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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association of pulmonary hypertension with portal hypertension, also called portopulmonary hypertension (PPHTN), is a known complication of chronic liver disease. Previously, the presence of PPHTN was considered to be a contraindication to orthotopic liver transplantation (OLT). Although there are selected case reports of successful OLT in the setting of PPHTN, an excessive mortality rate is associated with OLT and PPHTN. Heretofore, therapy for chronic management of PPHTN was lacking. Recently, continuous intravenous infusion of epoprostenol has been demonstrated to improve symptomatology and survival in the general population of patients with primary pulmonary hypertension. We now report the use of epoprostenol in the more specific instance of PPHTN. Over a period of 6-14 months, epoprostenol (10-28 ng/kg/min) therapy was associated with a 29-46% decrease in mean pulmonary artery pressure, a 22-71% decrease in pulmonary vascular resistance, and a 25-75% increase in cardiac output in a group of four patients. These results suggest that effective chronic therapy for PPHTN is available. In conjunction with inhaled nitric oxide as acute intraoperative therapy, epoprostenol infusion represents an additional therapeutic option for treatment of PPHTN in the liver transplant candidate.
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PMID:Continuous intravenous infusion of epoprostenol for the treatment of portopulmonary hypertension. 904 58

The significant advances achieved in the last years in the field of liver transplantation have led to an almost routinely performance of this therapeutic approach throughout North America and Western Europe. This has led to an increased demand so that today the real problem is the organ availability and the need to use those supplied only for patients with best chances of success. For this reason timing of the operation and patient selection are of critical importance. The ultimate success depends on better surgical procedures and advances in immunosuppressive therapy, but perhaps even more on an accurate patient evaluation. The patient selection is based on standardized medical criteria which constitute the indication in patients with end-stage liver disease and on a careful search for risk factors. To this purpose the evaluation of the tolerance of the hemodinamic stress during clamping of the inferior vena cava is of critical importance and must be carefully evaluated both in patients with known and unknown coronary disease. Another condition to be considered is lung hypertension which is frequently associated with portal hypertension. Finally, important conditions for a good evaluation are the epatopulmonary syndrome and diabetes. The last condition is not a contraindication unless associated with severe vascular, cardiac or renal complications.
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PMID:[Liver transplantation. Selection criteria and risk evaluation]. 914 74

The presence of naturally portacaval shunts has been investigated in the vasculature of normal and Schistosoma mansoni-infected Rattus rattus. Using the technique of injecting Polystyrene microspheres in the superior mesenteric vein, we demonstrated that the presence of adult schistosomes in the lungs of R. rattus was not due to an innate anomaly of the rat vasculature but resulted from the formation of portacaval shunts during infection. In rats harbouring a bisexual infection, microspheres were only detected in the lungs from week 7. The development and increasing size of the shunts were maximal between weeks 7 and 10 and coincident with the translocation of adult worms from the portal tract to the lungs. At weeks 20-25, only 1-2% of the microspheres were recovered from the lungs, suggesting that the portacaval anastomoses have regressed due to reduction in portal hypertension after worm translocation. R. rattus with a male-only schistosome infection harboured adult worms in the lungs, indicating that the development of shunts does not solely depend upon egg deposition in the liver to generate hypertension. The relationships between the presence of the schistosomes in the lungs, the portacaval shunting and the resistance to reinfection is discussed.
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PMID:Schistosome-induced portacaval haemodynamic changes in Rattus rattus are associated with translocation of adult worms to the lungs. 955 Feb 17

The article presents summarized results of treatment and examinations of 216 patients with gastro-intestinal bleedings due to acute errosive hemorrhagic gastritis and gastroduodenitis, cancer and polyposis of the stomach, liver cirrhosis and portal hypertension, hemorrhage against the background of atherosclerosis and arterial hypertension by administration of hemostatic medicine into the lymphatic system for activation and reinforcement of the reserve monocyte-macrophage mechanism of hemocoagulation. The results obtained confirm the expedience of this method of influencing the monocyte-macrophage hemostasis, having no complications and giving better medical effects.
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PMID:[Hemostatic therapy of gastroduodenal hemorrhage of non-ulcer genesis by the use of reserve mechanisms of hemostasis]. 961 18

The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathophysiology of both syndromes may involve vasoactive mediators and angiogenic factors.
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PMID:Pulmonary vascular disorders in portal hypertension. 964 72

