Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen patients with advanced hepatic cirrhosis underwent cardiopulmonary assessment by means of Swan-Ganz catheters combined with indocyanine green clearance studies to measure functioning hepatic cell mass. The indocyanine green clearance test was found to have a statistically significant linear correlation with such indicators of the hyperdynamic circulatory state as cardiac index and total peripheral resistance. Results from these studies also showed that the hyperdynamic state in cirrhosis is associated with limited oxygen consumption as compared with a control series of patients. Of the 14 patients who required operations, eight survived and six died. The mean indocyanine green clearance was a statistically significant predictor of death.
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PMID:Functioning hepatic cell mass and the hyperdynamic state in cirrhosis. 341 47

Prostaglandin E1 (PGE1, Prostin VR) in doses of 30 ng/kg . min was studied in two series of severely ill surgical patients with adult respiratory distress syndrome (ARDS). First the drug was administered in an initial trial in six patients; then a prospective, randomized, blinded trial was conducted in 10 studies on nine patients. PGE1 markedly decreased pulmonary artery pressure, pulmonary and systemic vascular resistance indexed, and venous pressures, while increasing cardiac output, arterial PO2 (PaO2), oxygen delivery, and oxygen consumption when compared with the baseline preinfusion control values and with the response of the placebo-treated control series. The PGE1 responses were greater in patients whose ARDS was primarily attributed to the postoperative state with or without sepsis and least in patients with cirrhosis. The data are consistent with the concept that the drug reduces vasoconstriction primarily in the pulmonary circulation but also in the systemic circulation; improved PaO2 usually follows the hemodynamic effect. We conclude that PGE1 may be a useful adjunctive therapy for ARDS.
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PMID:Effects of prostaglandin E1 in adult respiratory distress syndrome. 351 57

The aim of the study in alcoholic cirrhotic patients was to determine if a relationship exists between the areas of hepatocytes and their nuclei and the area of the nodules to which these cells belong as well as the thickness of the fibrous tracts which delimit these nodules. It was found that hepatocyte and nuclear areas were enlarged the smaller the nodules and the thicker the surrounding fibrous tracts. Considering that oxygen supply in liver cirrhosis decreases with increasing fibrosis, our results permit the hypothesis that a low oxygen supply causes an increase not only in liver cell size but also in nuclear size, which is an index of nuclear activity.
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PMID:Hepatocyte and nuclear areas in alcoholic liver cirrhosis: their relationship with the size of the nodules and the degree of fibrosis. 360 94

Blood gas analyses and hepatic blood flow were determined during hepatic vein catheterization in order to establish a possible hypoxic component in alcoholic liver disease. Fifty-six patients (9 non-cirrhotic liver disease, 14 cirrhosis Child-Turcotte class A, 23 class B, 10 class C) and 10 control subjects were studied. Mean hepatic venous oxygen saturation and tension were almost the same in all groups, and hepatic blood flow was inversely correlated to the arteriohepatic venous oxygen difference (r = -0.53, P less than 0.01). Splanchnic oxygen uptake was similar in all groups studied. The arterio-hepatic venous difference of base excess was small and of the same size in all groups, indicating no enhanced production of lactic acid in the liver. Our results do not support the concept that hepatic venous oxygen content is low in alcoholic liver disease and thereby contributes to hypoxic liver damage.
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PMID:Hepatic venous oxygen content in alcoholic cirrhosis and non-cirrhotic alcoholic liver disease. 361 86

