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At least 37 records · Page 2Linked to original sources
PubMed1994

Outcome of portal-systemic shunt surgery for portal hypertension associated with intrahepatic obstruction in patients with agnogenic myeloid metaplasia.

Life-threatening portal hypertension (PHN) in patients with chronic myeloproliferative disorders may result from increased portal flow caused by marked splenomegaly or an increased resistance to portal flow from either a large vein thrombosis or an intrahepatic obstruction usually associated with agnogenic myeloid metaplasia (AMM). The former cause is correctable by splenectomy alone, whereas the latter requires portal-systemic shunt surgery. Few data exist regarding the outcome of portal-systemic shunt surgery in patients with AMM and intrahepatic obstruction. During the past 25 years, 13 patients with chronic myeloproliferative disorders underwent portal-systemic shunt surgery at our institution. The cause of PHN was intrahepatic obstruction in ten patients and hepatic vein thrombosis in three. Ten of the thirteen patients had AMM as initial diagnosis. Only one patient had intraoperative complications, and four patients had either sepsis or thrombosis during the postoperative period. Twelve patients survived the postoperative period and had a median postsurgical survival of 3 years (range, 0.25 to 19 years). The long-term complications of the operation were very few and included hepatic encephalopathy (one patient), portal vein thrombosis (one patient), and shunt occlusion (one patient). The procedure was successful in alleviating complications of PHN in all but one patient. Deterioration of hepatic function and subsequent hepatomegaly were unusual. Portal-systemic shunt surgery seems to be a useful option in patients with AMM and life-threatening PHN from intrahepatic obstruction.

Adult↗
PubMed2000

[Magnetic resonance angiography in assessing changes of pre-and post-disconnective portal system in patients with portal hypertension].

OBJECTIVE: To evaluate the role of magnetic resonance angiography (MRA) in assessing the portal system changes in patients with portal hypertension after pericardial devascularization and splenectomy. METHODS: The portal diameter, blood velocity and flow, collateral circulation, variceal vein and other portal parameters of 15 patients with portal hypertension receiving pericardial devascularization and splenectomy and splenectomy were comparatively evaluated with Siemens 1.5 T MRI 1 week before operation and 2 weeks after operation. RESULTS: The portal diameters decreased after operation, with the disappearance or alleviation of esophageal and fundal variceal veins. In 15 patients, 9 showed. The blood velocity and flow of the portal veins were lower postoperatively. than those preoperatively; In 15 patients, 9 showed increased gastric imaging intensity after operation. CONCLUSIONS: MRA can provide high quality and concrete 3-dimensional information about the portal system and hemodynamics of portal hypertensive patients. It is an important non-invasive way in evaluating the effects of operations and long-term follow-up. Postoperative gastric venous congestion possibly causes increased portal hypertensive gastropathy after disconnection.

Blood Flow Velocity↗
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↗
PubMed2005

Inhibition of VEGF receptor-2 decreases the development of hyperdynamic splanchnic circulation and portal-systemic collateral vessels in portal hypertensive rats.

BACKGROUND/AIMS: Portal hypertension is characterized by the development of a hyperdynamic splanchnic circulation. To determine whether this process is angiogenesis-dependent, we assessed the effects of SU5416, a specific inhibitor of VEGF receptor-2, in portal hypertensive rats. METHODS: Rats with portal hypertension induced by partial portal vein ligation were treated with SU5416 or vehicle during 5 days. Then, hemodynamic studies were performed using radioactive microspheres. Protein expressions of CD31, VEGF receptor-2 and VEGF were also determined by Western blotting. RESULTS: Treatment of portal hypertensive rats with SU5416 resulted in a significant and marked decrease (by 44%) in portal venous inflow, and increases in splanchnic arteriolar resistance (by 68%) and portal venous resistance (by 93%). In addition, SU5416 administration significantly inhibited the formation of portal-systemic collateral vessels (52% inhibition), as well as the splanchnic CD31 and VEGF receptor-2 protein expressions in portal hypertensive rats, compared with those receiving vehicle. CONCLUSIONS: This study demonstrates that the development of hyperdynamic splanchnic circulation and the formation of portal-systemic collateral vessels in portal hypertensive rats are angiogenesis-dependent processes that can be markedly inhibited by blockade of the VEGF signaling pathway. Therefore, modulation of angiogenesis may represent a potential target in the treatment of portal hypertension.

