Influence of anesthesia on bladder hyperactivity induced by middle cerebral artery occlusion in the rat.

Abstract

The effect of anesthesia or an N-methyl-D-aspartate (NMDA) glutamatergic antagonist (MK-801) on bladder hyperactivity induced by unilateral middle cerebral artery (MCA) occlusion was examined in female rats. Before infarction, control bladder contractions were monitored in two groups of rats: 1) awake and 2) urethan anesthetized. The awake rats were 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 occlusion but not changed in urethan-anesthetized rats. MK-801 (0.1 mg/kg i.v.) administered before MCA occlusion blocked the reduction in bladder capacity in awake rats 1.5-4.5 h after MCA occlusion. Bladder capacity was not changed by sham operation in either the awake or urethan-anesthetized rats. Urethan administered after recovery from halothane anesthesia increased bladder capacity in MCA-occluded awake rats but not in sham-operated awake rats. Infarct areas in halothane, urethan-anesthetized, or MK-801-treated rats were not significantly different. These results indicate that cerebral infarction induces bladder hyperactivity in awake rats and that urethan or MK-801 inhibits the development of this hyperactivity, most likely by blocking glutamatergic transmission in the brain.