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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↗
PubMed1999

Effects of vasopressin on portal-systemic collaterals in portal hypertensive rats: role of nitric oxide and prostaglandin.

This study investigated the effect of vasopressin on portal-systemic collaterals in portal hypertensive rats and the influence of nitric oxide (NO) and prostaglandin on the responsiveness of collateral vessels to vasopressin. The vascular responsiveness to graded concentrations of vasopressin was tested with or without the incubation of n(omega)-nitro-L-arginine (NNA) (100 micromol/L) and/or indomethacin (10 micromol/L) in perfused collateral vascular beds of rats with portal hypertension induced by partial portal vein ligation. In addition, concentration-response curves to vasopressin with incubation of a vasopressin V(1) receptor antagonist d(CH(2))(5)Tyr(Me) arginine vasopressin and concentration-response curves to a V(2) receptor agonist 1-desamino-8-D-arginine vasopressin were performed. Vasopressin significantly increased the perfusion pressure of collaterals, and this effect was suppressed by the addition of the V(1) receptor antagonist. Perfusion with the V(2) receptor agonist had no effect on the collaterals. Incubation with NNA, indomethacin, or both significantly potentiated the response of collaterals to vasopressin. In addition, the pressor response to vasopressin in the combination group was significantly higher than that in the NNA-alone group. The results show that vasopressin produces a direct vasoconstrictive effect on the portal-systemic collaterals of portal hypertensive rats. This effect is mediated by the vasopressin V(1,) but not V(2), receptors. The attenuation of the response to vasopressin by NO and prostaglandin suggest a function role of both mediators in the regulation of the portal-systemic collateral circulation in portal hypertensive rats.

Animals↗
PubMed2001

Myxedema accompanied by huge portal-systemic shunt without portal hypertension.

A 43-year-old woman with a huge portal-systemic shunt accompanied by myxedema showed slow speech and behavior. Several imaging studies revealed a bold portal-systemic shunt from the splenic vein to the left renal vein. In addition, hypothyroidism caused by chronic thyroiditis was diagnosed, and synthesized thyroxine replacement was effective for the symptoms. However, the serum ammonia and indocyanin green retention remained in the abnormal range, nevertheless the portal vein pressure was normal and findings of liver cirrohsis were not recognized histologically. Surgical shunt closure was performed, resulting in normalized serum ammonia levels and serum branched chain amino acids /aromatic amino acids ratio, and improvement of the ammonia tolerance test.

Adult↗
PubMed1993

Administration of N omega-nitro-L-arginine ameliorates portal-systemic shunting in portal-hypertensive rats.

BACKGROUND: Nitric oxide, a vasodilator synthesized from L-arginine by vascular endothelial cells, may play a role in the development of portal-systemic collaterals. This study investigated the effect of long-term inhibition of NO secretion on portal systemic shunting. METHODS: Systemic and splanchnic hemodynamics and the degree of portal-systemic shunting were evaluated in partial portal vein-ligated rats after administration of placebo (0.9% saline) or N omega-nitro-L-arginine (NNA) (approximately 2 micrograms.kg-1 x min-1) intravenously for 6 days. RESULTS: NNA treatment induced increases in splanchnic arterial resistance (P < 0.001) and portal-collateral resistance (P < 0.05) and a decrease in portal venous inflow (P < 0.05). Portal pressure was not changed (NS). The splenic-systemic shunting was significantly decreased from 81% +/- 5% in the placebo-treated group to 69% +/- 4% in the NNA-treated group (P < 0.05), paralleled by an insignificant reduction in the mesenteric-systemic shunting (64% +/- 7% vs. 50% +/- 6%, NS). The attenuation of portal-systemic shunting by NNA was further shown by an increase in the vascular resistance of portal-systemic collateral venous bed using an in situ portal-systemic collateral perfusion model (1.27 +/- 0.05 vs. 1.07 +/- 0.03 cm H2O.mL-1 x min-1; P < 0.001). CONCLUSIONS: The results show that in portal hypertensive rats, NNA reduces portal-systemic shunting without reducing portal pressure, suggesting that NO plays a role in the collateralization of the portal system. In addition, high flow through the portal-collateral bed is probably an important driving force that is independent of portal hypertension for the development of portal-systemic shunting in portal-hypertensive rats.

Animals↗
PubMed2002

Effects of somatostatin and octreotide on portal-systemic collaterals in portal hypertensive rats.

BACKGROUND/AIMS: Somatostatin and its long-acting analogue, octreotide, have been used to cease variceal bleeding with uncertain mechanisms. This study investigated whether somatostatin and octreotide have a direct vasoconstrictive effect on the portal-systemic collaterals of portal-hypertensive rats and potentiate the vasoconstriction induced by endothelin-1 in these vascular beds. METHODS: The vascular responses of collateral vessels to graded concentrations of somatostatin (10(-9)-10(-5) mol/l), octreotide (10(-10)-10(-6) mol/l), norepinephrine (10(-9)-10(-5) mol/l) and vehicle (Krebs solution) were evaluated in perfused collateral vascular beds of rats with portal hypertension induced by partial portal vein ligation. In addition, the perfusion pressure changes of collateral vessels to endothelin-1 (10(-8) mol/l) in the presence of vehicle(control), somatostatin (10(-6) mol/l) and octreotide (10(-6) mol/l) were tested. RESULTS: Compared with the vehicle group, norepinephrine significantly increased the perfusion pressure of collateral vessels at concentrations between 10(-7) and 10(-5) mol/l. In contrast, neither somatostatin nor octreotide significantly changed the perfusion pressure. Somatostatin and octreotide significantly enhanced the endothelin-1-induced vasoconstrictive effect on the collaterals. CONCLUSIONS: Somatostatin and octreotide exert no direct vasoconstrictive effect on the collateral vessels of portal hypertensive rats. In the presence of endothelin-1, somatostatin and octreotide exert a local vasoconstrictive effect on these vascular beds.