Angiogenesis Inhibitors↗
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↗
PubMed1999

Elevated serum levels of astroglial S100beta in patients with liver cirrhosis indicate early and subclinical portal-systemic encephalopathy.

Portal-systemic encephalopathy is the prototype among the neuropsychiatric disorders that fall under the term Hepatic Encephalopathies. Ammonia toxicity is central to the pathophysiology of Portal-systemic encephalopathy, and neuronal ammonia toxicity is modulated by activated astrocytes. The calcium-binding astroglial key protein S100beta is released in response to glial activation, and its measurement in serum only recently became possible. Serum S100beta was determined by an ultrasensitive ELISA in patients (n=36) with liver cirrhosis and transjugular intrahepatic portosystemic stent-shunt. Subclinical portal-systemic encephalopathy and overt portal-systemic encephalopathy were determined by age-adjusted psychometric tests and clinical staging, respectively. Serum S100beta, was specifically elevated in the presence of subclinical or early portal-systemic encephalopathy, but not arterial ammonia. S100 levels elevated above a reference value (S100beta < or = 110pg/ml) or the cut off value determined in our group of patients (112pg/ml) predicted subclinical portal-systemic encephalopathy with a specificity and sensitivity of 100 and 56.5%, respectively. Serum S100beta was significantly dependent on liver dysfunction (Child-Pugh score), but was more closely related to cognitive impairments than the score. Serum S100beta seems to be a promising biochemical surrogate marker for mild cognitive impairments due to portal-systemic encephalopathy.

Astrocytes↗
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↗
PubMed2002

Effects of long-term octreotide treatment on the response of portal-systemic collaterals to vasopressin in portal hypertensive rats.

BACKGROUND: Chronic portal hypertension is associated with the development of portal-systemic collaterals. Long-term octreotide treatment has been shown to enhance the constrictive response to vasopressin in the mesenteric arteries of portal hypertensive rats. This study investigated the effects of long-term octreotide treatment on the response of portal-systemic collaterals to vasopressin in portal hypertensive rats. METHODS: Partially portal vein-ligated rats were divided into two groups to receive subcutaneous injection of either placebo (5% dextrose in water) or octreotide (30 microg kg(-1)) twice daily for 7 days. Two series of experiments were performed to measure: (a) the systemic and portal hemodynamics and cumulative concentration-response curves of collateral vessels to vasopressin (10(-10) to 10(-7 )M) and (b) the slopes of the flow-pressure curves of collaterals (an index of portal-systemic shunting). The cumulative concentration-response curves and flow pressure curves were determined by the in situ collateral perfusion. RESULTS: Long-term octreotide treatment significantly lowered the portal pressure without changes in the mean arterial pressure. Vasopressin significantly and similarly increased the perfusion pressure of collateral vessels in both the placebo- and octreotide-treated groups. In addition, long-term octreotide treatment exerted no effect on the EC(50) of vasopressin (-8.25 +/- 0.19 vs. -8.20 +/- 0.10, P > 0.05) and the slopes of flow-pressure curves (0.97 +/- 0.02 vs. 0.94 +/- 0.04, P > 0.05) in the collaterals. CONCLUSION: Despite lowering the portal pressure, long-term octreotide treatment did not enhance the vasoconstrictive effect of vasopressin in the collateral vessels of portal hypertensive rats and ameliorate the degree of portal-systemic shunting.

Animals↗
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↗
PubMed2004

Anti-VEGF receptor-2 monoclonal antibody prevents portal-systemic collateral vessel formation in portal hypertensive mice.

