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Biomedical subjects

R Zuin

Publications and source records attributed to R Zuin.

At least 37 records · Page 2Linked to original sources
PubMed1987

Nadolol for prevention of variceal rebleeding in cirrhosis: a controlled clinical trial.

Nadolol, a nonselective beta-blocker, has been shown to decrease portal pressure in patients with cirrhosis at the same degree as propranolol. No data are available, however, about its effect on rebleeding rate and mortality in patients undergoing prevention of rebleeding from esophageal varices. A prospective randomized clinical trial was performed in patients with cirrhosis who survived a documented episode of variceal hemorrhage. 12 patients received nadolol, 12 placebo. Patients with child's C grade, tense ascites, renal failure, contraindications to beta-blocker, or age greater than 70 were not included. After a follow-up of up to 145 weeks, 9 patients in the nadolol group and 4 in the placebo group survived free from rebleeding (log-rank test: chi 2 = 4.35, p less than 0.05). Survival was not statistically different in the two groups (1 death in the nadolol group, 3 in the placebo group). In conclusion, nadolol appears to represent an effective therapy in the prevention of variceal rebleeding in cirrhotic patients.

Adult↗
PubMed1986

Redistribution of renal blood flow in patients with liver cirrhosis. The role of renal PGE2.

Cirrhotic patients frequently show a decrease in renal blood flow and redistribution of the flow from the outer cortex to the juxtamedullary cortex. The cause of the maintenance of juxtamedullary perfusion is not presently known. Prostaglandin E2 (PGE2) has its vasodilating effect on medullary and juxtamedullary vessels where it is synthesized. Therefore, its increased production, frequently shown in cirrhotics, could be responsible for the relative preservation of juxtamedullary blood flow. To verify this hypothesis we examined 13 cirrhotic patients. In these patients we determined mean renal blood flow (MRBF), blood flow in the 1st compartment (ICBF) and in the 2nd compartment (IICBF) with the 133-Xenon washout technique and PGE2 plasma levels in the renal veins (PGE2V). MRBF and ICBF were significantly reduced as compared to control subjects (P less than 0.01); IICBF resulted unaltered. Significant correlation was found between IICBF and PGE2V (P less than 0.01). Our data confirm the decrease in renal blood flow and the redistribution of intrarenal blood flow in cirrhotic patients. The maintenance of IICBF is likely to be a consequence of PGE2 renal production.

Adult↗
PubMed1986

Effect of nadolol on liver haemodynamics and function in patients with cirrhosis.

Beta-adrenoceptor blockers used in the medical management of portal hypertension decrease liver blood flow. The sporadic onset of hepatic encephalopathy during propranolol treatment was ascribed to this decrease. The aim of the present study was to evaluate the effect of chronic treatment with nadolol on liver blood flow and liver function. Nadolol, a non-cardioselective beta-adrenoceptor blocker, has been reported to be as powerful as propranolol in decreasing portal pressure. Before and after 1 month of treatment with nadolol at a dose reducing heart rate by 25%, in 15 cirrhotic patients with portal hypertension, the following parameters were determined: hepatic venous pressure gradient, hepatic blood flow, galactose eliminating capacity, aminopyrine metabolic activity, ICG clearance and intrinsic hepatic clearance. Hepatic venous pressure gradient and hepatic blood flow were decreased by nadolol. However liver function was not affected by the drug. We conclude that, despite a lowered hepatic blood flow, liver function is not affected by 1 month of nadolol treatment.

Adult↗
PubMed1985

Splenic haemodynamics and portal hypertension in patients with liver cirrhosis and spleen enlargement.

The relationships between portal hypertension and spleen enlargement, in patients with liver cirrhosis, are not clearly defined; as well as those between splenic haemodynamics and portal hypertension. In 25 cirrhotics with spleen enlargement and portal hypertension and in seven controls, the following parameters were determined: estimated splenic volume (ESV) from the radiographic view of the spleen, according to Blendis, Williams and Kreel (1969), specific splenic blood-flow (SSBF), total splenic blood-flow (TSBF), porto-hepatic gradient (PHG), specific splenic resistance (SSR) and total splenic resistance (TSR). Moreover, the size and extension of oesophageal varices, at oesophagoscopy, were classified according to Dagradi (1973). PHG, ESV and TSBF were increased in all subjects, SSBF was increased in two cases, SSR was increased in two cases and decreased in two cases, TSR was decreased in all cases and ESV was not correlated to the level of portal hypertension. Neither TSBF nor TSR were found to be correlated to the level of portal hypertension, as estimated by PHG or by oesophageal varices. It is concluded that, in patients with liver cirrhosis and spleen enlargement, splenomegaly is likely to be the consequence of pulp hyperplasia and not of passive congestion, and that increases in splenic blood-flow do not contribute significantly to portal hypertension.

