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Biomedical subjects

A Blanchart

Publications and source records attributed to A Blanchart.

10 recordsLinked to original sources
PubMed1988

Urinary excretion and glomerular synthesis of prostaglandin E2 and prostaglandin F2 alpha in cirrhotic, non-ascitic rats: the effects of sodium overload.

The urinary excretion of aldosterone, kallikrein and prostaglandin E2 (PGE2) was studied in sodium-retaining (RC) and nonretaining (NRC), nonascitic cirrhotic rats, under basal conditions and after an oral sodium load (5 mmol). The glomerular synthesis of PGE2 was measured in RC rats under the same conditions. Both groups of cirrhotic animals showed a decreased urinary excretion of PGE2. Isolated glomeruli of RC rats produced less PGE2 than those of the control animals, both under basal conditions and after the sodium load. The NRC group was the only one able to increase the urinary excretion of kallikrein in response to the sodium load. These findings could contribute to explain the early physiopathological events of hepatic cirrhosis.

Aldosterone↗
PubMed1988

Plasma catecholamines and urinary excretion of their main metabolites in three models of portal hypertension.

We have measured, by a specific radioenzymoassay, the plasma concentration of dopamine (DA) and norepinephrine (NE) and by gas chromatography the urinary excretion of some catecholamine metabolites (HVA, homovanillic acid, DOPAC, dihydroxyphenyl acetic acid; VMA, vanilmandelic acid, and DOPEG, dihydroxyphenyl glycol) in three groups of rats with portal hypertension: cirrhotic rats (CR), rats with progressive portal hypertension (PPH) and rats with progressive hepatic congestion (PHC). The three groups of rats had portal hypertension. PPH and PHC had also intrahepatic hypertension. CR rats showed an increased urinary excretion of NE and DA metabolites with a normal plasma concentration of these catecholamines, suggesting an increased turnover of NE and DA in this experimental model. PPH animals had a high plasma DA concentration with a decreased urinary excretion of catecholamine metabolites. PHC showed high plasma DA and NE levels with normal or increased urinary excretion of its metabolites. These results suggest that an increased neural activity is present in the early stages of experimental cirrhosis in rats and this alteration does not seem directly related to the portal hypertension but perhaps to the intrahepatic hypertension or to the hepatocellular damage.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Haemodynamic effects of angiotensin II in conscious, non-ascitic cirrhotic rats.

The effect of angiotensin II (AII) on systemic and regional haemodynamics was studied in 18 control and 18 cirrhotic, non-ascitic conscious rats (CCl4/phenobarbital model). Cirrhotic rats were found to retain sodium and to have normal plasma renin and plasma aldosterone concentrations when compared with control animals. Cirrhotic rats showed an enhanced cardiac output (34.4 +/- 0.5 vs. 27.5 +/- 2.0 ml/min in controls) and decreased peripheral resistances (2.96 +/- 0.25 vs. 3.95 +/- 0.31 mm Hg/min/100 g/ml in controls) under basal conditions. When AII was administered cardiac output decreased by 10.7 +/- 1.2% in cirrhotic rats, whereas it increased in control animals (11.2 +/- 2%, p less than 0.005). The AII-induced increase in arterial pressure was lower in cirrhotic than in control rats. The renal blood supply was particularly impaired by AII in cirrhotics, with a maintained flow to other organs (muscle, testes). It is concluded that the response to AII is disturbed in rats with hepatic cirrhosis even in a stage without ascites and with plasma renin and aldosterone concentrations similar to those of control animals.

Aldosterone↗
PubMed1987

Effect of chronic and progressive hepatic outflow blockade on renal function in rats.

Systemic and splanchnic hemodynamics, plasma concentration, and urinary excretion of several hormones and the changes in renal function induced by saline infusion were studied in rats with a chronic and progressive model of postsinusoidal hypertension by hepatic vein ligation (HVL) and in a control group. HVL rats showed no differences in systemic hemodynamics compared with control rats, with the exception of decreased renal blood flow and increased renal vascular resistance. HVL rats showed increased portal and intrahepatic pressure, without other differences in splanchnic hemodynamics or in portal-systemic shunts. Clearance studies revealed that under basal conditions, HVL rats showed lower glomerular filtration rate, renal plasma flow, urinary flow, and sodium, chloride, and potassium excretion than control rats. After saline infusion (3% body weight, 15 ml/hr) differences in glomerular filtration rate became nonsignificant, but urinary flow and electrolyte excretion remained lower in HVL than in control rats. Under basal conditions, plasma norepinephrine and dopamine concentrations were higher and urinary prostaglandin E2 (PGE2) and prostaglandin F2 alpha levels were lower in HVL than in control animals. These results demonstrate that chronic and progressive hepatic congestion results in impaired renal function with decreased water and electrolyte excretion, and suggest the involvement of a hepatorenal sympathetic reflex in these alterations. Renal effects could also be mediated by the low levels of PGE.

Animals↗
PubMed1986

Lack of a direct regulatory effect of atrial natriuretic factor on prostaglandins and renin release by isolated rat glomeruli.

We have tested the direct regulatory effect of synthetic Atrial Natriuretic Peptide (ANP, 8-33aa) on prostaglandins and renin release by isolated rat glomeruli. Variable incubation times and doses of ANP did not modify the rate of PGE2, PGF2a and TXB2 production. Similar results were obtained for renin release. These data do not support a role for ANP in the regulation of prostaglandins and renin release by rat glomeruli.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Lack of effect of indomethacin on systemic and splanchnic haemodynamics in portal hypertensive rats.

