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)

Propranolol, a beta-blocking agent, has been proposed in the prevention of gastro-intestinal bleeding in cirrhotic patients, and is known for its bronchoconstrictive effects. Since hypoxemia is a frequent finding in patients with cirrhosis, this work was undertaken to study the effects of intravenous propranolol on pulmonary function and on gas exchange in these patients. The 10 patients studied had cirrhosis associated with an increase in the alveolar arterial O2 difference, (A-a)DO2, an index of arterial oxygenation impairment. Their 1-s forced expiratory volume/forced vital capacity (FEV1/FVC) was normal, but in most a reduction of the forced expiratory flow of 25-75% of vital capacity was observed (FEF 25-75), suggestive of some degree of small airway obstruction. Although propranolol induced a significant decrease of FEF 25-75 from 67.7 +/- 19.3% to 55.4 +/- 21.5% (P less than 0.01), suggesting a bronchoconstriction of the small airways, there was no significant decrease in mean arterial oxygen partial pressure (PaO2) (74.1 +/- 6.4 mmHg before and 77.0 +/- 6.5 mmHg after propranolol). Indeed, a slight but significant improvement of the (A-a)DO2 was observed, from 39.1 +/- 5.9 mmHg to 34.4 +/- 4.9 mmHg (P less than 0.02). Although the mechanism of this beneficial effect remains to be elucidated, we conclude that in spite of its bronchoconstrictive action, propranolol is not contra-indicated in cirrhotic patients with hypoxemia who have normal expiratory flow.
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PMID:Effects of propranolol on pulmonary gas exchange in patients with cirrhosis. 280 64

The influence of a long-acting somatostatin octapeptide analogue (SMS 201-995) on splanchnic circulation and metabolism has been studied in healthy subjects and in patients with liver cirrhosis. In healthy subjects doses of 5, 10, 50, or 100 micrograms SMS and in the cirrhotic patients 25 micrograms SMS were infused intravenously during 1 h. Measurements were obtained before, during, and for 1 h after SMS infusion. SMS infusion in healthy subjects resulted in a 25-35% reduction in hepatic blood flow. This effect was largely independent of the dose used. Splanchnic oxygen uptake was unchanged before and during SMS infusion. Insulin and glucagon levels fell markedly in response to SMS administration, and the blood concentration and splanchnic output of glucose decreased transiently. Patients with liver cirrhosis responded to SMS infusion similarly to the healthy subjects. Hepatic blood flow decreased by 25-35% and remained suppressed for at least 1 h after infusion. Wedge hepatic venous pressure was 18 +/- 2 mm Hg in the basal state and decreased progressively during and after SMS infusion (60 min after infusion, 15 +/- 2 mm Hg; P less than 0.01). The marked hyperinsulinaemia and hyperglucagonaemia seen in the basal state decreased significantly during SMS administration. As in the case of the controls, blood concentration and splanchnic output of glucose fell transiently during and after SMS infusion. It is concluded that SMS exerts a marked and prolonged suppressive effect on hepatic blood flow in both healthy subjects and patients with liver cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of a long-acting somatostatin analogue on splanchnic haemodynamics and metabolism in healthy subjects and patients with liver cirrhosis. 287 92

The influence of SMS 201-995 (octreotide, Sandostatin), a long-acting somatostatin analogue, on splanchnic haemodynamics was studied in 15 patients with liver cirrhosis and in 5 healthy individuals before, during, and after 60 min of intravenous SMS infusion (25 and 50 micrograms/h, respectively). No adverse effects of the SMS infusion were seen. In the basal state the estimated hepatic blood flow was 1.04 +/- 0.08 l/min (mean +/- SE) in the patients and 1.62 +/- 0.09 l/min (P less than 0.001) in the controls. At 15 min after the beginning of the infusion the blood flow had already decreased by 15-30% (P less than 0.05-0.01). The reduction was more marked in controls than in patients, and it persisted in both groups during and for 60 min after the infusion. Wedged hepatic venous pressure, measured in the patients, was 20 +/- 2 mmHg in the basal state and 18 +/- 1 mmHg during the infusion (P less than 0.05), and it remained at this level for 60 min after the infusion. Free hepatic venous pressure was unchanged throughout the study. Splanchnic oxygen uptake was similar in the two groups in the basal state and remained unaltered during and after SMS infusion. Both heart rate and arterial systolic and diastolic blood pressure remained unchanged during SMS administration. In summary, SMS infusion results in a fall in hepatic blood flow and a slight but significant decrease in wedged hepatic venous pressure, whereas no effect was noted on the systemic circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemodynamic effects of a long-acting somatostatin analogue in patients with liver cirrhosis. 289 Nov 84

