Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PORTAL SYSTEM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1993

Effect on liver and splanchnic circulation of graded flow rates through portal-systemic bypass during acute portal occlusion.

Using graded flow rates through a passive portal-systemic bypass during 2-hr portal occlusion in dogs, splanchnic, hemodynamic, and metabolic changes and liver insults were evaluated to determine critical bypass flow. To exclude effects caused by reduced circulating blood volume, constant preocclusion levels of cardiac output were maintained throughout the study by increasing intravenous infusion rates. With the decrease in bypass flow rates during portal occlusion, portal pressure increased, superior mesenteric arterial flow decreased, and hepatic arterial flow rapidly increased and these parameters maintained their individual levels during occlusion. These hemodynamic parameters recovered to nearly normal levels 3 hr after release of the portal clamp. Metabolic acidosis progressed with decreasing bypass flow, but portal potassium and inorganic phosphorus levels showed a significant rise only when there was no bypass. Portal levels of creatine phosphokinase BB, beta-glucuronidase, and endotoxin did not show significant changes corresponding to bypass flow. The amounts of infusion required were 3 to 6 times the basal level (10 ml/kg/hr) during occlusion and 1.7 to 3 times after release in 30% or less bypass groups. Upon ceasing infusion 3 hr after release, dogs in the 10% or less bypass groups underwent circulatory insufficiency. Changes in total adenine nucleotide and energy charge ratio of the liver, postoperative changes in transaminase levels, and animal survival indicated that a 2-hr interruption of the portal flow, either sufficiently or insufficiently bypassed, caused only minimal insults of the liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

[Portal-systemic shunting and hemodynamics of prehepatic portal hypertensive rat models].

Hemodynamics and relationship between portal-systemic shunting and portal pressure were measured by radioactive microsphere techniques in 31 rats after various degree portal vein constriction. Prominent hyperdynamic state was present in prehepatic portal hypertensive rats models. Both cardiac output and index were increased, the mean arterial pressure and pripheral resistance were reduced significantly. The total splanchnic blood flow was increased but splanchnic resistance reduced remarkably. Portal-systemic shunting flow was higher. There was a significant positive correlation between them, Y = 26.14 + 5.32X (r = 0.76, P < 0.001). For this reason, elevated systemic and portal venous flow provided main impetus for maintaining portal hypertension.

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↗
PubMed1996

[Reversal of portal-systemic encephalopathy by shunt-preserving disconnection of portal and systemic circulation].

Obliteration of portal-systemic shunts surgically or by interventional radiological techniques is fairly effective in reversing intractable portal-systemic encephalopathy (PSE), but is often associated with ascites accumulation and/or formation of esophageal varices. This study reports four patients with incapacitating PSE who were treated by interventional radiological techniques via percutaneous transhepatic route. One case had the shunt embolized directly. In the other three the blockage was placed on the proximal part of the splenic vein, whereby disconnecting the mesenteric-portal blood flow from the systemic circulation while preserving the shunt. The patient of shunt closure showed transient correction of encephalopathy, but developed massive ascites and esophageal varices, encephalopathy recurred, resulting in death from hepatic failure two months after the procedure. In the cases of shunt-preserving disconnection of portal and systemic circulation (SPDPS) immediate and permanent clearing of encephalopathy was achieved without manifestation of ascites or esophageal varices during the follow-up period of 10 to 31 months. The difference of portal pressure between before and after the procedure was 18 mmHg in the shunt-closed patient and 3 mmHg in SPDPS group. We conclude from this limited experience that SPDPS can be an effective and safe method in treating PSE in adequately selected patients.

Aged↗
PubMedDate not supplied

Effects of alpha 1 and beta-adrenergic antagonists and 5-hydroxytryptamine receptor antagonist on portal-systemic collateral vascular resistance in conscious rats with portal hypertension.

