Platelet proaggregatory effect associated with gentamicin-induced nephrotoxicity in mice

Gentamicin chronic treatment (5, 20, 40 and 80 mg/kg/day, i.p. tor 6 days) caused a dose-dependent reduction in mouse renal function, indicated by creatinine plasma concentration. The 40 and 80 rag/kg increased creatinine plasma concentration by 35 and 60% respectively (P < 0.01). When given in the same doses but for 1 day only, gentamicin caused no change in renal Junction. After acute and chronic administration of gentamicin, platelet aggregation in pial microvessels of control (normal saline) and gentamicin-treated mice was assessed by photochemical means. Results showed that gentamicin given for 6 days reduced the time for the appearance of the first platelet aggregate and to full occlusion of the pial arterioles. The maximum effect was manifested at doses of 20 and 40 mg/kg (73 and 69 sec, respectively) compared to control (230 sec). Other measured paramètre were not affected by gentamicin treatment When gentamicin was given for 1 day, no difference was found in any of the measured platelet aggregation parameters. It is concluded that gentamicin-induced nephrotoxicity in mice but not gentamicin per se may have a platelet proaggregatory effect in vivo.