Kakihana M, Shino A, Nagaoka A
Jpn J Pharmacol. 1983 Feb;33(1):17-26. doi: 10.1254/jjp.33.17.
Systemic arterial pressure was markedly increased in the early phase of cerebral ischemia induced by bilateral carotid artery occlusion (BCAO) in stroke-prone spontaneously hypertensive rats (SHRSP). The elevated level of arterial pressure was gradually returned to the initial level, and hypotension followed in the late phase. Severe neurological symptoms such as "ischemic seizure", dyspnea and coma were developed in the late phase. All SHRSP died within 6 hr after BCAO. The heart rate continued to increase during the brain ischemia. Cardiac arrhythmias, significant increases in plasma levels of creatine phosphokinase (CPK) and CPK-MB isozyme and disruption of myofibrils were observed after BCAO, particularly after the development of ischemic seizure. In contrast, in stroke-resistant SHR (SHRSR) and Wistar-Kyoto rats (WKY), ischemic seizure did not develop, yet all died within 8 hr after BCAO. Arterial pressures were moderately increased and never decreased to below the initial levels during the observation periods. Increases in CPK-MB isozyme activities in plasma from SHRSR and WKY were not detected. Pretreatments with propranolol and reserpine inhibited the increases in heart rate, reduced the frequency of arrhythmias and prolonged the survival time following BCAO in SHRSP. Our results indicate that cardiac dysfunction, which is a consequence of the cerebral ischemia, may be one of the causes of death following BCAO in SHRSP.
在易患中风的自发性高血压大鼠（SHRSP）中，双侧颈动脉闭塞（BCAO）诱导的脑缺血早期，体循环动脉压显著升高。动脉压升高水平逐渐恢复至初始水平，后期出现低血压。后期出现了“缺血性惊厥”、呼吸困难和昏迷等严重神经症状。所有SHRSP在BCAO后6小时内死亡。脑缺血期间心率持续增加。BCAO后，尤其是在缺血性惊厥发生后，观察到心律失常、血浆肌酸磷酸激酶（CPK）和CPK-MB同工酶水平显著升高以及肌原纤维破坏。相比之下，在抗中风的SHR（SHRSR）和Wistar-Kyoto大鼠（WKY）中，未发生缺血性惊厥，但所有大鼠在BCAO后8小时内死亡。观察期间动脉压适度升高，从未降至初始水平以下。未检测到SHRSR和WKY血浆中CPK-MB同工酶活性增加。普萘洛尔和利血平预处理可抑制SHRSP的心率增加，减少心律失常频率，并延长BCAO后的存活时间。我们的结果表明，心脏功能障碍作为脑缺血的后果，可能是SHRSP中BCAO后死亡的原因之一。
