The effects of nimodipine on regional cerebral blood flow, brain water and electrolyte contents in rats with subarachnoid hemorrhage.

Secondary cerebral ischemic injury is a major cause of mortality and disability from subarachnoid hemorrhage (SAH). In this study, the protective effects of nimodipine were investigated. Rat SAH models were divided into a sham-operated group, a saline-controlled, and a nimodipine-treated group by an endovascular piercing method. Nimodipine, 100 microg/kg BW was injected intraperitoneally 30 minutes before operation and was repeated every 6 hours. Dynamic changes in cortical regional cerebral blood flow (rCBF) using a laser Doppler flow-meter probe, and somatosensory evoked potentials (SEP) were estimated. Brain water content, sodium, potassium and calcium contents at different time points were determined. rCBF, latency of SEP, brain water and electrolyte contents did not statistically change in sham-operated rats. In saline-controlled rats, rCBF decreased immediately after SAH, and stabilized at low levels within 24 hours. The latency of SEP delayed gradually after SAH. Brain water and sodium increased, while potassium decreased at 6 hours and 24 hours. Brain calcium content increased significantly from 1 hour to 24 hours after induction of SAH. Extents of alterations of the above parameters caused by SAH in the nimodipine-treated group were less than those in the saline-controlled group, statistically. In conclusion, nimodipine partly prevents a decrease in cerebral blood supply and attenuates secondary cerebral ischemic injury after SAH.