In order to study the acute effects of pharmacological agents on the vascular resistance of portal-systemic collaterals, a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the conscious rat. The haemodynamic effects of several vaso-active substances were evaluated in this model and compared with those obtained after saline administration. Prazosin (0.5 mg), an alpha 1-adrenergic antagonist, significantly reduced mean arterial pressure by 29%, portal pressure from 13.8 +/- 1.0(mean +/- s.e.m.) to 10.1 +/- 0.4 mmHg and portal tributary blood flow (radioactive microspheres) from 13.6 +/- 2.1 to 11.7 +/- 1.2 mL/min. It also decreased portal-systemic vascular resistance from 95 +/- 16 to 73 +/- 9 dyn s/cm5 x 10(3). Propranolol (4 mg), a beta-adrenergic antagonist, significantly reduced mean arterial pressure by 12% and portal pressure from 15.5 +/- 1.2 to 13.3 +/- 0.9 mmHg while reducing portal tributary blood flow from 14.6 +/- 1.5 to 11.0 +/- 1.7 mL/min and increasing portal systemic collateral vascular resistance from 88 +/- 7 to 103 +/- 8 dyn s/cm5 x 10(3). Ketanserin (0.25 mg/kg), a 5-hydroxytryptamine receptor antagonist, reduced portal pressure from 15.8 +/- 1.0 to 13.3 +/- 0.7 mmHg at a dose that did not alter mean arterial pressure or portal tributary blood flow. It achieved this by reducing portal-systemic collateral vascular resistance from 90 +/- 14 to 74 +/- 13 dyn s/cm5 x 10(3). Saline had no significant effect on systemic and splanchnic haemodynamics. This study shows that ketanserin decreases vascular resistance of portal-systemic collaterals while propranolol increases it. Thus, it is suggested that collateral vascular resistance is accessible to pharmacological manipulation.

Animals↗
PubMed1998

Alterations of neurotransmitter-related gene expression in human and experimental portal-systemic encephalopathy.

Portal-systemic encephalopathy (PSE) is a serious neuropsychiatric condition that results from chronic liver failure and portal-systemic shunting of venous blood. PSE is particularly prevalent following treatment of portal hypertension or ascites by the TIPS procedure. Recent studies both in autopsied brain tissue from PSE patients as well as in experimental animal models of PSE reveal that chronic liver failure results in altered expression of several genes coding for proteins having key roles in the control of neuronal excitability. Such alterations include increased expression of monoamine oxidase (MAO-A isoform), the "peripheral-type" benzodiazepine receptor (PTBR) as well as constitutive, neuronal nitric oxide synthase (nNOS). Such changes result in altered protein expression and in increased degradation of monoamine neurotransmitters, increased synthesis of neurosteroids with inhibitory properties and increased production of nitric oxide (respectively) in brain in chronic liver failure. In the case of PTBR and nNOS, increases in expression result from exposure to ammonia and/or manganese, two neurotoxic agents shown previously to be increased in brain in chronic liver failure. Further elucidation of the consequences of neurotransmitter-related gene expression could identify new pathophysiologic mechanisms and result in new approaches to the prevention of PSE in chronic liver disease in humans.

Animals↗
PubMedDate not supplied

[Correlation of Doppler ultrasound of the portal system with endoscopic changes caused by portal hypertension in cirrhotic patients].

BACKGROUND: The portal hypertension in cirrhotic patients is the main cause of this illness complication, that are clinically translated to visible collateral circulation in the abdominal wall, ascites and esophageal varices. AIM: To evaluate if the portal system echodoppler is able to estimate the presence of esophageal varices, gastric varices and congestive gastropathy in patients with hepatic cirrhosis. PATIENTS AND METHODS: One hundred and eighty six patients of the gastroenterology and hepatology ambulatory of the Clinical Hospital of the Federal University of Paraná, Curitiba, PR, Brazil, had been selected for evaluation. Of those, 145 had completed all the stages of the evaluation and 133 had been enclosed in the final analysis. All had been submitted to high digestive endoscopy for evaluation of esophagogastric varices and congestive gastropathy and then to Doppler ultrasound of the portal system with study of the systolic peak speed of the portal vein, diameter of the portal and splenic vein and spleen size, presence of the umbilical vein recanalization and hepatofugal flow. RESULTS: The patients with esophagogastric varices had significant difference of the spleen size when compared to patients without these change. However, none of the Doppler ultrasound parameters showed good accuracy and specificity in this group of cirrhotic patients. Congestive gastropathy patients had their diagnosis predict with significant manner not only by the portal and splenic vein diameter but also by the spleen size. Similarly to that described above, they do not have a good accuracy and specificity. These evaluations were validated by the construction of ROC (Receiver Operating Characteristic) curves, whose areas below the curves had always been less than 0,8. CONCLUSION: There was not a good correlation of the Doppler ultrasound parameters of the portal system to the presence of the main endoscopic alterations (esophagogastric varices and congestive gastropathy) in patients with hepatic cirrhosis.

Blood Flow Velocity↗
PubMed1993

Application of CDFI and portal system pressure measurement in the study of portal hypertension hemodynamics.

