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)

Portal hemodynamics were studied in 69 patients with cirrhosis and 29 patients with idiopathic portal hypertension to investigate the effects of an operative procedure for varices that consists of transabdominal esophageal mucosal transection, paraesophagogastric devascularization, pyloroplasty, and splenectomy. Portal venous flow measured by the pulsed Doppler flowmeter in 14 patients with cirrhosis and nine patients with idiopathic portal hypertension, who underwent operation 2-5 yr earlier, was significantly reduced compared with that in unoperated 49 patients with cirrhosis and 17 patients with idiopathic portal hypertension who had esophageal varices (410 +/- 158 versus 660 +/- 263 ml/min in cirrhosis; 443 +/- 185 versus 912 +/- 189 ml/min in idiopathic portal hypertension). In nine patients (six cirrhosis, three idiopathic portal hypertension), portal venous flow and portal vein pressure were measured before and after operation. In patients with cirrhosis, portal vein pressure did not change significantly postoperatively even though portal venous flow was reduced. In contrast, portal vein pressure decreased in two patients with idiopathic portal hypertension in whom portal venous flow was reduced. Portal vein pressure was elevated in one patient with idiopathic portal hypertension in whom portal venous flow was increased postoperatively as a result of resection of a large gastro- and splenorenal shunt conducted additionally.
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PMID:Effects of esophageal transection combined with splenectomy on portal hemodynamics. 379 75

Changes of portal hemodynamics with the progression of chronic liver disease and changes caused by body posture and physical exercise were investigated using an ultrasonic pulsed Doppler flowmeter in healthy adults and in patients with chronic persistent hepatitis, chronic active hepatitis, and cirrhosis. Portal venous velocity was significantly reduced in patients with chronic active hepatitis, cirrhosis without a large splenorenal shunt, and cirrhosis with a large splenorenal shunt, compared with normal subjects and patients with chronic persistent hepatitis. Portal venous flow, by contrast, was significantly reduced only in patients with cirrhosis and a large splenorenal shunt compared with normal subjects and with the other three groups; there was no significant difference in portal venous flow among the latter four groups. Both portal venous velocity and flow showed a tendency toward further reduction in patients with cirrhosis who had hepatofugal flow of part of the superior mesenteric venous blood into the splenic vein and a large splenorenal shunt. Both exercise and posture change from supine to sitting significantly reduced portal venous velocity and portal venous flow in normal subjects, as well as in the patients with chronic liver disease.
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PMID:Portal venous hemodynamics in chronic liver disease: effects of posture change and exercise. 389 4

The portal venous system was studied by ultrasonography (US) in 18 patients with cirrhosis of the liver who had previous bleeding from large esophageal varices. Portal-tract pressure for ten of these patients also was measured by hepatic vein catheterization. After 21 days of treatment with atenolol, the calibers of their splanchnic veins decreased during expiration, while a response to breathing maneuvers was restored. The decrease in the caliber of the splenic and superior mesenteric veins seen by US appeared to correlate significantly with the decrease in portal pressure (P less than .05). Nonresponse to treatment also was detected by US. Real-time US may be routinely carried out as a noninvasive, easy-to-repeat technique for the study of portal system hypertension in patients with cirrhosis undergoing therapy with beta-adrenergic blocking agents.
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PMID:Portal pressure changes induced by medical treatment: US detection. 389 6

Net acetate uptake/release by various tissues was studied in vivo in fed, starved and Paromomycin-treated rats and in patients with cirrhosis of the liver. In humans the portal vein, hepatic vein and hepatic arterial blood flow rates were determined simultaneously. In rats acetate is only intestinally produced and released into the portal vein. Intestinal production is decreased by 33% in starved and Paromomycin-treated rats compared to fed animals. Portal vein hepatic vein acetate differences are linearly related to the portal vein acetate concentration (r = 0.92). Acetate uptake from the portal vein by the liver was found when the portal venous concentration exceeded 180 mumol l-1. In humans the hepatic net acetate uptake from the portal vein/net acetate release into the hepatic vein, measured as mmol min-1, is linearly related to the portal vein acetate concentration (r = 0.96). The data indicate that the liver may homeostatically regulate the systemic acetate concentration in rat and man.
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PMID:Role of gastrointestinal tract and liver in acetate metabolism in rat and man. 393 Feb 58