Adult↗
PubMed1985

Effect of somatostatin on splanchnic hemodynamics in patients with liver cirrhosis and portal hypertension.

The effect of somatostatin on splanchnic hemodynamics in patients with liver cirrhosis is not clearly defined, as some authors report a decrease in portal pressure and in liver blood flow during intravenous administration of this hormone, while others do not. In 19 subjects with liver cirrhosis and portal hypertension the following parameters were measured before and during intravenous administration of somatostatin (7.5 micrograms/min): porto-hepatic gradient, estimated hepatic blood flow, specific splenic blood flow, cardiac index. Estimated hepatic blood flow decreased significantly during somatostatin infusion (p less than 0.05), averaging a 13% decrease; porto-hepatic gradient, splenic specific blood flow and cardiac index did not vary significantly. These data indicate that somatostatin infused at a dose of 7.5 micrograms/min induces a slight decrease in liver blood flow without affecting portal hypertension.

Adult↗
PubMed1985

Use of a nonselective beta-blocker, nadolol, in the treatment of portal hypertension in cirrhotics.

Recently a medical treatment with propranolol has been proposed in order to decrease portal pressure and lessen the risk of recurrent gastrointestinal bleeding in cirrhotic patients. No data are available about another beta-blocker, nadolol, which, unlike propranolol, has a low hepatic metabolism, a low lipid solubility, a long serum half-life and does not reduce renal blood flow in patients with arterial hypertension. In 18 cirrhotics with portal hypertension, the effects of nadolol were studied on systemic and hepatic haemodynamics and liver function, at a dosage which reduced the heart rate by 25%. After one month of treatment, a significant decrease in cardiac output, portohepatic gradient and estimated hepatic blood flow were found. The degree of oesophageal varices was reduced in 11 patients, unchanged in the other seven. Hepatic function, evaluated by galactose eliminating capacity, did not change significantly. Although the small number of treated patients does not allow definitive conclusions, nadolol seems to have the features needed to be used in the medical treatment of portal hypertension in patients with liver cirrhosis.

Cardiac Output↗
PubMed1984

[Effect of somatostatin on splanchnic hemodynamics in liver cirrhosis].

The effect of somatostatin on splanchnic haemodynamics in patients with liver cirrhosis is not clearly defined, as some Authors reported a decrease in portal pressure and in liver blood flow during i.v. administration of this hormone, while others did not. In 19 subjects with liver cirrhosis and portal hypertension the following parameters were measured before and during i.v. infusion of somatostatin (7.5 micrograms/min): porto-hepatic gradient, effective hepatic plasma flow, specific splenic blood flow, cardiac output. Moreover the gastrin-G-17 plasma levels, those of insulin and growth hormone were measured. Effective hepatic plasma flow decreased significantly during somatostatin infusion (P less than 0.05), averaging a 15% decrease. Porto-hepatic gradient, specific splenic blood flow, cardiac output did not vary significantly. Gastrin, insulin and growth hormone plasma levels decreased significantly (P less than 0.02, 0.01, 0.05). These data indicate that somatostatin infused at the dose of 7.5 micrograms/min provokes endocrine effects, but as far as the splanchnic circulation is concerned, it induces a slight decrease in liver blood flow without affecting portal hypertension.

Adult↗
PubMed1984

[Therapeutic action of Piroxicam administered rectally in rheumatic diseases. Controlled double-blind study].

In a 15 day double-blind clinical trial 39 patients affected with rheumatic disease have been enrolled to evaluate the therapeutic effect of rectal administration of Piroxicam, in comparison with Indomethacin. At the end of the study, 20 patients had been treated with Piroxicam and 19 with Indomethacin. Nine patients in the Indomethacin group and one in the Piroxicam group dropped-out. Both drugs safety resulted good in the patients who completed the study, whereas 5 out of 10 dropped-out patients stopped the trial in consequence of severe side-effects of Indomethacin. Piroxicam induced a very good improvement in 76% of the patients, moderate in 19% and no improvement in 5%; Indomethacin induced a very good improvement in 75% of the patients, moderate in 15% and no improvement in 10%. No significative modifications resulted from the control of the laboratory blood tests. Piroxicam (30 mg/die) showed a therapeutic activity similar to Indomethacin (100 mg/die). The rectal administration of Piroxicam can be then considered a very good alternative to the oral one, particularly in the patients in which oral use of NSAID is counter-indicated.

