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M A Boim

Publications and source records attributed to M A Boim.

At least 37 records · Page 2Linked to original sources
PubMed1994

Acute, subacute, and chronic x-ray effects on glomerular hemodynamics in rats.

In order to evaluate the effects of x-rays on glomerular hemodynamics, surgically exposed left kidneys of Munich-Wistar rats were irradiated with 15 Gy in a single dose. The animals were studied 45 min (acute group, n = 8), 14 days (subacute group, n = 7), and 60 days (chronic group, n = 7) after irradiation and compared with their respective controls. A decrease in total glomerular filtration (55%) and renal plasma flow (40%) rates with marked elevation of total renal vascular resistance (180%), p < 0.05, occurred within 45 min. Significant changes also occurred in the microcirculation; i.e., single-nephron glomerular filtration (SNGFR), glomerular plasma flow (QA), and glomerular capillary hydraulic pressure (PGC) declined by 35%, 40%, and 12%, respectively, due to an increase in total arteriolar resistance (90%), p < 0.05. Within 14 days, SNGFR was similar to control in spite of a moderate elevation of afferent arteriolar resistance (26%) and reduction in PGC (11%), p < 0.05, and QA (20%). Kf was significantly elevated (46%), p < 0.05. The chronic group presented a response pattern similar to that of the acute group, although less severe. Histopathological changes were not relevant and were restricted to tubules. The present results suggest that: (a) Acutely, there was a marked reduction in filtration, flow, and PGC with significant elevation of resistances. (b) Within 14 days, the maintenance of SNGFR was probably the result of an offsetting effect between QA and PGC decreases and Kf elevation. (c) After 60 days, the homeostatic mechanism was not sufficient to maintain normal renal function. (d) A functional effect is probably the most important pathogenetic mechanism, at least during the initial phase, for the development of radiation nephropathy since no morphological alterations were observed.

Animals↗
PubMed1994

Glomerular hemodynamics during abortion induced by RU 486 and sepsis in rats.

1. Acute renal failure is a very common consequence of septic abortion. Whole kidney and glomerular hemodynamics were evaluated in virgin (V), pregnant (PREG) and aborted (ABOR) euvolemic Munich-Wistar rats before and after E. coli (0111-B4) endotoxin (LPS) infusion in order to evaluate the effect of septic abortion on the renal microcirculation. 2. Abortion induced by RU 486 blunted the increase in glomerular filtration rate (GFR) induced by normal pregnancy (0.86 +/- 0.03 vs 0.63 +/- 0.07 ml/min, P < 0.05). In virgin rats, RU 486 did not modify the parameters of renal function. Significant alterations occurred in whole kidney and single nephron function. However, the changes in whole kidney function in the ABOR group were significantly higher than those observed for the V group (reductions in GFR were 42% in V and 80% in ABOR, RPF decreased 34% in V and 76% in ABOR, TRVR increased 82% in V and 400% in ABOR). 3. Mean single nephron glomerular filtration rate (SNGFR) was reduced in all groups after LPS (44% in V, 43% in V+RU, 55% in PREG, 60% in ABOR), due to significant decreases in glomerular plasma flow rate, QA (42% in V, 55% in V+RU, 53% in PREG, 57% in ABOR) and in glomerular ultrafiltration coefficient, Kf (46% in V, 47% in V+RU, 45% in PREG, 67% in ABOR). 4. These data show that LPS induced significant alterations in renal function in all groups. However, aborted rats were more sensitive to the effects of LPS than V rats. These results indicate that abortion may potentiate the effects of endotoxemia on renal function elevating the extent of acute renal failure and thus the mortality rate.

Abortion, Induced↗
PubMed1993

Effect of cicletanine on the progression of chronic renal failure in rats.

