Debdi M, Seylaz J, Sercombe R
Centre National de la Recherche Scientifique U.A. 641, Université Paris VII, France.
Stroke. 1992 Aug;23(8):1154-62. doi: 10.1161/01.str.23.8.1154.
Subarachnoid hemorrhage frequently leads to long-term cerebral artery narrowing called vasospasm. Very early changes in cerebral arteries have not been studied extensively and may be critical for the later pathological developments. We therefore determined what changes in the reactivity of cerebral arteries could be observed after 10 minutes' or 24 hours' contact with subarachnoid blood.
Ten minutes or 24 hours after the injection of blood or physiological solution (sham hemorrhage) into the cisterna magna of anesthetized rabbits or no injection (control rabbits), segments of the middle cerebral, basilar, and vertebral arteries were removed for conventional in vitro tension measurements. Concentration-response curves to four endogenous constrictors likely to be released after hemorrhage were obtained, and the maximum relaxation to acetylcholine was determined.
There were no significant differences between the sham hemorrhage and control groups. Compared with control rabbits, treated animals showed increased reactivity to uridine triphosphate in the basilar and vertebral arteries at 10 minutes but not at 24 hours, whereas reactivity was increased in the middle cerebral artery only at 24 hours. Reactivity to serotonin was greatly increased in all arteries at both latencies (up to 2.7 times). Reactivity to noradrenaline was unchanged in the basilar and vertebral arteries at 10 minutes; reactivity in both the basilar and middle cerebral arteries was increased at 24 hours, which is compatible with denervation supersensitivity. There were only minor changes in the reactivity to histamine, and only at 10 minutes. Relaxation to acetylcholine was increased for the middle cerebral artery at 10 minutes but otherwise was not significantly changed.
Reactivity to uridine triphosphate, serotonin, and noradrenaline greatly increases by 10 minutes to 24 hours after subarachnoid hemorrhage, and this increase is not owing to the mechanical effects of intracranial hypertension, nor is it related to impaired endothelium-dependent relaxation. It is suggested that these and other spasmogens cause excessive muscular calcium loading with a very rapid onset after subarachnoid hemorrhage.
蛛网膜下腔出血常导致称为血管痉挛的长期脑动脉狭窄。脑动脉的极早期变化尚未得到广泛研究，可能对后期病理发展至关重要。因此，我们确定在与蛛网膜下腔血液接触10分钟或24小时后，脑动脉反应性会发生哪些变化。
向麻醉兔的大池内注入血液或生理溶液（假出血）10分钟或24小时后，或不进行注射（对照兔），取出大脑中动脉、基底动脉和椎动脉节段进行传统的体外张力测量。获得对出血后可能释放的四种内源性收缩剂的浓度-反应曲线，并确定对乙酰胆碱的最大舒张反应。
假出血组与对照组之间无显著差异。与对照兔相比，处理组动物在10分钟时基底动脉和椎动脉对三磷酸尿苷的反应性增加，但在24小时时未增加，而大脑中动脉的反应性仅在24小时时增加。在两个时间点，所有动脉对5-羟色胺的反应性均大幅增加（高达2.7倍）。10分钟时基底动脉和椎动脉对去甲肾上腺素的反应性未改变；24小时时基底动脉和大脑中动脉的反应性均增加，这与去神经超敏反应相符。对组胺的反应性仅在10分钟时有微小变化。大脑中动脉在10分钟时对乙酰胆碱的舒张反应增加，但其他情况下无显著变化。
蛛网膜下腔出血后10分钟至24小时，对三磷酸尿苷、5-羟色胺和去甲肾上腺素的反应性大幅增加，这种增加并非由于颅内高压的机械作用，也与内皮依赖性舒张功能受损无关。提示这些及其他血管痉挛原在蛛网膜下腔出血后极短时间内导致肌肉钙负荷过度增加。
