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Biomedical subjects

H Ajzen

Publications and source records attributed to H Ajzen.

At least 55 records · Page 3Linked to original sources
PubMed1989

Renal function and glomerular hemodynamics in male endotoxemic rats.

The renal effects of a single intravenous dose of two different E. coli lipopolysaccharides (LPS 0111:B4 and LPS 0127:B8), at the same dose of 100 micrograms/kg, were evaluated in euvolemic Munich-Wistar (MW) rats by whole kidney clearance techniques and micropuncture studies. Following LPS infusion, a significant decrease (8%) in mean BP was observed only in the LPS 0127:B8 treated group. Inulin clearance fell 57% (LPS 0111:B4), P less than 0.01, and 38% (LPS 0127:B8), P less than 0.01. Para-aminohippuric (PAH) clearance decreased 31% (P less than 0.01) and total effective renal vascular resistance rose 70% (P less than 0.03) in response to LPS 0111:B4. No significant change in PAH clearance was noted in the LPS 0127:B8 group. Superficial single nephron glomerular filtration rate (SNGFR) was reduced 69% (LPS 0111:B4), P less than 0.03, and 33% (LPS 0127:B8), P less than 0.02. Superficial glomerular plasma flow fell 48% (LPS 0111:B4), P less than 0.03, and 24% (LPS 0127:B8), P less than 0.03. Both lipopolysaccharides were associated with an increase in afferent arteriolar resistance (RA) which accounted for a reduction in the glomerular capillary hydraulic pressure (PGC). There was no change in the proximal tubular pressure in either group and, therefore, the net transcapillary hydraulic pressures were reduced. No measurable change in the ultrafiltration coefficient. Kf, was observed in either group. In a second set of protocols, the effect of prior administration of indomethacin or captopril on LPS 0111:B4 action was investigated. A significant decrease in BP occurred when animals were pretreated with captopril. Both indomethacin and captopril prevented the renal effects of LPS 0111:B4.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1987

Glomerular hemodynamics and hormonal participation on cyclosporine nephrotoxicity.

The mechanism of cyclosporine A (CyA) nephrotoxicity is unclear. In order to evaluate renal microcirculation seven euvolemic Munich-Wistar (MW) rats were studied after acute CyA treatment (50 mg/kg, i.v.). Both total glomerular filtration rate (GFR, 0.96 +/- 0.04 vs. 0.47 +/- 0.07 ml/min) and single nephron GFR (27.90 +/- 3.39 vs. 14.02 +/- 3.49 nl/min) declined significantly (P less than 0.001). It was observed an increase in afferent (RA, increases 188%) and efferent (RE, increases 360%) arteriolar resistances that caused a decrease on glomerular plasma flow rate (QA) from 100.99 +/- 17.09 to 44.37 +/- 13.37 nl/min (P less than 0.001). Mean glomerular capillary hydraulic pressure (PGC) increased from 45 +/- 1 to 55 +/- 4 mm Hg (P less than 0.05) and the glomerular ultrafiltration coefficient (Kf) decreased by 70% (0.096 +/- 0.030 to 0.031 +/- 0.010 nl/sec X mm Hg, P less than 0.05). Additionally, in order to study hormonal participation in this nephrotoxicity, other three groups of MW rats were previously treated with captopril (2 mg/kg, i.v.), verapamil (20 micrograms/kg/min, i.v.) or indomethacin (2 mg/kg, i.v.). Both captopril and verapamil minimized the renal effects of CyA, with a decline of approximately 25% instead of approximately 50% on GFR and RPF. Moreover, two groups of Brattleboro rats were studied. Acute CyA administration in homozygote Brattleboro rats produced a decline of only approximately 22% and approximately 31%, respectively, in GFR and renal plasma flow (RPF), when compared with MW rats (P less than 0.05). Similar results were observed in heterozygote Brattleboro rats when compared with MW rats, disclosing differences due to a different strain of rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Acute hemodynamic action of captopril in congestive heart failure: contrasts between refractory and untreated patients.

