INFLUENCE OF ANESTHESIA ON BLADDER HYPERACTIVITY INDUCED BY MIDDLE CEREBRAL-ARTERY OCCLUSION IN THE RAT

The effect of anesthesia or an N-methyl-D-aspartate (NMDA) glutamaterg ic antagonist (MK-801) on bladder hyperactivity induced by unilateral middle cerebral artery (MCA) occlusion was examined in female rats. Be fore infarction, control bladder contractions were monitored in two gr oups of rats: I) awake and 2) urethan anesthetized. The awake rats wer e then anesthetized with halothane, and MCA occlusion was performed in both groups. After recovery from halothane, bladder capacity in awake rats was significantly reduced (60.8 +/- 1.3%) 0.5-4.5 h after MCA oc clusion but not changed in urethan-anesthetized rats. MK-801 (0.1 mg/k g iv) administered before MCA occlusion blocked the reduction in bladd er capacity in awake rats 1.5-4.5 h after MCA occlusion. Bladder capac ity was not changed by sham operation in either the awake or urethan-a nesthetized rats. Urethan administered after recovery from halothane a nesthesia increased bladder capacity in MCA-occluded awake rats but no t in sham-operated awake rats. Infarct areas in halothane, urethan-ane sthetized, or MK-801-treated rats were not significantly different. Th ese results indicate that cerebral infarction induces bladder hyperact ivity in awake rats and that urethan or MK-801 inhibits the developmen t of this hyperactivity, most likely by blocking glutamatergic transmi ssion in the brain.