BACKGROUND & AIMS: Portal hypertension is a frequent syndrome that develops in patients with chronic liver diseases, which are one of the most common causes of death in adults worldwide. The most serious clinical consequences of portal hypertension are related to the development of portal-systemic collateral vessels. Those include hepatic encephalopathy and massive bleeding from ruptured gastroesophageal varices. The high relevance of these collateral vessels prompted us to investigate the mechanism underlying its formation in a murine model of portal hypertension. METHODS: To determine whether the development of portal-systemic collateral vessels in portal hypertension is a vascular endothelial growth factor (VEGF)-dependent angiogenic process, we assessed the effects of a monoclonal antibody against VEGF receptor-2 on the formation of these collateral vessels in mice with portal hypertension induced by partial portal vein ligation. We also studied the effects of a selective and specific inhibitor of VEGF receptor-2 autophosphorylation in partial portal vein-ligated rats. RESULTS: A significant and marked inhibition in the formation of portal-systemic collateral vessels was observed in both partial portal vein-ligated mice and rats treated with anti-VEGF receptor-2 monoclonal antibodies or with the inhibitor of VEGF receptor-2 autophosphorylation, respectively, compared with animals receiving control solutions. CONCLUSIONS: Our present study shows that formation of collateral vessels is an angiogenesis-dependent process that can be markedly inhibited by blockade of the VEGF signaling pathway. These findings will make angiogenesis a focal point of research in portal hypertension and may lead to novel approaches for therapy of patients with chronic liver diseases.

Animals↗
PubMed1980

Renal and intrarenal blood flow in patients with cirrhosis before and after portal-systemic shunt.

Portal hypertension has been considered a pathogenetic factor in the onset of renal haemodynamic alterations in patients with cirrhosis. This hypothesis is based on experimental evidence, whereas the clinical data are few and contradictory. Mean and cortical renal blood flows were studied in 16 patients with liver cirrhosis before and 20-40 days after a portal-systemic shunt performed by different techniques: nine patients had a non-selective shunt and seven a selective shunt (distal splenorenal according to Warren). Despite a decrease in portal pressure, mean and cortical renal blood flows did not change significantly after surgery, and there was no significant correlation between decrease in portal pressure and modification of renal blood flow. It is concluded that portal hypertension is not a pathogenetic factor in renal hypoperfusion in cirrhosis.

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↗
PubMed1998

The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.

BACKGROUND: Portal hypertension is associated with gross haemodynamic disturbances characterised by high cardiac output, low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting. AIMS: To study the relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver. METHODS: Different sized microspheres were sequentially injected into the portal vein of male Wistar rats. RESULTS: Steady state portal venous pressure was increased by 102.2 (35.6)% (14.9 (3.6) mm Hg) and 272.3 (78.0)% (24.0 (2.2) mm Hg) above the basal pressure following sequential injections of 15 and 80 microns diameter microspheres, respectively. Sequential injection of 15, 40, and 80 microns diameter microspheres in either ascending or descending order of size did not generate further increases in portal venous pressure. A single injection of 1.8 x 10(5) 80 microns microspheres consistently produced a steady state portal venous pressure of 19.0 (1.3) mm Hg but did not approach the much higher value of 36.6 (43.2) mm Hg measured during clamping of the portal vein. These data indicate that the opening of patent intrahepatic shunts was responsible for the reduced pressures observed during microsphere injections and further evidence for this was provided by the location of microspheres in the pulmonary vascular bed. The elevation in portal venous pressure achieved by microsphere injections was not significantly different to that produced in rats subjected to partial portal vein ligation (20.7 (0.5) mm Hg, p > 0.05). Wedged hepatic venous pressure decreased from 6.7 (0.7) to 3.0 (0.6) mm Hg following injection of 80 microns microspheres, suggesting a decrease in total hepatic blood flow. Conversely, injection of 15 microns microspheres induced an increase in wedged hepatic venous pressure from 7.0 (1.0) mm Hg to 12.4 (1.8) mm Hg, indicating a localised redistribution of blood flow at the presinusoidal level of the portal venous vascular network and increased intrahepatic shunt flow. CONCLUSION: It is suggested that there may be a protective pathophysiological role for these shunts when the liver is subjected to changes which induce acute portal hypertension.

Acute Disease↗
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↗