To compare the hemodynamic mode of action of captopril in patients with Congestive Heart Failure (CHF) with high- or low-plasma renin activity, we studied the systemic and renal hemodynamic changes induced by this drug in patients with refractory CHF (Group I) or untreated CHF (Group II). Plasma Renin Activity (PRA) was 7.46 +/- 3.7 ng/ml/hr in Group I and 1.15 +/- 0.45 ng/ml/hr in Group II. After the administration of captopril, these values increased to 14.35 +/- 6.19 and to 1.99 +/- 0.76 ng/ml/hr respectively (p less than 0.05). We observed that patients of Group I responded with increases in cardiac index and stroke volume and diminutions in total peripheral resistance, but Group II did not show any significant change in these variables. In contrast to this difference in responses between the refractory and untreated patients, both groups showed similar decreases in pulmonary artery and wedge pressures. Both groups also showed similar increases in plasma volume and effective renal plasma flow, and decreases in renal vascular resistance. These results show that captopril has predominantly venodilator effects in patients with CHF with low PRA levels, and it acts as a mixed vasodilator in patients refractory to conventional therapy, receiving high doses of diuretics, and in whom PRA is elevated. Our results also suggest that the venodilator action of captopril is not mediated by the Renin-Angiotensin System.

Adult↗
PubMed1986

Renal haemodynamics in spontaneously hypertensive rats with superficial glomeruli.

Spontaneously hypertensive rats (SHR) were mated with Munich-Wistar rats (MW), and the F1 hybrids were called Escola Paulista de Medicina (EPM) rats. The EPM rats present spontaneous hypertension and superficial glomeruli, allowing a study of glomerular haemodynamics. Mean whole kidney (GFR) and single nephron glomerular filtration rate (SNGFR), and mean total and glomerular plasma flow, were similar in EPM and MW rats. However, a higher glomerular capillary hydraulic pressure and a reduced ultrafiltration coefficient (Kf) of EPM rats were observed. The glomerular hypertension may be the cause of low Kf, a possible initial lesion of glomerular sclerosis. When mean arterial pressure levels were reduced to about 90 mmHg, a maintenance of SNGFR, with a 40% reduction in GFR, in EPM rats were achieved, suggesting an autoregulatory mechanism in the superficial but not in the juxtamedullary nephrons. The decrease on urinary sodium excretion (UNaV) in this condition, which was also lower than in MW rats, showed an impaired sodium handling by EPM kidneys, a possible role in the hypertension genesis. Thus, the data suggest that EPM rats can be a useful model for glomerular haemodynamics and microcirculatory studies in the spontaneously hypertensive state.

Animals↗
PubMed1985

Inadequate aldosterone response to hyperkalemia during angiotensin converting enzyme inhibition in chronic renal failure.

To assess the mechanism involved in hyperkalemia during angiotensin converting enzyme inhibition with captopril in chronic renal failure, captopril, 150 mg/day, was administered to 16 patients with hypertension with plasma creatinine levels between 1.6 and 12.4 mg/dl. After 4 weeks of therapy, plasma potassium levels increased from 3.9 +/- 0.1 to 5.5 +/- 0.2 mEq/L (P less than 0.001) and the final plasma potassium levels correlated with plasma creatinine levels (r = 0.67; P less than 0.01). In six patients with plasma creatinine levels greater than or equal to 3 mg/dl, aldosterone excretion decreased after 4 weeks of captopril, from 7.5 +/- 3.1 to 1.8 +/- 0.5 micrograms/24 hr, whereas plasma renin activity increased from 0.6 +/- 0.2 to 4.4 +/- 1.1 ng/ml/hr (P less than 0.05). This was associated with increases in plasma potassium levels from 3.9 +/- 0.2 to 5.4 +/- 0.4 mEq/L (P less than 0.005) and a significant reduction in fractional excretion of potassium from an average of 34% to 25%. No significant changes in plasma creatinine levels were observed during therapy. There was a significant positive correlation between aldosterone excretion and the potassium excretion fraction (r = 0.53; P less than 0.01). Increases in plasma potassium levels were not able to increase aldosterone excretion, although the greater the plasma potassium level attained, the smaller the reduction in aldosterone excretion (r = 0.47; P less than 0.05). Our results indicate that adequate aldosterone production is essential to preserve potassium homeostasis in chronic renal failure. Moreover, angiotensin II appears necessary for an adequate aldosterone response to potassium stimulation.

Adolescent↗
PubMed1985

Role of the prostaglandin and kallikrein-kinin systems in aminoglycoside-induced acute renal failure.