The effect of glucagon on hepatic regional hemodynamics was investigated in patients with chronic liver disease during peritoneoscopy with reflectance spectrophotometry. When glucagon was infused intravenously in patients with a non-cirrhotic liver, the regional hepatic tissue oxygen consumption, as estimated spectrophotometrically, increased significantly, whereas the index of hepatic tissue blood volume did not change appreciably, and consequently, the oxygen saturation of hemoglobin in the hepatic tissue blood decreased. In contrast, the administration of glucagon in patients with liver cirrhosis resulted in a significant increase in the index of hepatic tissue blood volume and produced a minor increase in hepatic tissue oxygen consumption. The oxygen saturation of hepatic blood hemoglobin tended to increase in the cirrhotics. The result suggests the presence of functional vasoconstriction at the presinusoidal and/or sinusoidal vessels in the cirrhotic liver, possibly due to a decreased vasomotor activity and/or an abnormal regulatory function of vasoactive substances, which are released by glucagon.
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PMID:Characterization of hepatic hemodynamics in cirrhotics and non-cirrhotics. Effect of glucagon infusion. 292 37

We investigated the estimated hepatic oxygen consumption by reflectance spectrophotometry during peritoneoscopy and the rate of in vitro oxygen consumption of liver slices obtained by liver biopsy using the oxygen electrode apparatus in patients with chronic liver diseases. The estimated hepatic oxygen consumption decreased concomitantly with the decrease in blood supply, expressed as the regional hepatic blood hemoglobin concentration, and it was significantly decreased in cirrhosis compared to chronic hepatitis. The estimated hepatic oxygen consumption also was significantly correlated with the serum albumin level, 15-min retention rate of indocyanine green, and prothrombin time. There was no correlation between the estimated hepatic oxygen consumption calculated from the reflectance spectra and the rate of in vitro oxygen consumption measured by the oxygen electrode apparatus. Most cirrhotic liver slices had a respiratory rate comparable to that in chronic hepatitis. Thus, it is concluded that the reduction of estimated hepatic oxygen consumption in cirrhosis of the liver is mainly due to the reduction of oxygen supply secondary to the decrease of hepatic blood flow.
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PMID:Estimated hepatic oxygen consumption in patients with chronic liver diseases as assessed by organ reflectance spectrophotometry. 293 79

Alterations in protein and amino acid metabolism have been postulated to explain the frequent observations of muscle wasting and decreased plasma branched-chain amino acid concentrations in cirrhosis. In order to investigate the changes in protein metabolism, we have measured the rates of leucine turnover and oxidation in six stable, biopsy-proven cirrhotics and six age and sex-matched healthy control subjects after an overnight fast, using [1-13C]leucine tracer. Following a primed constant-rate infusion of [1-13C]leucine, the 13C enrichments of plasma leucine and expired CO2 were used to estimate leucine turnover and oxidation, respectively. Fat-free body mass was estimated from the measurements of total body water as quantified by H2[18O] tracer dilution. The rates of CO2 production and oxygen consumption were measured hourly during the study period, using open-circuit respiratory calorimetry. Urinary urea, ammonia and total nitrogen excretion rates were quantified from timed urine samples. Even though the plasma leucine levels were lower in cirrhotics as compared with controls (100.5 +/- 17.1 vs. 138.3 +/- 20.4 mumoles per liter, mean +/- S.D., p less than 0.001), the rates of leucine turnover were not significantly different in the two groups (89.4 +/- 19.0 vs. 87.8 +/- 19.0 mumoles per kg X hr). In contrast, the rates of leucine oxidation were significantly reduced in cirrhosis (8.1 +/- 2.5 vs. 12.7 +/- 3.1 mumoles per kg X hr, p less than 0.01). When all subjects were considered, the leucine oxidation rate was correlated with plasma leucine concentration (r = 0.62, p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Leucine metabolism in stable cirrhosis. 308 96

