Biomedical subjects

V Martin-Paredero

Publications and source records attributed to V Martin-Paredero.

5 recordsLinked to original sources

PubMed1991

Renal function derangements induced by portacaval anastomosis in normal rats.

The purpose of this study was to determine the renal function derangements that portacaval shunting caused in previously normal rats. Eight rats suffered a surgical portacaval shunt (PCS) and another 8 a sham operation (SHAM). Renal function was investigated by determining urinary volume, sodium, potassium, creatinine and aldosterone excretion, in basal conditions and after sodium overload. Plasma renin concentration and urinary excretion of PGE2, 6-keto-PGF1 alpha and TXB2 were also determined in basal conditions. PCS rats showed increased urinary volume, creatinine excretion and endogenous creatinine clearance, either in basal conditions or after sodium load. After the latter, PCS animals also showed sodium retention and hyperaldosteronuria. PCS caused in basal conditions a striking diminution in urinary excretion of all prostaglandins and no changes in plasma renin. In conclusion, PCS in the normal rat caused a renal dysfunction consisting of polyuria, possibly related to ADH disfunction and an inability to manage a sodium load.

Aldosterone↗

PubMed1990

Hepatic haemodynamic changes after portacaval anastomosis in normal, cirrhotic and chronic prehepatic portally hypertensive rats.

Radioactive microspheres were used to determine the hepatic haemodynamic response to portacaval anastomosis in normal, cirrhotic and chronic prehepatic portally hypertensive rats 20 days after operation, and in normal rats 2 months after operation. After 20 days portacaval anastomosis caused a decrease in liver mass only in normal and cirrhotic animals, whereas hepatic arterial blood flow per unit of mass increased in normal (+488 per cent), cirrhotic (+191 per cent) and prehepatic portally hypertensive rats (+133 per cent). Despite these facts, animals with portacaval anastomosis showed a reduced hepatic total perfusion (arterial plus portal inflow) per unit of mass with respect to controls in normal (-53 per cent) and cirrhotic rats (-68 per cent), but not in those with prehepatic portal hypertension. Comparing studies carried out at 2 months with those performed 20 days after portacaval anastomosis in normal rats, some recovery of liver mass and total liver blood flow was observed. In conclusion, portacaval anastomosis produced a limited increase in hepatic arterial blood flow which was unable to preserve liver mass and its total perfusion in normal and cirrhotic animals. In contrast, portacaval anastomosis did not significantly alter liver mass or its perfusion in animals with chronic prehepatic portal hypertension, as both values were previously diminished in controls. Thus, the risk of liver failure after portacaval anastomosis is higher in normal and cirrhotic rats than in those with chronic prehepatic portal hypertension.

Animals↗

PubMed1990

Role of glucagon in the splanchnic and systemic hemodynamic changes induced by portal-systemic blood shunting.

Portal-systemic blood shunting is often accompanied by hyperglucagonemia and hemodynamic changes. To determine this causal relation, splanchnic and systemic hemodynamics (radioactive microspheres) and plasma glucagon levels (radioimmunoassay) were assessed in conditions of total portal-systemic shunting in portacaval-shunted (PCS) rats and in sham-operated (SO) normal rats. To compare these results, another hemodynamic study was undertaken basally and during glucagon infusion in nonoperated normal rats. PCS rats showed a threefold greater plasma glucagon concentration than SO animals (924 +/- 134 vs. 309 +/- 18 pg/ml, p less than 0.01), and they developed a hyperdynamic splanchnic circulation with higher portal venous inflow than SO rats (8.29 +/- 1.1 vs. 5.09 +/- 0.4 ml/min/100 g, p less than 0.05). Infusion of a pharmacological dose of glucagon in normal rats increased portal venous inflow (from 4.92 +/- 0.33 to 6.24 +/- 0.48 ml/min/100 g, p less than 0.05) so as to imply this hormone in the development of the hyperdynamic splanchnic circulation in conditions of portal-systemic shunting. However, the discrepancies in systemic hemodynamics between PCS and glucagon-infused rats may be a result of the different plasma glucagon levels reached in the two groups.

Animals↗

PubMed1985

Effect of captopril infusion on systemic and renal haemodynamics in conscious hypertensive rats with chronic, progressive aortic ligation.

The effect of the converting enzyme inhibitor captopril (5 mg (kg bwt)-1) on systemic and renal haemodynamics has been studied in conscious rats in which a progressive hypertension has been induced by progressive aortic ligation (AL) between the renal arteries, and in a sham-operated (SO) group. Cardiac output (CO), organ blood flow and vascular resistances have been measured using radioactive microsphaeres. Captopril infusion caused increases in CO in both groups of rats, but the increase was higher in SO (9.2 +/- 0.7%) than in AL rats (5.2 +/- 0.6%; P less than 0.005). Plasma renin concentrations were similar in both groups but increased more in AL (10.3 microIU +/- 1.0) than in SO (5.81 microIU +/- 0.62; P less than 0.05) after captopril. Captopril induced also a larger decrease in arterial pressure (36 +/- 4 mmHg), and of the pressure gradient across the stenosis (19 +/- 3) mmHg in AL than in SO rats (5.6 +/- 1.4 and 1.1 +/- 1.3 mmHg, P less than 0.005 for both cases). Vascular resistance of the kidney above the ligature decreased more in AL than in SO rats, but this difference was not observed in the other kidney. From these data it can be concluded that captopril has an acute hypotensive effect despite the normal renin levels of this model of chronic hypertension. In addition, blood flow to the high-pressure perfused kidney seems to be dependent on the increased renin production by the contralateral kidney.

Animals↗

PubMed1985

Acute renal dysfunction after major arteriography.

The incidence of acute renal dysfunction (ARD) after major arteriography was evaluated by assessment of the change in serum creatinine in 364 patients undergoing arteriography. Major arteriography was defined as abdominal aortography, abdominal aortography with lower-extremity runoff, aortic arch studies, or aortic arch plus selective carotid angiography. The influence of the volume of contrast material received, hydration, and associated risk factors was evaluated. In the entire group, the frequency of postarteriographic ARD was 7.1%. Although most patients recovered, 1.4% required renal dialysis. The frequency of renal dysfunction was significantly higher in patients with preexisting renal disease (14.8%), and 3.7% of these patients went on to require dialysis. In the total group and in those with normal renal function prearteriographically, the frequency of ARD was found to be related to the volume of iodinated contrast material received. Hydration before, during, and after angiography did not prevent this complication. Several risk factors, namely preexisting renal disease, advanced age, volume of contrast material used, type of study performed, diabetes mellitus, and coexistent heart disease were found to be associated with a statistically significant increased risk of postangiographic ARD.

Acute Kidney Injury↗