The role of humoral factors in the pathogenesis of gentamicin and tobramycin aminoglycoside-induced acute renal failure was studied in rats. Renal function was evaluated after inhibition of prostaglandin synthesis with indomethacin and inhibition of the kallikrein-kinin system with aprotinin. Plasma and urinary kallikrein levels were measured in aminoglycoside-treated rats, as was in vitro effect of of these antibiotics on plasma kallikrein activity and prekallikrein activation by dextran sulfate. Indomethacin treatment (2 mg kg-1 day-1, ip, for 13 days) of rats which received gentamicin or tobramycin (40 mg kg-1 day-1, ip, for 10 days) caused a further fall in glomerular filtration rate (GFR) and renal blood flow and an impressive increase in renal resistance. The effect of indomethacin on GFR was more evident for gentamicin- than tobramycin-treated animals. Aprotinin administration had no additional effects on the renal function of antibiotic-treated rats. Plasma and urinary kallikrein levels in aminoglycoside-treated rats were significantly lower than in untreated controls. Both aminoglycosides at concentrations of 0.1 mg/ml inhibited dextran sulfate activation of plasma prekallikrein, and 2.0 micrograms/ml tobramycin, but not gentamicin, inhibited the hydrolysis of H-D-Pro-Phe-Arg-p-nitroanilide by rat plasma. These data suggest that prostaglandins may protect against aminoglycoside nephrotoxicity.

Acute Kidney Injury↗
PubMed1985

Characteristics of spontaneously hypertensive, Wistar Kyoto and Munich Wistar rats bred in Brazil.

The breeding of imported strains of isogenic rats was started in 1981 because of the lack of experimental rat models in Brazil. The imported strains were: Spontaneously Hypertensive Rats (SHR) and their normotensive controls Wistar Kyoto Rats (WKY) from the National Institutes of Health, Bethesda, MD, and Munich Wistar (MW) rats which present superficial renal glomeruli, from Simonsen Laboratories, Gilroy, CA. Breeding of these strains was carried out without strict barriers (conventional breeding), under Standard Operating Procedures and strict inbreeding. Environmental factors such as ration, light, temperature, type of shavings and bedding, size of cages and their population were constant. Body weight growth curves were constructed for the three strains. The productivity of imported rats and local breeding colonies in 1981, 1982 and 1983 was compared on the basis of the following parameters: mean litter size, productivity of the females, pre- and post-weaning mortality, and effective yield. Systolic blood pressure was also measured for SHR and WKY rats. MW rats showed a high and relatively stable reproduction performance. The productivity of SHR and especially WKY animals declined progressively during the first three years, making the breeding of these strains of isogenic rats very difficult.

Animals↗
PubMed1983

Effect of positive pressure breathing on plasma antidiuretic hormone and renal function in dogs.

The effect of intermittent mechanical ventilation and positive end-expiratory pressure on plasma antidiuretic hormone concentration was determined in 14 pentobarbital anesthetized dogs. The study was divided into a control period (spontaneous respiration), and two consecutive 30 and 60 min periods after the start of controlled respiration: Group I - intermittent positive breathing (IPPB); Group II - positive end-expiratory pressure (PEEP) with 5 cm H2O. A decrease in urinary flow (36.9%) was observed during end-expiratory pressure breathing. An increase in plasma antidiuretic hormone in group II from 4.5 +/- 2.4 to 24.6 +/- 16.0 pg/ml (P less than 0.01) was associated with a significant reduction of free water clearance from 1.2 +/- 0.6 to 0.3 +/- 0.4 ml/min and an increase of the urine/plasma osmolality ratio (143%, P less than 0.05). The decrease in urinary output and concurrent reduction of urinary sodium excretion also suggest an influence of the fall in glomerular filtration rate and renal plasma flow on renal function. IPPB only reduced total Na+ and K+ excretion. These results indicate that the mechanisms underlying the renal response to positive end-expiratory pressure breathing may be due to an increase in antidiuretic hormone plasma levels leading to a fall in urinary flow and in part to a decrease in sodium excretion.

Animals↗
PubMed1982

Properties of the isolated rabbit proximal convoluted tubule and pars recta after long-term storage in a modified Collins solution.