The hypoxaemia associated with hepatic cirrhosis is classically attributed to an intrapulmonary shunt caused by small vascular abnormalities. Severe hypoxaemia (47 mmHg) associated with dyspnoea, cyanosis and clubbing was observed in a 57-year old man who presented with cirrhosis of the liver. At contrast echocardiography, a right-to-left shunt was demonstrated by the appearance of microcavities in the left atrium and ventricle after peripheral intravenous injection of the contrast medium. The intrapulmonary location of the shunt was determined by a 4 cardiac cycles interval between the arrival of the microcavities in the right heart and their appearance in the left heart. The right-to-left shunt was confirmed by the pure oxygen ventilation test and by pulmonary perfusion scintigraphy with radiolabelled albumin microaggregates. Pulmonary angiography proved normal. Thus, contrast echocardiography is capable of diagnosing right-to-left shunts associated with hepatic cirrhosis and to demonstrate their intrapulmonary location.
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PMID:[Intrapulmonary right-left shunt associated with liver cirrhosis: diagnosis by contrast echocardiography]. 313 12

Liver cirrhosis was induced in rats by the combined action of oral phenobarbitone and inhalations of carbon tetrachloride vapors. These rats manifested hepatosplenomegaly, hypoalbuminemia, and 2- to 17-fold elevations in serum transaminases and alkaline phosphatase levels. The hepatic antioxidant enzymes, superoxide dismutase and catalase, showed 28 and 60% decreases, respectively. There was, however, no increase in the hepatic lipid peroxidation. These studies suggest that in cirrhosis liver cell damage may result due to the direct attack of the oxygen free radicals. Lipid peroxidation in the liver may not be a prerequisite for the development of cirrhosis, as is generally believed.
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PMID:Hepatic antioxidant enzymes and lipid peroxidation in carbon tetrachloride-induced liver cirrhosis in rats. 321 29

The acute effects of the peritoneovenous shunt (LeVeen) on hemodynamics and pulmonary gas exchange in 6 consecutive patients with intractable ascites and cirrhosis were evaluated. After opening the peritoneovenous shunt, there was a marked increase in cardiac index, (from 3.78 +/- 0.4 to 5.86 +/- 0.4 1/min. m2, p less than 0.01), and mean pulmonary artery pressure (from 17.3 +/- 1.9 to 23.3 +/- 1.5 mmHg, p less than 0.05), while a significant decrease in systemic vascular resistances (from 1086 +/- 116 to 694 +/- 52 dynes.sec.cm-5, p less than 0.05) was observed. In all patients there was a drop in arterial oxygen tension (PaO2) (from 76 +/- 3 to 67 +/- 3 torr, p less than 0.01) and an increase in venous admixture (Qsp/Qt) from 13.1 +/- 2 to 18.9 +/- 2%, p less than 0.01). The comparable increase in cardiac output and in venous admixture produced by opening the peritoneovenous shunt, might be related to the massive transfusion of ascitic fluid into the intravascular compartment. It is therefore concluded that this impairment of tas exchange further support discarding an appropriate amount of ascitic fluid at the time of shunt insertion.
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PMID:Acute effects of peritoneovenous shunt (Le Veen) on the hemodynamics and gas exchange in patients with hepatic intractable ascites. 322 74

In animals, there may exist a hyperemic response in the portal circulation during intravenous administration of hypertonic glucose, but a hemodynamic response of this kind has never been described in man. This study was designed to evaluate if hyperglycemia itself could induce systemic or splanchnic hemodynamic changes in patients with cirrhosis. Sixteen patients with cirrhosis were studied before and during i.v. infusions of hypertonic (900 mOsmoles per liter) glucose (n = 8), mannitol (n = 4) or saline (n = 4) at 2 ml per min. In the group receiving glucose, there were significant increases in hepatic venous pressure gradient (+12%), azygos blood flow (+27%) and pulmonary capillary pressure (+32%), while calf blood flow decreased (-26%). No changes occurred in the mannitol or saline groups. Changes in plasma osmolality, plasma volume, splanchnic oxygen extraction and vasoactive hormones, including vasoactive intestinal polypeptide and glucagon, did not appear to be involved in the mechanism of these vasoactive phenomena. It is suggested that the possible deleterious effects of increase in portal pressure and azygos blood flow should be taken into consideration when administering hypertonic glucose to patients with portal hypertension.
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PMID:Systemic and splanchnic hemodynamic effects of intravenous hypertonic glucose in patients with cirrhosis. 337 82


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