A 30-year-old man with presinusoidal portal hypertension was transplanted for cryptogenic cirrhosis. On the explanted liver, few intrahepatic stones, biliary cirrhosis, chronic cholangitis of the large bile ducts and a peculiar proliferation of small dilated bile ducts at the periphery of the portal tracts led to the diagnosis of secondary biliary cirrhosis and cholangitis, possibly linked to ductal plate malformation, including congenital hepatic fibrosis associated with a minor form of Caroli's disease. Ex vivo portogram and histology showed the paucity of portal vein branches and the hypertrophy of the peribiliary vascular plexus. This hypertrophy, which has been reported in livers with presinusoidal hypertension, is another indirect argument to suggest the diagnosis of congenital hepatic fibrosis.
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PMID:Case report: secondary biliary cirrhosis possibly related to congenital hepatic fibrosis. Evidence for decreased number of portal branch veins and hypertrophic peribiliary vascular plexus. 971 24

Although the underlying mechanisms no doubt differ, activation of the sympathetic nervous system is an important pathophysiological feature in primary arterial hypertension, in portal hypertension accompanying hepatic cirrhosis, and in heart failure, and is a logical therapeutic target for centrally acting sympathetic nervous system suppressant drugs. Portal hypertension: The sympathetic outflows to skeletal muscle vasculature, the heart, the kidneys and to the hepatomesenteric circulation are stimulated in patients with alcoholic cirrhosis of the liver, perhaps as a reflex response to the vasodilatation and vascular shunting present. Acute dosing with clonidine produces dose dependent reduction in noradrenaline spillover from visceral organs and reduction in hepatic vein wedge pressure, with preservation of hepatic blood flow and negligible fall in arterial pressure. These findings indicate the clinical potential of drugs such as clonidine, moxonidine and rilmenidine for chronically lowering portal venous pressure in cirrhosis. Arterial hypertension: Activation of the sympathetic outflow to the heart, kidneys and skeletal muscle vasculature is commonly present in younger (< 45 years) patients with essential hypertension. The sympathetic stimulation appears to have adverse consequences in hypertensive patients beyond blood pressure elevation. Neural vasoconstriction in skeletal muscle has metabolic effects by impairing glucose delivery, which is a basis for insulin resistance and hyperinsulinemia. Within the heart a trophic effect of sympathetic activation on cardiac growth, contributing to the development of left ventricular hypertrophy, and an arrhythmogenic effect are also likely. Cardiac failure: The cardiac sympathetic nerves are preferentially stimulated in severe heart failure, with norepinephrine release from the failing heart at rest being increased as much as 50-fold, similar to the level seen in healthy people during near maximum exercise. This preferential activation of the cardiac sympathetic outflow contributes to arrhythmogenesis and possibly to progression of the heart failure, and has been directly linked to mortality; a high rate of spillover of noradrenaline from the heart is a strong, independent predictor of poor prognosis in severe cardiac failure. The mechanisms underlying sympathetic nervous stimulation are not entirely clear. Increased intracardiac diastolic pressure seems to be one peripheral signal, and increased forebrain norepinephrine turnover an important central mechanism. Following the demonstration of the beneficial effect of the beta-adrenergic blocker, carvedilol, and with second generation centrally acting sympathetic suppressants now under clinical investigation, elucidation of the abnormalities in central nervous control of sympathetic outflow in heart failure has become clinically relevant.
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PMID:Increased sympathetic nervous system activity and its therapeutic reduction in arterial hypertension, portal hypertension and heart failure. 985 71

Pulmonary hypertension associated with increased pulmonary vascular resistance (PVR) and occurring in the setting of portal hypertension is referred to as "portopulmonary hypertension." Intravenous epoprostenol (prostacyclin) is a potent pulmonary and systemic vasodilator with antithrombotic properties. It can decrease PVR and pulmonary artery pressure in patients with primary (idiopathic) pulmonary hypertension. Using right-heart catheterization, we evaluated the acute pulmonary hemodynamic effects of intravenous epoprostenol in patients with moderate to severe pulmonary hypertension (mean pulmonary artery pressure [MPAP] >/=35 mm Hg) associated with clinical manifestations of portal hypertension. Effects of long-term infusion of epoprostenol were also evaluated. We studied 15 consecutive patients with portopulmonary hypertension; 14 underwent acute administration of epoprostenol, and no significant side effects were noted. Ten patients received continuous epoprostenol (range, 8 days-30 months). Acute changes in PVR (-34% +/- 18%), MPAP (-16% +/- 10%), and cardiac output (CO) (+21 +/- 18%), were statistically significant (P <.01). Long-term use of epoprostenol further lowered PVR (-47% +/- 12% from baseline and -31% +/- 22% from the acute change; P <.05) in the 6 patients restudied by right-heart catheterization. Death occurred in 6 of 10 (60%) of those receiving long-term epoprostenol. In moderate to severe portopulmonary hypertension, intravenous epoprostenol resulted in a significant improvement (both acute and long-term) in PVR, MPAP, and CO. Potential adverse effects on portal hypertension and implications for orthotopic liver transplantation (OLT), however, require further study.
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PMID:Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension. 1046 69

