunts is likely to cause hepatic encephalopathy rather than to develop bleeding varices. Thus, it is necessary to perform abdominal angiography in patients with hematochezia of unknown etiology or recurrent episodes of hepatic encephalopathy.

Aged↗
PubMed1990

Role of glucagon in the splanchnic and systemic hemodynamic changes induced by portal-systemic blood shunting.

Portal-systemic blood shunting is often accompanied by hyperglucagonemia and hemodynamic changes. To determine this causal relation, splanchnic and systemic hemodynamics (radioactive microspheres) and plasma glucagon levels (radioimmunoassay) were assessed in conditions of total portal-systemic shunting in portacaval-shunted (PCS) rats and in sham-operated (SO) normal rats. To compare these results, another hemodynamic study was undertaken basally and during glucagon infusion in nonoperated normal rats. PCS rats showed a threefold greater plasma glucagon concentration than SO animals (924 +/- 134 vs. 309 +/- 18 pg/ml, p less than 0.01), and they developed a hyperdynamic splanchnic circulation with higher portal venous inflow than SO rats (8.29 +/- 1.1 vs. 5.09 +/- 0.4 ml/min/100 g, p less than 0.05). Infusion of a pharmacological dose of glucagon in normal rats increased portal venous inflow (from 4.92 +/- 0.33 to 6.24 +/- 0.48 ml/min/100 g, p less than 0.05) so as to imply this hormone in the development of the hyperdynamic splanchnic circulation in conditions of portal-systemic shunting. However, the discrepancies in systemic hemodynamics between PCS and glucagon-infused rats may be a result of the different plasma glucagon levels reached in the two groups.

Animals↗
PubMed1990

[Physiology of the portal system and physiopathology of portal hypertension].

Circulation in the territory of the portal vein is made up of blood flows in the organs of this territory. Each of these organs has an intrinsic and extrinsic regulatory system. Portal hypertension results from a simultaneous increase of intrahepatic portal vascular resistances and blood flow rates. The rise in vascular resistance is due to a decrease of the intrahepatic vascular space consecutive to fibrosis and lesions of the liver cells. The cause of the increase in blood flow is imperfectly known. Physical, metabolic, hormonal and nervous factors may be responsible for these splanchnic circulatory changes, and they also produce changes in systemic haemodynamics.

Animals↗
PubMed1990

Effects of haemorrhage and volume expansion on portal-systemic collateral vascular resistance in conscious portal hypertensive rats.

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.

Animals↗