Adult↗
PubMed1984

Effects of nadolol treatment on renal and hepatic hemodynamics and function in cirrhotic patients with portal hypertension.

Twelve cirrhotic patients with portal hypertension and esophageal varices were treated with nadolol for 1 month, and the effects on renal and hepatic hemodynamics and function were studied. A significant decrease in cardiac output, portohepatic gradient, and effective hepatic blood flow was found, whereas mean arterial pressure, liver function, effective renal blood flow, glomerular filtration rate, and urinary sodium and potassium excretions were not affected. In seven patients esophageal varices were also reduced. A significant correlation was found between the decrease in portohepatic gradient and that in cardiac output. The percentage of cardiac output distributed to the kidneys was significantly increased after nadolol treatment. In conclusion, nadolol seems to have properties useful for the treatment of portal hypertension in patients with liver cirrhosis.

Adrenergic beta-Antagonists↗
PubMed1984

Carbohydrate and lipid metabolism in cirrhosis. Evidence that hepatic uptake of gluconeogenic precursors and of free fatty acids depends on effective hepatic flow.

Splanchnic arteriovenous differences for several intermediary metabolites of carbohydrate and lipid metabolism were determined simultaneously with hepatic blood flow in seven normal subjects, eight patients with cirrhosis, and six patients with cirrhosis after surgical portosystemic shunt ( SPSS ) after an overnight fast. Arteriovenous differences in the legs were also determined together with flux measurement. The individual turnover rates of acetoacetate (AcAc) and 3 hydroxybutyrate (beta OHB) were also determined by means of isotopic techniques. Splanchnic gluconeogenic precursors and FFA uptakes were lower in cirrhotic patients with SPSS than in normal subjects (P less than 0.05 and P less than 0.01, respectively). Splanchnic triglyceride output was also lower in cirrhotic patients with SPSS than in normal subjects (P less than 0.01), whereas no significant differences were found for AcAc, beta OHB, and glucose release. In the group of cirrhotic patients without SPSS , those patients with negligible signs of portal systemic shunt and normal splanchnic blood flow had uptake of gluconeogenic precursors and of FFA normal or higher than that of normal subjects, whereas those patients with signs of spontaneous portal systemic shunt behaved like cirrhotic patients with SPSS . Alanine release from the leg was lower in both cirrhotic patient groups. Tracer determined hepatic output of AcAc and beta OHB was higher in cirrhotic patients with SPSS (P less than 0.05). Plasma clearance rates of AcAc and beta OHB were significantly elevated in both cirrhotic patient groups. Close agreement was found between tracer and catheterization techniques in the evaluation of ketone body production in cirrhotic patients with SPSS , whereas in cirrhotic patients without SPSS tracer determined hepatic output was slightly lower, possibly because of extrahepatic splanchnic tissue ketone body uptake. In conclusion, our data in patients with cirrhosis indicate that: 1) splanchnic uptake of gluconeogenic precursors and of FFA was related to the degree of portal systemic shunt, e.g. to the degree of effective hepatic blood flow; 2) liver triglyceride but not ketone body output was decreased by the impaired FFA (and glycerol) liver uptake; 3) the higher circulating levels of gluconeogenic precursors (except alanine) and of FFA appeared at least partially due to lower hepatic removal of these metabolites; and 4) peripheral use of ketone bodies was increased and alanine release from the leg reduced in patients with cirrhosis.

Adult↗
PubMed1983

Pathogenetic relationships between renal tubular acidosis and sodium metabolism alterations in liver cirrhosis.

5 cirrhotic patients with latent distal renal tubular acidosis (RTA) and 5 cirrhotic patients with normal distal acidification ability were studied. All the patients were maintained on a 80 mEq/day sodium diet for at least 5 days before the study. Only 2 of the 5 patients with RTA showed a reduced daily sodium excretion while the 3 other patients with RTA had a normal natriuresis. Acidification ability was retested in all the patients after increasing sodium distal delivery by intravenous administration of ethacrynic acid. Some hours after the maximal natriuretic effect induced by ethacrynic acid, a normalization of the acidification test was seen in all patients with RTA. These findings support the concept that although sodium metabolism alterations are not the only factor in the pathogenesis of RTA in liver cirrhosis, reduced availability of sodium at the distal tubule may impair tubular acidification, probably by influencing the distal transtubular potential difference.

Acidosis, Renal Tubular↗
PubMed1982

Lack of correlation between endotoxaemia and renal hypoperfusion in cirrhotics without overt renal failure.

