Talman W T, Dragon D M, Heistad D D, Ohta H
Department of Neurology, Department of Veterans Affairs Medical Center, Iowa City, Iowa.
Am J Physiol. 1991 Sep;261(3 Pt 2):H707-13. doi: 10.1152/ajpheart.1991.261.3.H707.
We used the microsphere technique and laser flowmetry to assess cerebral blood flow in 43 anesthetized rats. Cerebral blood flow did not increase significantly when the fastigial nucleus was stimulated 15 min after administration of alpha-chloralose. In animals that received maintenance doses of alpha-chloralose, the modest (50%) increase in cerebral blood flow that did occur returned toward control during stimulation despite a continued stable elevation of arterial pressure. Stimulation of fastigial nucleus 2 h after alpha-chloralose elicited a 20 +/- 3 mmHg increase in arterial pressure; cerebral blood flow increased gradually for 30-60 s after the rise in arterial pressure and reached a peak that was approximately 90% (P less than 0.05) above baseline. The stimuli did not significantly reduce vascular resistance or impair autoregulation. We did not stimulate the fastigial nucleus for more than 2 h after administration of alpha-chloralose because anesthesia was effective for only 2 h. This study demonstrates that stimulation of the fastigial nucleus in rat produces a delayed increase in cerebral blood flow that is blocked by alpha-chloralose anesthesia. The delay in increases of cerebral blood flow suggests that a metabolic mechanism, not a direct neurogenic vascular effect, may account for increases in flow with fastigial stimulation.
我们使用微球技术和激光血流测定法评估了43只麻醉大鼠的脑血流量。给予α-氯醛糖15分钟后刺激顶核时,脑血流量并未显著增加。在接受α-氯醛糖维持剂量的动物中,尽管动脉压持续稳定升高,但在刺激期间确实出现的适度(50%)脑血流量增加又恢复到了对照水平。给予α-氯醛糖2小时后刺激顶核,动脉压升高了20±3 mmHg;动脉压升高后,脑血流量在30 - 60秒内逐渐增加,并达到比基线高出约90%(P<0.05)的峰值。这些刺激并未显著降低血管阻力或损害自动调节功能。由于麻醉仅持续2小时,因此在给予α-氯醛糖后2小时以上我们未再刺激顶核。本研究表明,刺激大鼠顶核会使脑血流量出现延迟增加,而这种增加会被α-氯醛糖麻醉所阻断。脑血流量增加的延迟表明,代谢机制而非直接的神经源性血管效应可能是顶核刺激后血流量增加的原因。