Portal hypertension was produced experimentally in rats by partial constriction of the portal vein. Twelve rats were injected daily with indomethacin, 4 mg/kg body weight, and 12 with the vehicle (80% ethanol, 0.5 ml/day). There were no differences in portal-systemic shunts nor systemic or splanchnic haemodynamics between indomethacin-treated and untreated rats. These results suggest that cyclo-oxygenase products do not play a significative role in haemodynamic alterations shown by portal-ligated rats.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Systemic and splanchnic hemodynamic disturbances in conscious rats with experimental liver cirrhosis without ascites.

Rats with CCl4-induced cirrhosis of the liver show histological and clinical features that closely resemble those of the disease in humans. Metabolic cages were used and hemodynamic studies (15-micrograms radioactive microspheres) were performed on 10 conscious, nonascitic, cirrhotic rats and in 10 control rats. Compared with control animals, cirrhotic rats showed lower sodium excretion (0.80 +/- 0.07 vs. 1.01 +/- 0.07 meq/day), total solute excretion (12.52 +/- 0.79 vs. 19.38 +/- 3.7 mosmol/day), and increased aldosterone excretion. No differences were observed in urinary epinephrine and norepinephrine excretion. Cirrhotic rats showed also slight hypotension, increased cardiac output (48.97 +/- 3.94 vs. 26.97 +/- 2.3 ml X min-1 X 100 g-1) without tachycardia, and decreased total peripheral resistance, which was mainly attributed to reduced renal and skeletal muscle resistances with increased blood flow throughout these areas. Cirrhotic rats showed increased hepatic vascular resistances by both portal and arterial inputs with portal hypertension (16.15 +/- 1.01 vs. 9.60 +/- 0.77 cmH2O) but without differences in total hepatic blood flow or portal-systemic shunt rate with respect to control rats. Plasma renin content was not significantly different between the groups of rats. From these data it can be concluded that nonascitic, cirrhotic rats show a hyperdynamic circulatory state, which seems to be caused by a peripheral vasodilation of unknown mechanism; portal-systemic shunting does not seem to be a necessary condition for the hyperdynamic status at this early stage of the hemodynamic disturbances.

Animals↗
PubMed1985

Effect of chronic and progressive increase of portal venous pressure on renal handling of water and electrolytes in rats.

Systemic and splanchnic hemodynamics and the changes in renal function induced by saline infusion (3% body weight) were studied in rats with a chronic and progressive model of portal hypertension (CPH) and in a control group. CPH rats showed a hyperdynamic circulatory status with increased cardiac output, decreased total peripheral resistances, and decreased portal inflow. Portal hypertension was accompanied by intrahepatic hypertension. Clearance studies revealed that in basal conditions CPH rats showed lower glomerular filtration rate (GFR), renal plasma flow (RPF), urinary flow, and potassium excretion than control rats, while the difference in Na and Cl excretion was not statistically significant. After saline infusion (3% body weight, 15 ml/h), differences in GFR and RPF became nonsignificant, but CPH rats showed lower Na, Cl and osmolar excretion and urinary flow than control rats. In basal conditions, plasma renin content was higher in CPH than in control rats, and decreased in both groups after volume expansion, the difference then being not statistically significant. These results demonstrate that chronic portal hypertension results in impairment of GFR, RPF and renal handling of water and electrolytes and suggest the involvement of a hepatorenal sympathetic reflex in these alterations. This reflex could be stimulated by the increase in intrahepatic pressure rather than by portal hypertension per se.

Animals↗
PubMedDate not supplied

Effect of volume expansion on hemodynamics, capillary permeability and renal function in conscious, cirrhotic rats.

General and splanchnic hemodynamics (radioactive microspheres), renal function, spontaneous and histamine-mediated vasopermeability and albumin distribution space were studied in conscious control and nonascitic cirrhotic rats, before and after a moderate and sustained saline infusion (3% of body weight per 30 min + repletion of urinary losses). In basal conditions, cirrhotic rats showed lower fractional sodium excretion than did control rats (0.09 +/- 0.01 vs. 0.15 +/- 0.01%, p less than 0.005). In addition, cirrhotic animals showed higher cardiac output (161.4 +/- 12.8 ml per min) and lower total peripheral resistance (0.63 +/- 0.05 mm Hg . min per ml) and mean arterial pressure (102.9 +/- 3.9 mm Hg) than did control rats (cardiac output: 89.0 +/- 7.6; total peripheral resistance: 1.31 +/- 0.11; mean arterial pressure: 117.5 +/- 5.11; p less than 0.005). No differences in portal-systemic shunt rate or vasopermeability between both groups were observed. After saline infusion, fractional sodium excretion increased to 4.31 +/- 0.16% in controls but only 2.11 +/- 0.02% in cirrhotic animals. In this group, cardiac output decreased by 49.6 +/- 5.1% whereas mean arterial pressure and total peripheral resistance increased by 7.1 +/- 0.6 and 112 +/- 10%, respectively. In control rats, no significant hemodynamic changes were observed. Blood gases did not change after expansion in any group. Saline infusion induced an increase in histamine-mediated vasopermeability in cirrhotic rats but not in control rats. Also albumin distribution space increased more in cirrhotic than in control animals. Heart weight was higher in cirrhotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