1. The effects of chronically administered cicletanine (CICL), an antihypertensive and prostacyclin stimulating agent, on glomerular hemodynamics were evaluated after 30 (CRF-30) or 60 (CRF-60) days of chronic renal failure (CRF) induced by 5/6 nephrectomy in Munich-Wistar rats. 2. CICL administration (3 mg kg-1 day-1, N = 5) for 60 days did not modify glomerular hemodynamics of normal rats (control group). The CRF-60 group (N = 6) presented a significant increase in mean arterial pressure (MAP) compared with control (122 +/- 7 vs 98 +/- 2 mmHg, P < 0.05), which was attenuated by CICL (113 +/- 7 vs 122 +/- 7 mmHg). 3. Hyperfiltration and hyperperfusion were observed in both CRF groups after 30 (N = 5) but not after 60 days of CRF, 73.9 +/- 6.3 and 48.2 +/- 3.2 vs 36.8 +/- 2.6 nl/min for SNGFR and 200 +/- 17 and 147 +/- 8 vs 112 +/- 8 nl/min for QA in CRF-30, CRF-60 vs control group, respectively. However, glomerular hypertension was demonstrable for both CRF groups only after 60 days. CICL treatment starting 7 days prior to nephrectomy reduced the transcapillary hydraulic pressure difference (delta P) in both groups, 36 +/- 3 vs 30 +/- 2 mmHg (30 days) and 41 +/- 4 vs 34 +/- 2 (60 days), but did not significantly modify arteriolar resistances or glomerular hemodynamics, suggesting that the reduction in MAP in response to CICL may have been responsible for the decrease in delta P. CICL administration did not prevent the proteinuria or glomerular sclerosis associated with CRF. 4. The results suggest that the administration of CICL for 30 (N = 4) to 60 days (N = 7) was sufficient to prevent systemic hypertension associated with CRF but not to reduce the additional glomerular hemodynamic factors that participate in the progression of CRF.

Animals↗
PubMed1993

Effect of time on remnant glomerular function.

1. Although hypertrophy and hyperfiltration have been identified in remnant nephrons, the time of their appearance and the relationship between them have not been established. In order to evaluate remnant glomerular hemodynamics over different periods of time, we studied Munich-Wistar rats 7, 30 and 60 days after 5/6 renal mass ablation. 2. Kidney weight increased after 7 days, continued to increase after 30 days and decreased after 60 days. Glomerular filtration rate (GFR) and renal plasma flow decreased by 67% and 7 days, were 35% lower than normal after 30 days, and after 60 days presented the same values as after 7 days. Single-nephron GFR and glomerular plasma flow increased slightly after 7 days, were 118% higher than control after 30 days, and decreased after 60 days. Hydraulic glomerular capillary pressure tended to increase after 30 days (6%), reaching statistical significance after 60 days (45 vs 62 mmHg). The glomerular ultrafiltration coefficient increased significantly after 30 days (82%) and decreased to values similar to the control group after 60 days. 3. These data suggest that kidney hypertrophy occurs early after reduction of renal mass, before the hemodynamic adaptations are complete. Glomerular hypertension was observed after 60 days, when single-nephron GFR and the glomerular ultrafiltration coefficient were decreased compared to rats studied after 30 days. 4. These data may indicate that, once glomerular hypertension starts, structural abnormalities are followed by a decline in glomerular function.

Animals↗
PubMed1992

Possible role for chondroitin sulfate in urolithiasis: in vivo studies in an experimental model.

The effect of chondroitin sulfate upon the growth of calcium oxalate crystals was measured in vivo by using an experimental model in rats. Adult male Wistar rats were treated by chronic i.p. injections of chondroitin sulfate solutions (1, 5 or 10 mg in 0.3 ml of saline, every 2 days). This treatment led to a dose-dependent increase in the urinary chondroitin sulfate concentration. Urolithiasis was induced by the introduction of a calcium oxalate seed into the bladder of the animals. Urine samples were collected and the calculi formed were removed after 42 days. The chondroitin sulfate concentration have decreased in the lithiasic urines, as compared to controls and higher chondroitin sulfate doses correlated with larger calculi. The presence of chondroitin sulfate in the matrices of stones obtained from chondroitin sulfate-treated animals suggested that there was some adsorption of chondroitin sulfate on to the growth sites of the calcium oxalate crystals. In contrast to the chondroitin sulfate effect observed in vitro, which inhibits the growth of calcium oxalate crystals, our results suggest that in vivo chondroitin sulfate promotes the growth of stones in the urinary tract.

Adult↗
PubMed1992

Glomerular hemodynamics and hormonal evaluation during starvation in rats.