The effect of storage of cortical slices in modified Collins solution on the viability of rabbit proximal convoluted tubules (PCT) and pars recta (PR) was evaluated by microperfusion of isolated tubules in vitro. Cortical slices of rabbit kidney were stored for 1, 24, 48, 72 and 97 h at 4 degrees C in modified Collins solution. PCT and PR were dissected from these slices and perfused with a modified Krebs-Henseleit solution in vitro. Fluid absorption (JV) was 1.21 +/- 0.3 nl min-1 mm-1 (N = 8) and the transepithelial potential difference (PD) was -2.3 +/- 0.3 mV (N = 6) for PCT from cortical slices stored 0 to 3 h. JV was 1.01 +/- 0.09 nl min-1 mm-1 (N = 8) and PD was -1.9 +/- 0.6 mV (N = 5) for PCT from tissue stored 23 to 97 h. JV of PR from tissue stored 5 to 26 h was 0.75 +/- 0.1 nl min-1 mm-1 (N = 5) and PD was -1.5 +/- 0.3 mV (N = 5). JV was 0.76 +/- 0.1 nl min-1 mm-1 (N = 3) for PR stored 72 to 74 h, and PD was not measured. There was no correlation between storage time and JV or PD. Furthermore, the JV and PD values for these tubules were similar to those obtained for freshly dissected tubules. These results show that the isolated tubule preparation is useful for the direct assessment of the efficacy of different kidney preservation solutions on nephron function.

Animals↗
PubMed1982

Pulmonary gas exchange and ventilation during hemodialysis.

Hemodialysis-induced hypoxemia has been explained by several mechanisms: pulmonary microembolization, decreased pulmonary diffusing capacity, fall in alveolar oxygen tension, hypoventilation and ventilation/perfusion abnormalities. The objective of this study was to analyze the factors influencing pulmonary ventilation and gas exchange of 20 patients with chronic renal failure during hemodialysis performed under the following conditions: Group 1 (9 patients) dialyzed against an acetate dialysate with a cuprophan membrane; Group 2 (7 patients) dialyzed against acetate bubbled with CO2 with a cuprophan membrane; Group 3 (4 patients) similar to Group 1, but using a polyacrylonitrile membrane. Arterial and venous blood samples were obtained from the respective lines during the predialysis period (zero), at 30, 60, 120 180 and 240 min of hemodialysis, and 60 min post dialysis (300 min) for the measurement of pH, PCO2, PO2, HCO-3 and total CO2. The minute expired volume (VE), expired fractions of O2 (FEO2) and CO2 (FECO2), O2 consumption (VO2), CO2 elimination through the lungs (VCO2) and dialyzer, respiratory exchange ratio (R), dead space to tidal volume ratio (VD/VT), alveolar ventilation (VA) and alveolar-arterial O2 difference (delta AaPO2) were measured and a leukocyte count was performed for each period of hemodialysis. The patients in Groups 1 and 3 showed a significant drop in ventilation and PaO2, a slight decrease in PAO2 and a significant increase in delta AaPO2. The patients in Groups 1 and 2 showed a significant leukopenia at 30 min of hemodialysis. The volume of CO2 eliminated across the dialyzer was very similar for the three groups of patients. Group 2 did not show any drop in ventilation or PaO2. For Group 2 venous line pH was very low and PCO2 was within the normal range, in contrast to the normal or high pH and low PCO2 shown by Groups 1 and 3. This study indicates that the drop in PaO2 was partially the consequence of a slight decrease in PAO2, but mainly due to the increase in delta AaPO2. Thus the most likely cause of the decrease in PaO2 was the VA/Q imbalance brought about by a drop in ventilation. The drop in ventilation was linked not only to the volume of CO2 eliminated across the dialyzer, but also to the amount of CO2 delivered to the lungs, and to the pH and PCO2 of the venous line.

Adult↗
PubMed1979

[Effect of saralasin infusion on glomerular filtration rate and sodium excretion in hypertensive patients (author's transl)].

Saralasin (S) infusion, at a dose of 10 micrograms/kg/min IV, decreased Glomerular Filtration Rate (GFR) in 18 hypertensive patients. This effect was more pronounced in those patients with angiotensinogenic hypertension due to the somation of the effects of S upon renal vasculature and systemic arterial pressure. A decrease in urinary sodium excretion was also observed being more intense in those patients whose systemic pressure also decreased during S infusion. In group II (10 hypertensive patients) infusion of S in increasing doses (0.1, 0.5, 1.0, 5.0 and 10.0 micrograms/kg/min) a progressive decrease in GFR was observed only when the arterial pressure also decreased. However urinary sodium excretion decreased progressively as S doses increased. This effect was not related to S effect upon arterial pressure. This observation indicates that S, like angiotensin II, has a direct effect upon the renal tubules evoking an increase of sodium reabsorption.

Angiotensin II↗