Animals↗
PubMed2001

Endothelin-1 induces vasoconstriction on portal-systemic collaterals of portal hypertensive rats.

Portal hypertension is associated with increased hepatic and collateral resistance to an increased portal blood flow. Endothelin-1 (ET-1) can induce intrahepatic vasoconstriction and consequently increase portal pressure. It is unknown if ET-1 also modulates portal pressure by a direct vasoconstrictive effect on collaterals. 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. The portal-systemic collaterals of partially portal vein-ligated rats were tested by in situ perfusion. The concentration-response curves of collaterals to graded concentrations of ET-1 (10(-10)-10(-7) mol/L) with or without BQ-123 (ET(A) receptor antagonist, 2 x 10(-6) mol/L), BQ-788 (ET(B) receptor antagonist, 10(-7) mol/L) or both were recorded. In addition, the collateral responses to ET-1 with preincubation of n(omega)-nitro-L-arginine (NNA; 100 mol/L), indomethacin (INDO; 10 mol/L), or in combination were performed. ET-1 increased the perfusion pressure of collaterals and its effect was significantly suppressed by BQ-123 alone and BQ-123 plus BQ-788, but not BQ-788 alone (P <.05). Incubation with NNA, INDO, or both significantly enhanced the response of collaterals to ET-1 (P < .05). These results show that ET-1 produces a direct vasoconstrictive effect on the collateral vessels of portal hypertensive rats. This effect is mediated by ET(A,) but not ET(B), receptors. Both nitric oxide and prostaglandin modulate the collateral vascular response to ET-1 and may therefore participate in the development and maintenance of portal hypertension.

Animals↗
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↗
PubMed1995

Extrahepatic portal-systemic encephalopathy without portal hypertension.

We report three cases of extrahepatic portal-systemic encephalopathy (EHPSE), two of which did not show portal hypertension (PH) and in the other of which precirrhotic state with chronic active hepatitis was detected at liver biopsy. Our review of the literature regarding EHPSE without PH leads us to conclude that a part of the shunts is congenitally or spontaneously formed, that PH is not always essential to shunt formation. Since the clinical symptoms most often do not manifest until middle age, cases with only mild disturbance of consciousness are not easily distinguished from dementia. Furthermore, all reported patients underwent shunt closure followed by marked improvement of clinical symptoms and uneventful postoperative course. EHPSE without PH which can be corrected by shunt closure should always be differentiated from EHPSE with PH.

Aged↗
PubMed1996

Local absorption kinetics into the portal system using the portal-venous concentration difference after an oral dose of diclofenac in the awakening rat. Accelerative effect of bile on intestinal absorption of diclofenac.

The local absorption kinetics from the intestinal tract into the portal system was evaluated using the portal-venous concentration difference (P-V difference) after oral administration of diclofenac in conscious rats. The local absorption ratio (Fa), mean local absorption time (ta), and relative variance (sigma 2/ta2) from the intestinal tract into the portal system were estimated by simultaneously measuring the portal and venous concentrations, using diclofenac as a model drug. The effect of bile on diclofenac intestinal absorption was also investigated. The awakening rats simultaneously cannulated into the jugular and portal veins were divided into group A with intact enterohepatic circulation (EHC) and into another group with bile-duct cannulation to block EHC. The rats in the latter group were further divided into group B without the bile supply to the intestinal tract and into group C with the bile supply from the other rat. After oral administration of diclofenac to rats in groups A, B, and C, the portal and venous concentrations of diclofenac in each rat were simultaneously monitored by HPLC method at proper time intervals. The absorption time profile of diclofenac into the portal system was directly predicted from P-V difference. Plasma concentrations of diclofenac in the portal vein were constantly higher than those in the jugular vein after the oral administration. It was demonstrated that P-V difference was caused by absorption from the intestinal tract into the portal system. Fa in groups A, B, and C were estimated to be 91.5% for 8 hr, 33.8% for 3 hr, and 57.8% for 3 hr, respectively. ta in groups A, B, and C were estimated to be 2.26 hr, 0.65 hr, and 0.96 hr, respectively. sigma 2/ta2 in groups A, B, and C were 1.31, 0.48, and 0.55, respectively. Fa and ta of diclofenac extensively increased in the presence of the bile in the intestinal tract, whereas sigma 2/ta2 was unaffected by the bile. The mean absorption time (MAT) almost agreed with ta, which demonstrates that the mean transit time through the liver (tH) is negligible in MAT(= ta+tH).

Administration, Oral↗
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↗