The effects of total food deprivation on renal function were evaluated in normal Munich-Wistar rats submitted to starvation (S) periods of two to eight days (Groups S2 to S8). A prompt and sustained decrease in renal plasma flow (RPF) and an increase in total renal vascular resistance (TRVR) were observed after the second day, together with a gradual decrease in glomerular filtration rate (GFR) until the fourth day (40% in the S4 group, P less than 0.05). After this period, a spontaneous and progressive increase in GFR occurred in spite of continuing low RPF and high TRVR. Glomerular hemodynamics were evaluated in additional animals from groups S4 and S7. As observed for whole kidney GFR, mean single nephron (SN) GFR was reduced in group S4, but not in group S7. The decline in SNGFR in S4 was the result of a decline (approximately 40%) in glomerular plasma flow rate (QA) and glomerular capillary hydraulic pressure (PGC), due to a predominant increase (approximately 60%) in afferent arteriolar resistance. In S7, SNGFR and its determinants did not differ from the control. Angiotensin II (Ang II), prostaglandin (but not thromboxane A2, TxA2) inhibition blunted the alterations in whole kidney function observed in S4. Conversely in S7, the inhibition of vasoconstrictor agents (Ang II and TxA2) did not normalize GFR, suggesting that the intrarenal vasoconstriction could be an important factor to maintain GFR after a prolonged period of starvation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effect of eicosapentaenoic acid on the progression of chronic renal failure in rats.

Eicosapentaenoic acid (EPA) can induce a shift in prostaglandin and leukotriene synthesis. The effects of EPA supplementation of the diet on the progression of chronic renal failure (CRF) were evaluated in a model of 5/6 renal mass ablation in rats. After 30 or 60 days of CRF, elevation in single-nephron glomerular filtration rate due to an increase in glomerular plasma flow and hydraulic pressure was observed. These hemodynamic alterations were followed by a rise in proteinuria and glomerular sclerosis. EPA treatment for 30 or 60 days did not substantially modify the hemodynamic or morphological profiles induced by renal mass ablation. In the present non-immune model of CRF, preglomerular vasodilation with glomerular hyperperfusion and hypertension were responsible, at least in part, for the presence of proteinuria and glomerular sclerosis. No additional vasodilation was observed in the present model of CRF, and, thus, hemodynamic effects induced by EPA did not modify renal damage, in contrast to the EPA effects observed in immune-mediated models of CRF.

Animals↗
PubMed1992

Renal sodium conservation during starvation in rats.

The natriuresis of fasting has been well characterized in man and rabbits but not in rats. The daily effects of fasting on glomerular filtration rate (GFR) and urinary sodium and potassium excretion were evaluated in Munich-Wistar rats (260-310 g) submitted to prolonged starvation (2-8 days). Rats do not present the natriuresis of fasting. Sodium excretion was reduced since the first few hours (0-4 h) of starvation. Antinatriuresis was abrupt during the early periods (1st and 2nd days) and stabilized at very low levels. During the early phase (4 days), sodium retention occurred due to both reduced glomerular filtration and increased tubular reabsorption. However, during the late phase (after the 4th day), antinatriuresis was mainly induced by the elevation in tubular reabsorption, since a normalization of GFR was observed. Thus, these homeostatic mechanisms permit adequate renal sodium conservation during starvation in rats.

Animals↗
PubMed1991

Nephrotoxicity of cyclosporine: the role of platelet-activating factor and thromboxane.

Cyclosporine (CsA), an immunosuppressive agent, is potentially nephrotoxic. We had previously observed that acute administration of CsA to Munich-Wistar rats induced a decrease in single nephron glomerular filtration rate, due to a decline in glomerular plasma flow, and in the glomerular ultrafiltration coefficient. Moreover, these alterations were prevented when an antagonist of platelet-activating factor (PAF) was administered. In the present study we examined whether the protective effect of the PAF blocker in CsA nephrotoxicity could have been mediated by thromboxane (TxA2). Our data show that the PAF effects were not mediated by TxA2, since administration of dazmegrel, a thromboxane synthetase inhibitor, did not ameliorate the acute renal failure caused by CsA. Thus, PAF appears to be a direct mediator of acute CsA nephrotoxicity, while TxA2 is not significantly involved in this process.

Animals↗
PubMed1991

Effect of platelet-activating factor antagonist BN 52063 on the nephrotoxicity of cisplatin.