It has been discovered in portal system hemodynamics research using CDFI and pressure measurement, that among 40 portal hypertension patients the demonstrating rate of left gastric vein (LGV) was 77.5%, and all were hepatofugal. The demonstrating rates of spontaneous splenorenal vein shunt collaterals and of patency umbilical vein (UV) with blood signal were 85%, 12.5% respectively, and the thrombosis rate of portal system was 10%. Blood flow direction of main portal vein (MPV) in all patients was hepatopetal, and one case of superior mesenteric vein (SMV) and another one of splenic vein (SV) were hepatofugal. The patients with MPV thrombosis or portal system hepatofugal should be operated on by shunt. Shunt capacity of portal vein in gastroplenic region was 34.07% on average. This demonstrated that devascularization was applicable. Internal diameter, blood capacity and time average velocity (TAV) of the left portal vein (LPV) and right portal vein (RPV) with portal hypertension were almost equal, their difference being not significant (P > 0.2). This should be a basis for the diagnosis of portal hypertension. Free portal pressure (FPP) and internal diameter, blood capacity and TAV of MPV, SV, SMV, LGV were not correlative with each other.

Adult↗
PubMed2003

Central nervous system alterations in liver cirrhosis: the role of portal-systemic shunt and portal hypoperfusion.

The role of portal-systemic shunting and portal liver hypoperfusion in the pathophysiology of central nervous system dysfunction (CNSD) of cirrhosis is not yet well defined. It is well known that one of the most important collateral vessels (CVs) is a patent paraumbilical vein (PUV), but there is controversy regarding its clinical significance. We have evaluated the relationships between neuropsychological and EEG alterations, ammonia plasma level (NH4), hepatic function, and portal hemodynamics (Doppler Ultrasound) in 95 cirrhotic patients. Patency, diameter, or flow of PUV or the presence of other CVs were not related to an increased prevalence of neuropsychological or EEG abnormalities. Patients with effective portal flow (EPF = portal flow - PUV flow) lower than 692 mL/min (median) had a significantly higher risk of failing the neuropsychological test, or of having an altered EEG. Low EPF and prothrombin time (<50%), and high NH4 (51 micromol/L) were independent predictors of an abnormal EEG. Considering both low EPF and the numerosity of CVs, only low EPF was found to explain EEG alterations. In conclusion, portal liver hypoperfusion and decreased liver function were associated with an increased risk of CNSD in cirrhotic patients, whereas PUV patency per se was not.

Brain↗
PubMed1991

[Catecholamine fluorescent, acetylcholinesterase positive and peptide immunoreactive nerve fibers in the rat hepatic portal system].

Innervation of rat hepatic portal system consisting of stem (portal vein) and peripheral portions (superior mesenteric vein, inferior mesenteric vein, splenogastric vein) was investigated by catecholamine fluorescence, acetylcholinesterase and immunohistochemical methods. Catecholamine fluorescent and Neuropeptide Y (NPY) immunoreactive (ir) nerve fibers were distributed throughout the hepatic portal system. Greater density was demonstrated in the peripheral portions. Catecholamine fluorescent and NPY ir nerve fibers formed ground plexus around the hepatic portal system. Acetylcholinesterase positive and vasoactive intestinal polypeptide-ir nerve fibers were sparsely distributed and no significant difference in density was noticed in the stem and the peripheral portions. Density of substance P ir, neurokinin A ir and calcitonin gene-related peptide ir nerve fibers was greater in the peripheral than the stem portion. All these fibers reticular showed pattern.

Acetylcholinesterase↗
PubMed1991

Propranolol ameliorates the development of portal-systemic shunting in a chronic murine schistosomiasis model of portal hypertension.

We investigated the role of early portal hypotensive pharmacotherapy in preventing the development of portal-systemic shunting in a portal hypertensive model of chronic murine schistosomiasis induced by infecting C3H mice with 60 cercariae of Schistosoma mansoni. Propranolol was administered in drinking water to 20 animals for a period of 6 wk at a dose of 10 mg.kg-1d-1, starting at 5 wk of schistosomal infection. 32 age-matched mice with chronic schistosomal infection served as controls. All animals were studied 11 wk after the infection. Compared with controls the portal pressure (10.8 +/- 0.40 mmHg) was significantly lower (P less than 0.001) in the propranolol-treated animals (7.9 +/- 0.80 mmHg). Portal-systemic shunting was decreased by 79%, from 12.2 +/- 3.34% in controls to 2.5 +/- 0.99% in the propranolol group (P less than 0.05). Portal venous inflow was reduced by 38% in the propranolol treated animals (2.50 +/- 0.73 ml/min; n = 6) compared with controls (4.00 +/- 0.34 ml/min; n = 8; P less than 0.05). The worm burden, the granulomatous reaction, the collagen content of the liver, and the serum bile acid levels were not significantly different between the two groups of animals. These results demonstrate that in chronic liver disease induced by schistosomiasis, the development of portal-systemic shunting can be decreased or prevented by the reduction of flow and pressure in the portal system.

Animals↗