Colloid osmotic pressure in plasma (IIP) and ascitic fluid (IIA) and hydrostatic pressures in the hepatoportal system were measured simultaneously in 20 patients with decompensated cirrhosis. IIP was significantly decreased (mean, 21 mm Hg, versus normal, 30 mm Hg; P less than 0.01), and IIA was significantly below that of plasma (average, 25% of IIP; P less than 0.01). Portal pressure (transmural), determined as wedged hepatic venous minus inferior vena caval pressure (WHV--IVCP), was significantly increased (mean, 18 mm Hg, versus normal, 3 mm Hg; P less than 0.01) and inversely correlated to IIA/IIP (r = -0.77, P less than 0.001). WHV--IVCP was in most patients in the same order as and closely correlated to effective colloid osmotic pressure (IIP--IIA) (r = 0.88, P less than 0.001). No relationship was found between WHV--IVCP and IIP. The results indicate that a fall in colloid osmotic pressure in the interstitial space and ascitic fluid is related to and most likely secondary to the elevated portal pressure in decompensated cirrhosis. Effective colloid osmotic pressure may therefore be regarded as a 'mirror image' of transmural portal pressure. The role of colloid osmotic pressure in the genesis and perpetuation of ascites should be reconsidered in the light of these findings.
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PMID:Colloid osmotic pressure in decompensated cirrhosis. A 'mirror image' of portal venous hypertension. 399 73

Portal pressure and systemic hemodynamics were evaluated for 30 minutes after intravenous injection of 400 mg of cimetidine in patients with and without liver cirrhosis when they were operated upon for varying surgical diseases. A transient fall of arterial pressure was seen in both groups of patients, but the change was statistically significant only in those with cirrhosis. Cimetidine did not substantially alter pulse rate, CVP, and portal pressure in both groups. The present results seem to indicate that rapid administration of cimetidine does not induce a fall of portal venous pressure in both cirrhotic and non-cirrhotic patients.
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PMID:Effect of cimetidine on portal pressure and systemic hemodynamics in patients with and without liver cirrhosis. 402 50

Propranolol decreases portal venous pressure in patients with cirrhosis but no method is available in man to study the effect of this beta-blocker on splanchnic organ blood flow. Because in rats, the microsphere method allows evaluation of regional blood flow, the acute effect of propranolol on both splanchnic and systemic circulations was studied in normal rats and in rats with portal hypertension due to portal vein stenosis. Portal venous pressure significantly decreased during propranolol administration in normal (5.6 +/- 1.0-4.7 +/- 1.1 mm Hg; mean +/- SD) as well as in portal hypertensive rats (11.7 +/- 2.3-10.3 +/- 1.8 mm Hg). Propranolol slightly decreased cardiac output and arterial pressure in all rats. Portal tributary blood flow was significantly reduced by propranolol in normal rats (17.4 +/- 3.0-11.3 +/- 2.2 ml/min) and in portal hypertensive rats (23.7 +/- 5.0-16.6 +/- 3.3 ml/min). Accordingly vascular resistance of the different organs in the portal venous territory increased in these rats receiving propranolol. The percentage of the decrease in portal tributary blood flow was significantly more marked than the percentage of reduction in cardiac output in portal hypertensive rats but, in normal rats, these percentages were parallel. Hepatic arterial blood flow did not change or slightly increased and, consequently, hepatic arterial vascular resistance decreased. These findings further clarify the marked effects of propranolol on splanchnic circulation.
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PMID:Acute effect of propranolol on splanchnic circulation in normal and portal hypertensive rats. 405 47