Cisplatin (DDP) is an effective anticancer agent that has been successfully applied against various solid tumors. However, DDP commonly causes nephrotoxicity. We observed that DDP led to significant alterations in renal microcirculation when administered to Munich-Wistar rats, with a concomitant decrease in single nephron glomerular filtration rate due to reduction in glomerular plasma flow and transcapillary hydraulic pressure difference. BN 52063, a platelet-activating factor antagonist, caused a striking change in acute renal failure induced by DDP leading toward normalization of all parameters of renal function. The results suggest that BN 52063 could be used as a novel drug to control DDP nephrotoxicity.

Animals↗
PubMed1991

Role of platelet activating factor in gentamicin and cisplatin nephrotoxicity.

The present study was undertaken to evaluate the effects of platelet activating factor (PAF) antagonists on nephrotoxicity induced by gentamicin (GENTA) and cisplatin (DDP) in rats. PAF infusion provoked a 56% decline in single nephron (SN) GFR due to a decrease in glomerular plasma flow (QA, 55%), glomerular transcapillary hydraulic pressure (delta P, 13%), and glomerular ultrafiltration coefficient (Kf, 37%). Four days after a single dose of DDP (6 mg/kg, i.p.) we observed non-oliguric acute renal failure (ARF) with reduced SNGFR (45%), QA (46%) and delta P (10%) and unchanged Kf. GENTA administration for 10 days (40 mg/kg, i.p. daily) induced a decline in SNGFR (40%), QA (41%) and Kf (41%). Chronic treatment with a GENTA + PAF antagonist (BN 52021) partially prevented the decline in SNGFR (22%) by an amelioration in QA (25%) and Kf (13%). However, simultaneous treatment with DDP and BN 52063 completely prevented the ARF induced by DDP, normalizing all parameters of renal function. Thus, PAF may be a potential mediator involved in the nephrotoxicity induced by GENTA and DDP.

Acute Kidney Injury↗
PubMed1990

Effects of systemic hypertension, antidiuretic hormone, and prostaglandins on remnant nephrons.

Renal function was evaluated in normal and after 30 days of 5/6 renal mass reduction (CRF) in Munich-Wistar (MW) rats, spontaneously hypertensive rats with superficial glomeruli (EPM), and in Brattleboro rats with congenital diabetes insipidus (DI). Mean arterial pressure was higher in EPM-Control and EPM-CRF rats as compared with MW and DI rats. MW and EPM rats with CRF showed increases of 120% and 196%, respectively, in single nephron glomerular filtration rate as compared with their controls. However, DI rats with CRF did not show any increase in single nephron glomerular filtration rate as compared with the control group. Therefore, the data suggest that the presence of hypertension enhances the adaptive mechanisms on remnant kidney's function. Conversely, in the absence of antidiuretic hormone, adaptive mechanisms of remnant nephrons did not occur. In addition, it was observed that rats with CRF submitted to prostaglandin blockade with indomethacin showed for MW rats a 55% and 20% reduction in ultrafiltration coefficient and in single nephron glomerular filtration rate, respectively. Decreases of 60% and 30% in ultrafiltration coefficient and single nephron glomerular filtration rate, respectively, were observed for EPM rats. In contrast, DI rats did not show any alteration on renal function after indomethacin. It seems, therefore, that prostaglandins play a role in remnant nephron function of MW and EPM rats, but in the absence of antidiuretic hormone, prostaglandins do not affect remnant glomerular hemodynamics.

Animals↗
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↗
PubMed1989

Effect of platelet-activating factor antagonist on cyclosporine nephrotoxicity. Glomerular hemodynamics evaluation.