Renal involvement in patients with liver cirrhosis is characterized by renal vasoconstriction, the aetiology of which remains obscure. Endotoxaemia, frequently found in patients with liver cirrhosis and renal failure, has been emphasized as a pathogenic factor. In fifty-seven patients with liver cirrhosis without overt renal failure endotoxin plasma level (Limulus Lysate test), mean renal blood flow (MRBF) (133Xe washout technique), and effective renal plasma flow (ERPF) (p-aminohippurate clearance) were determined. MRBF was decreased in nineteen out of twenty-seven patients, averaging 1.88 +/- 0.51 ml g-1 min-1 (in fourteen controls 3.17 +/- 0.51 ml g-1 ml-1). ERPF was decreased in seventeen out of thirty patients, averaging 380 +/- 164 ml/min (in eighteen controls 624 +/- 127 ml/min). Systemic endotoxaemia was found in sixteen out of fifty-seven patients, levels ranging from 0.62 to 200 ng/ml. No significant difference in renal blood flow values was found between patients with and without endotoxaemia (MRBF = 1.78 +/- 0.51 and 1.93 +/- 0.52 ml g-1 min-1 respectively; ERPF = 429 +/- 119 and 365 +/- 175 ml/min respectively). No significant difference in the frequency of endotoxaemia was found between patients with impaired and unimpaired renal blood flow. Moreover no relation was found between endotoxin plasma levels and MRBF and ERPF respectively. In conclusion in patients with cirrhosis without overt renal failure renal vasoconstriction does not seem to be related to endotoxaemia.

Adult↗
PubMed1982

Enhanced renal sympathetic tone in liver cirrhosis: evaluation by intrarenal administration of dihydroergocristine.

Mean renal blood flow (MRBF), cortical blood flow (CBF), glomerular filtration rate (GFR), heart rate, arterial blood pressure, Na+ and K+ excretion were determined before and 10 min after intrarenal administration of dihydroergocristine (0.017 mg/kg b.w.) in 13 patients suffering from liver cirrhosis. Cardiac output was also determined in 6 patients. Baseline values of MRBF and CBF were significantly lower in cirrhotics than in the 14 control subjects. Following intrarenal administration of the drug, renal hemodynamic parameters increased significantly, while GFR decreased. Systemic hemodynamic parameters, diuresis, Na+ and K+ excretions were unchanged. These data show that dihydroergocristine has a renal vasodilator effect, probably mediated by alpha-adrenergic blockade. The effect probably is prevalent at the postglomerular site, where the increase in vascular resistance is greatest. The effect of the drug suggests that patients with liver cirrhosis have enhanced renal sympathetic activity which is, at least in part, responsible for the renal vasoconstriction.

Adult↗
PubMed1982

Renal haemodynamic in essential hypertension assessed by 133-Xenon washout and selective renal angiography.

The renal and intrarenal haemodynamic pattern in 17 patients with essential hypertension of different severity and duration was studied by means of the 133-Xenon washout technique and the selective renal angiography. The mean and the cortical renal blood flows were on average significantly decreased as compared to the controls. A good agreement was found between the reduction in renal perfusion and the degree of vascular abnormalities as shown by angiography; on the contrary no correlation was found between the impairment in renal blood flow and the degree and/or duration of hypertension.

Adult↗
PubMed1981

Evaluation of renal tubular damage in liver cirrhosis by urinary enzymes and beta-2-microglobulin excretions.

To assess the renal tubular damage in liver cirrhosis the fractional clearances of beta-2-microglobulin (B2m-fr.cl) and malate-dehydrogenase (MDH-fr.cl) were measured respectively in sixty-four and in forty-six out of seventy-nine patients with liver cirrhosis of different aetiology; furthermore the fractional excretions of gammaglutamyl-transpeptidase (fr-GGT) and of alpha-glucosidase (fr-AGL) were determined in fifty-three and in forty of them respectively. In all patients glomerular filtration rate (GFR) and renal plasma flow (RPF) were also measured. Twenty-five subjects were studied as a control group for the enzyme excretions, sixteen for B2m-fr.cl. B2m-fr.cl and MDH-fr.cl--indexes of tubular functions--on the average were normal and only slightly increased respectively in cirrhotics compared to controls. Nevertheless fr-GGT and fr-AGL--indexes of cytolysis of tubular cells--on the average were massively increased in cirrhosis compared to controls, particularly in those with reduced RPF and/or GFR. No clear relationship between the indexes of tubular damage studied and the indexes of liver function was found. Our results show that (1) A renal tubular anatomical damage was found by means of an increase in the release of enzyme from tubular cells in patients with liver cirrhosis, particularly in those with a significant reduction of RPF and/or GFR; even so renal reabsorption of low molecular weight proteins is generally maintained. (2) The tubular damage does not seem to be related to the degree of liver impairment.

Adult↗