The aim was to study the relationships between portal hemodynamic parameters in cirrhotic patients. Portal hemodynamics was assessed by scintisplenoportography and sonography, and the measurement of portohepatic gradient. Gradient between wedged and free hepatic venous pressures was 2.71 +/- 0.90 kPa (SD), and extrahepatic shunting was 49 +/- 31 p. 100 (SD) in 27 cirrhotic patients. Intrahepatic shunting was present in 17 p. 100 out of 23 cirrhotics. Portal blood flow was 0.582 +/- 0.196 l/min (SD) and hepatic resistance to portal blood flow was 4.84 +/- 2.62 kPa/l/min (SD). Portal blood flow correlated neither with the pressure gradient, nor with portosystemic shunting. The pressure gradient was significantly correlated with portal systemic shunting (r = 0.64, p less than 0.001). Hepatic resistance to portal blood flow was significantly (p less than 0.05) correlated with portal systemic shunting, however the value of the correlation coefficient was low (r = 0.433). The pressure gradient and portosystemic shunting were higher in patients with large esophageal varices than in those with small ones (respectively t = 2.665, p less than 0.02 and t = 3.00, p less than 0.01). Hemodynamic pattern was not correlated with the degree of hepatocellular failure, as assessed by the Child-Pugh index. In conclusion this study provides further evidence for the forward theory of portal hypertension in human liver cirrhosis.
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PMID:[Correlation between hemodynamic parameters of the portal circulation in cirrhotic patients]. 406 89

A reduction in effective (nonportal) plasma volume is considered the basis for renal sodium retention, a spontaneous reduction in glomerular filtration rate (GFR), and a fall in GFR occurring during drug-induced diuresis in patients with cirrhosis and ascites. In the present study the concept of a reduced effective plasma volume in cirrhosis is challenged by two lines of evidence, even though effective plasma volume itself could not be measured. (a) Total plasma volume failed to rise in 10 patients with the spontaneous loss of ascites, the appearance of sodium in the urine, and a rise in GFR. Portal pressure remained constant in these patients as ascites left, suggesting that effective plasma volume had not increased while portal plasma volume decreased. (b) Reduction of GFR could not be prevented in five patients with cirrhosis and ascites while total plasma volume was prevented from falling with albumin infusions during drug-induced diuresis. Reduction of GFR during drug-induced diuresis in 15 patients with cirrhosis and ascites was completely reversed with saline infusion despite continued diuresis with the identical drugs, excluding drug nephrotoxicity as the cause for the reduced GFR. The ascites of cirrhosis might no longer be regarded as a cause of effective plasma volume contraction, stimulating renal sodium retention and a reduction in GFR. More likely, this form of ascites is a result of plasma volume expansion and sodium retention. The causes for renal sodium retention and a spontaneous reduction in GFR remain unknown. The cause for a fall in GFR during drug-induced diuresis also remains unknown, but effective plasma volume contraction and drug nephrotoxicity seem excluded.
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PMID:Effective plasma volume in cirrhosis with ascites. Evidence that a decreased value does not account for renal sodium retention, a sponteneous reduction in glomerular filtration rate (GFR), and a fall in GFR during drug-induced diuresis. 577 Nov 97

Portal blood flow (PBF) can be measured quantitatively using a B-mode combined pulsed Doppler (BCD) system. This system combines a real time B-mode linear type electroscanner and a pulsed Doppler (D-mode) flowmeter. Since both modes are displayed in realtime, Doppler blood flow signals can be retrieved at will from any depth. The blood flow velocity determined by the Doppler spectrogram and the vascular cross-sectional area measured from the B-mode tomographic image enables the quantitative calculation of blood flow volume. Using this system, PBF was measured quantitatively in 88 healthy adults, 54 patients with chronic hepatitis, 65 with cirrhosis of the liver, 27 with primary hepatoma and 12 with idiopathic portal hypertension (IPH). Results of PBF volume measurement were as follows: 889 +/- 284 ml/min (mean +/- S.D.) for healthy adults, 851 +/- 237 ml/min for patients with chronic hepatitis, 870 +/- 289 ml/min for cirrhosis of the liver, 966 +/- 375 ml/min for primary hepatoma and 1,047 +/- 381 ml/min for IPH. These preliminary results demonstrated that this ultrasonic Duplex system is clinically useful to determine the quantitative amount of PBF.
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PMID:Quantitative measurement of portal blood flow in patients with chronic liver disease using an ultrasonic Duplex system consisting of a pulsed Doppler flowmeter and B-mode electroscanner. 609 10


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