In order to evaluate the effect of platelet-activating factor (PAF) antagonist BN 52021 (5 mg/kg i.v.) on cyclosporine (50 mg/kg i.v.) nephrotoxicity, euvolemic Munich-Wistar rats were submitted to micropuncture studies. BN 52021 alone did not change the total (1.08 +/- 0.07 vs. 1.04 +/- 0.06 ml/min) or single nephron (SN) (29.1 +/- 50 vs. 31.3 +/- 4.0 nl/min) and glomerular filtration rate. The CsA administration caused a decline on GFR (0.47 +/- 0.07 vs. 0.96 +/- 0.04 ml/min, P less than 0.05) and on SNGFR (14.0 +/- 3.5 vs. 27.9 +/- 3.4 ml/min, P less than 0.05). An increase in afferent (RA) and efferent (RE) arteriolar resistances, 180% and 360%, respectively, 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 0.05) was observed. Moreover, the glomerular ultrafiltration coefficient (Kf) declined by 70% (0.096 +/- 0.003 to 0.031 +/- 0.10 ml/sec mmHg, P less than 0.05). The previous BN 52021 administration on rats treated with CsA blunted its effects on superficial nephrons. The SNGFR (22.3 +/- 3.0 vs. 28.0 +/- 25 nl/min), QA (72.2 +/- 5.9 vs. 91.7 +/- 12.1 nl/min) and KF (0.038 +/- 0.009 vs. 0.048 +/- 0.005 nl/s mmHg) remained unaltered. By contrast, the total renal function was not prevented by BN 52021 treatment: GFR 0.45 +/- 0.12 vs. 0.94 +/- 0.05 ml/min (P less than 0.05). Thus, this study suggests that PAF may participate in CsA nephrotoxicity. Furthermore, the protective effect of BN 52021 on superficial nephrons may indicate that BN 52021 is a drug that can minimize the impairment of renal function induced by CsA.

Animals↗
PubMed1989

Effect of cisplatin on glomerular hemodynamics.

1. The effects of cisplatin on renal microcirculation were evaluated in euvolemic Munich-Wistar rats submitted to micropuncture. Nine rats received a single dose of cisplatin (6 mg/kg, ip), and 6 control rats received the same volume (0.3 ml) of 150 mM NaCl 4 days before the measurements. 2. Cisplatin administration induced non-oliguric acute renal failure by decreasing glomerular filtration rate (GFR) from 0.96 +/- 0.05 to 0.33 +/- 0.04 ml/min (P less than 0.05) and by increasing urinary volume from 3.3 +/- 0.3 to 12.4 +/- 2.2 microliters/min (P less than 0.05). 3. Cisplatin administration decreased single nephron GFR from 34.2 +/- 2.1 to 20.1 +/- 2.3 nl/min (P less than 0.05) due to a reduction in both glomerular plasma flow from 106 +/- 9 to 61 +/- 6 nl/min (P less than 0.05) and transcapillary hydraulic pressure difference from 31 +/- 1 to 27 +/- 1 mmHg (P less than 0.05). An increase in arteriolar resistances, mainly afferent arteriolar resistance from 2.5 +/- 0.2 to 4.7 +/- 0.5 x 10(10) dyn.s.cm-5 (P less than 0.05), was observed. The glomerular ultrafiltration coefficient was unchanged.

Animals↗
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

Effects of cyclosporin on renal microcirculation.

To evaluate renal microcirculation during acute cyclosporin (CsA) administration (50 mg/kg, i.v.), seven euvolaemic Munich-Wistar rats were studied. CsA infusion caused a significant decrease in total glomerular filtration rate (GFR) (0.96 +/- 0.04 vs 0.47 +/- 0.07 ml/min) and in single-nephron GFR (SNGFR) (27.90 +/- 3.4 vs 14.02 +/- 3.5 nl/min). The efferent arteriolar resistance increased substantially (P less than 0.05) while the afferent resistance rose moderately. Consequently, there was an increase (P less than 0.05) in mean glomerular capillary hydraulic pressure (PGC), from 45 +/- 1 to 55 +/- 4 mmHg, together with an important decrease in mean glomerular plasma flow rate (QA), from 100 +/- 17 to 44 +/- 13 nl/min. Since tubular hydraulic pressure was maintained unaltered, an elevated transglomerular hydraulic pressure difference was observed (P less than 0.05). The lower values of SNGFR were accounted for by both the decrease in QA and in the glomerular ultrafiltration coefficient (Kf). The latter was reduced from 0.096 +/- 0.03 to 0.031 +/- 0.010 nl/sec per mmHg (P less than 0.05) by CsA. Additionally, three groups of Munich-Wistar rats were previously treated with captopril (2 mg/kg per h, i.v.), verapamil (20 micrograms/kg per min, i.v.) or indomethacin (2 mg/kg, i.v.). Both captopril and verapamil minimised the renal effects of CsA, with a decline of approximately 25% instead of approximately 50% on GFR and RPF. Thus CsA infusion caused a decline on SNGFR due to an important reduction in QA and Kf with an impressive increase on arteriolar resistance, a mark of angiotensin II stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