In patients with cirrhosis, elevation of azygos blood flow has been attributed on indirect grounds to cephalad portosystemic collaterals. To gather more information on the origin of the azygos blood, we studied the oxygen and bile acid content of the azygos and mixed venous blood in patients with portal hypertension. Azygos oxygen saturation was 59.6 +/- 6.0% in 8 controls, and significantly higher in 35 patients with cirrhosis (76.7 +/- 7.6%; P less than 0.01) as well as in 6 patients with noncirrhotic portal hypertension (84.0 +/- 8.2%; P less than 0.01). High oxygen saturation, however, was not correlated to azygos blood flow in patients with cirrhosis. In cirrhotic patients, total bile acid concentrations were 28.1 +/- 20.4 mumol/l in the pulmonary artery and 25.9 +/- 17.6 mumol/l in the azygos vein, giving an azygos to mixed venous ratio of 0.95 +/- 0.18. These results provide new evidence that elevated azygos blood flow in patients with portal hypertension is derived from the portal system, and perhaps predominantly from the splenic territory.
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PMID:Oxygen and bile acid content in the azygos blood. Clues to the azygos derivation in patients with portal hypertension. 365 14

A rat model was used to determine whether the metabolism of halothane is changed in the presence of cirrhosis and whether exacerbation of liver dysfunction is correlated with such a change. Cirrhosis was produced by gavaging enzyme-induced male Wistar rats with carbon tetrachloride in corn oil once weekly for 12 weeks. Control rats received corn oil only. After a 3-week period without treatment, blood and urine were collected from each rat for determination of background levels of inorganic fluoride, bromide, and trifluoroacetic acid (halothane metabolites) and for assessment of liver function. Rats were then anesthetized with 1.05% halothane in 50% oxygen for 3 h. Following anesthesia, serial blood and urine samples were taken to monitor halothane metabolism and liver function. No differences were observed between cirrhotic and non-cirrhotic rats in serum levels and urinary excretion of halothane metabolites. However, serum levels of SGOT and SGPT were significantly increased about 1.5-fold in the noncirrhotic group and about 2.5-fold in the cirrhotic group after anesthesia. The increased levels observed in the cirrhotic group were significantly greater than in the noncirrhotic group. The results imply that the exacerbation of liver dysfunction after halothane anesthesia is most likely related to an indirect effect, such as change in liver blood flow, rather than to toxic metabolites.
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PMID:Halothane metabolism in cirrhotic rats. 367 65

In order to elucidate the effect of beta-adrenergic blockade on liver metabolism and haemodynamics, splanchnic oxygen uptake, hepatic removal of indocyanine green (ICG) and splanchnic and systemic haemodynamics were studied in 13 patients with cirrhosis before and 1.5-2 h after an oral dose of 80 mg propranolol. All patients underwent hepatic vein catheterization and had a primed continuous intravenous infusion of ICG. Azygos vein catheterization was performed in six patients. Splanchnic (hepatic-intestinal) oxygen uptake (median control 68 ml/min vs. beta-blockade 56 ml/min, P less than 0.01), azygos venous oxygen saturation (76 vs. 67%, P less than 0.05), ICG clearance (263 vs. 226 ml/min, P less than 0.01), wedged-to-free hepatic vein pressure (16 vs. 13.5 mm Hg, P less than 0.01), hepatic blood flow (1.18 vs. 0.78 l/min, P less than 0.01), cardiac index (3.42 vs. 2.53 l/min . min 2, P less than 0.01), and heart rate (72 vs. 56 beats per min, P less than 0.01) decreased significantly after oral beta-blockade. The hepatic extraction ratio of ICG increased significantly (0.32 vs. 0.45, P less than 0.01), whereas estimated 'intrinsic' ICG clearance (289 vs. 300 ml/min, n.s.), arterial blood pressure, stroke volume, and systemic vascular resistance remained essentially unchanged. The results indicate that besides the well-known cardiovascular effects of propranolol, beta-adrenergic blockade may also reduce hepatic metabolic functions as evidenced by the significantly decreased splanchnic oxygen uptake. The raised hepatic extraction ratio of ICG may be caused by reduction in hepatic blood flow as well as in intrahepatic shunting.
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PMID:Effect of oral propranolol on splanchnic oxygen uptake and haemodynamics in patients with cirrhosis. 369 57

