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|Title:||Role of platelet activating factor in gentamicin and cisplatin nephrotoxicity|
|Authors:||Santos, Oscar Fernando Pavão dos [UNIFESP]|
Boim, Mirian Aparecida [UNIFESP]
Barros, Elvino José Guardão [UNIFESP]
Schor, Nestor [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
|Publisher:||Blackwell Science Inc|
|Citation:||Kidney International. Cambridge: Blackwell Science Inc, v. 40, n. 4, p. 742-747, 1991.|
|Abstract:||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 (Q(A), 55%), glomerular transcapillary hydraulic pressure (DELTA-P, 13%), and glomerular ultrafiltration coefficient (K(f), 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%), Q(A) (46%) and DELTA-P (10%) and unchanged K(f). GENTA administration for 10 days (40 mg/kg, i.p. daily) induced a decline in SNGFR (40%), Q(A) (41%) and K(f) (41%). Chronic treatment with a GENTA + PAF antagonist (BN 52021) partially prevented the decline in SNGFR (22%) by an amelioration in Q(A) (25%) and K(f) (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.|
|Appears in Collections:||Artigo|
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