In conclusion, surgical therapy in patients with chronic pancreatitis may be characterized as follows: 1. Independently, several investigators have found intraductal and intraparenchymatous hypertension in patients with chronic pancreatitis. Decompression of the ductal system as the main principle of surgical therapy achieves clinical pain relief in most patients with chronic pancreatitis. The precondition is a consequent drainage of the main pancreatic duct and tributary ducts of second and third order up to the prepapillary region. The presence of an inflammatory tumor in the head of the pancreas or ductal abnormalities in the prepapillary region or a pancreas divisum requires performance of an extended drainage operation (LPJ-LPHE) to achieve pain relief and an improved quality of life. An extended drainage operation effectively manages complications arising from adjacent organs, such as distal common bile duct stenosis, segmental duodenal stenosis, and internal pancreatic fistulas. The extent of decompression has to be tailored to the anatomic and morphologic situation of the patient. 2. In patients with chronic pancreatitis, the main pancreatic duct is usually dilated. A small duct (3-5 mm) is only small for the surgeon. For the sclerosing entity of chronic pancreatitis with a truly small duct, that is, less than 3 mm in diameter ("small duct disease"), a longitudinal V-shaped excision of the ventral pancreas, as opposed to left resection, provides a new perspective for a sufficient drainage. 3. In the presence of segmental portal hypertension, a simple or extended drainage operation does not result in a normalization of the portal venous blood flow; however, how often relevant upper gastrointestinal hemorrhage develops from segmental portal hypertension is unclear. Therefore, the clinical relevance of this special problem needs further evaluation. 4. Postoperative morbidity of LPJ-LPHE is significantly lower in comparison to resectional procedures, such as PD, PPPD, and DPRHP. A lower perioperative mortality rate is not justified anymore as a relevant criterion in favor of drainage procedures because resectional procedures are burdened by a minimal or no mortality in experienced centers; however, PD and PPPD are greatly hampered by a significantly decreased postoperative global quality of life as opposed to the LPJ-LPHE. This is reflected by a significantly lower rate of social and professional rehabilitation. 5. The incidence of exocrine and endocrine organ dysfunction is lower after LPJ-LPHE compared with PD or PPPD, but not compared with DPRHP. Preservation of the gastroduodenal passage and the continuity of the bile duct with its associated feedback mechanisms of exocrine pancreatic secretion and glucose metabolism seem to be responsible for this phenomenon. 6. An early surgical or endoscopic interventional drainage of the hypertensive pancreatic duct system possibly offers the chance to favorably manipulate the natural course of chronic pancreatitis with regard to a delayed onset of exocrine or endocrine insufficiency. 7. Late mortality reflects continued alcohol abuse rather than the effect of an operative procedure.
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PMID:Surgical treatment of chronic pancreatitis and quality of life after operation. 1047 Mar 35

Patients with end-stage liver failure, portal hypertension, and associated pulmonary artery hypertension (portopulmonary hypertension [PPHTN]) have a high mortality when undergoing liver transplantation. Successful transplantation in these patients may depend on efforts to reduce pulmonary artery pressure (PAP). To this end, a number of centers are using a continuous intravenous (IV) infusion of epoprostenol, which has been shown to improve symptoms, extend life span, and reduce PAP in patients with primary pulmonary hypertension. We report four cases in which treatment of patients with PPHTN with continuous IV epoprostenol was followed by the development of progressive splenomegaly, with worsening thrombocytopenia and leukopenia. This finding may limit the usefulness of epoprostenol in PPHTN and influence the timing of transplantation in such patients.
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PMID:Progressive splenomegaly after epoprostenol therapy in portopulmonary hypertension. 1047 35


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