Recent reports in the literature have promulgated nonresective treatment of abdominal aortic aneurysm as a safer procedure than conventional aneurysmectomy with graft replacement in high-risk patients. This review of 106 high-risk patients who underwent conventional aneurysm repair between 1980 and 1985 was undertaken to compare the relative risks, perioperative morbidity, and operative mortality of these patients to that reported for patients treated by nonresective therapy. Excluded were those patients who had rupture initially or underwent a concomitant renovascular procedure. Patients were considered to be at high risk if they met one or more of the following criteria: age equal to or greater than 85 years; receiving oxygen at home, PO2 less than 50 torr, or forced midexpiratory flow less than 25% of predicted; serum creatinine equal to or greater than 3 mg/dl; biopsy-proven cirrhosis with ascites; retroperitoneal fibrosis; or New York Heart Association functional class III-IV angina, left ventricular ejection fraction less than 30%, recent congestive heart failure, complex ventricular ectopy, large left ventricular aneurysm, severe valvular disease, recurrent congestive heart failure or angina after coronary artery bypass grafting, or severe unreconstructed coronary artery disease confirmed by angiography. The mortality rate for conventional aneurysm repair in high-risk patients was 5.7%, compared with a reported 7% mortality rate for nonresective therapy. In those patients with severe cardiac dysfunction, intraoperative pharmacologic manipulation and the selective use of intra-aortic balloon counterpulsation appeared helpful in achieving survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Conventional repair of abdominal aortic aneurysm in the high-risk patient: a plea for abandonment of nonresective treatment. 370 38

Changes of hepatic microcirculations in 22 autopsy cases of liver cirrhosis were analyzed by corrosion cast/scanning electron microscope (SEM) examination. By this method, the site of arterioportal (A-P) communication in liver cirrhosis was clearly demonstrated between proliferated portal venules and arterial capillaries. The communications were observed at the same site as in the normal liver and were not at larger arterial and portal vein branches. The findings indicate that the increase of A-P communication in liver cirrhosis may be called "capillary shunting". On the basis of the findings, it was postulated that the A-P shunt could not assist in the development of portal hypertension by the transmission of high arterial pressure to the portal vein but could only compensate for decreased portal flow and/or elevate the oxygen concentration in the sinusoids to improve the hypoxic state of the liver parenchyma. It was also demonstrated that the arterial capillarization of the interstitial septa in micronodular wide septal cirrhosis was more prominent than that in macronodular thin septal cirrhosis. A grade of portal vein reduction and compensatory arterialization in a fibrous septum have been regarded as an index to estimate the advancement of liver cirrhosis. Therefore, if alcoholic micronodular cirrhosis could change into macronodular, the process should have occurred at least before the establishment of micronodular wide septal cirrhosis.
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PMID:Hepatic microcirculation of liver cirrhosis studied by corrosion cast/scanning electron microscope examination. 371 92

The effect of the calcium channel blocking agent, verapamil, on microcirculatory patterns and hepatic function was investigated in the perfused liver of cirrhotic rats. Compared with controls, cirrhotic livers had higher vascular resistance, increased intrahepatic shunting, and smaller extravascular albumin space and larger extravascular sucrose space, as determined by a multiple-indicator dilution technique. Hepatic function, estimated by determining propranolol and antipyrine extraction, was markedly reduced in cirrhotic livers. Portal pressure was then reduced 25% either pharmacologically by verapamil or hydrodynamically by lowering inflow. Verapamil decreased vascular resistance by 22%. This was associated with a 38% reduction in intrahepatic shunting and a 62% increase in extravascular albumin space. Hydrodynamically lowering pressure had no or adverse effects. The verapamil-induced improvement in microcirculatory characteristics was associated with a significant improvement in oxygen consumption (+21%) and antipyrine clearance (+20%). We conclude that the microvascular distortions of liver cirrhosis in the rat are partially reversible by vasodilators like verapamil.
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PMID:Verapamil favorably influences hepatic microvascular exchange and function in rats with cirrhosis of the liver. 373


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