実験的脳幹部虚血における重症度別循環動態の検討

An Examination of Change in Blood Flow in the Brainstem of Rats under Various Grades of Ischemia

I．はじめに

　脳幹の血管運動中枢の局在や機能は現在においても論争中であるが^{5），下位脳幹に交感神経のトーヌスを発生し，主要な統合機能を営む中枢の存在があることはほぼ認められているようである9）．また，電気刺激により延髄網様体昇圧野，降圧野などの局所の機能を検討した報告は多いが9），実験的脳幹部虚血における脳幹血流動態の検討の報告は少ない．}

　以前われわれは，ラットにおいて実験的脳幹部再開通虚血を作製し，carbon perfusion法（Fig．1），Evans blue染色法（Fig．2）により，その病変の広がりを検討した^12）．今回，その脳幹部虚血において重症度別循環動態を検討した．

Abstract

A study was made of changes in brainstem blood flow (BBF) under various grades of ischemia in a rat recirculation model.

MATERIALS AND METHODS : Adult male Wis-tar rats were anesthetized with pentobarbital sodium (40mg/kg i.p.). After exposure of the cervical vertebra (C2 portion), embolic threads of various sizes prepared were inserted into the vertebral artery. By the hyd-rogen clearance technique, changes in BBF were mea-sured in 30 rats before, (luring and after brainstem ischemia.

RESULTS AND DISCUSSION : The mean arterial blood pressure (MABP) was 113 ± 5.8mmHg, and the mean BBF was 35.5±2.4m1/100g/min before ischemia. The alteration of BBF during and after ischemia was classified into three groups. The mildly ischemic group showed no significant changes in MABP ; BBF was above 15m1/100g/min during ischemia, with slight reactivity revealed by acetazolamide after recirculation. In the moderately ischemic group, MABP dropped sig-nificantly to 62.0± 12.4mmHg. After recirculation, it in-creased gradually to almost the control level. BBF de-creased to below 15m//100g/min immediately afterischemia, followed by a gradual increase to hyperperfu-sion after recirculation. After lhr of recirculation, BBF increased to more than 60m1/100g/min with inverse acetazolamide reactivity. In the severely ischemic group, both BBP and MABP decreased irreversibly even after recirculation. These data indicate that the changes in MABP and BBF could be classified accord-ing to the degree of ischemic damage in the brainstem,where the vasomotor center is located. Acetazolamide reactivity was disturbed during hyperperfusion. Such phenomena could be explained by the presence of para-lytically dilated vessels. If BBF falls below the critical level, as we showed here, it may induce postischemic hyperperfusion associated with dysfunction of autoreg-ulation and vasoparalysis in the brainstem.