Schürer L, Grögaard B, Gerdin B, Arfors K E
Institute for Surgical Research, Ludwig-Maximilians-University of Munich, Federal Republic of Germany.
Adv Neurol. 1990;52:57-62.
In the present investigation, the involvement of PMNLs and oxygen free radicals was explored in rats with postischemic perfusion disturbances of the brain. Reversible forebrain ischemia was induced by bilateral clamping of both carotid arteries in combination with hemorrhagic hypotension. This procedure resulted in a reproducible DPH 1 hr after start of recirculation. Neutropenia was induced by sheep ANS. One group received ANS before and a second group immediately after termination of ischemia. Two additional groups received SOD before or immediately after ischemia. Regional postischemic CBF was determined by [14C]iodoantipyrine autoradiography. It was found that CBF significantly improved in cortical structures of animals treated with ANS before ischemia. Treatment with ANS at the end of ischemia had no effect on the postischemic CBF depression. Neither was injection of SOD effective to influence DPH, irrespective whether given before or after ischemia. It is concluded that PMNLs play a role in the development of DPH of the brain, whereas free radical mechanisms seem to be less relevant.
在本研究中,探讨了中性粒细胞(PMNLs)和氧自由基在脑缺血后灌注紊乱大鼠中的作用。通过双侧颈总动脉夹闭联合出血性低血压诱导可逆性前脑缺血。该操作在再灌注开始1小时后导致可重复的二苯基六氢吡啶(DPH)。通过羊抗中性粒细胞血清(ANS)诱导中性粒细胞减少。一组在缺血前接受ANS,另一组在缺血结束后立即接受ANS。另外两组在缺血前或缺血后立即接受超氧化物歧化酶(SOD)。通过[14C]碘安替比林放射自显影术测定局部缺血后脑血流量(CBF)。发现缺血前用ANS治疗的动物皮质结构中的CBF显著改善。缺血结束时用ANS治疗对缺血后CBF降低没有影响。无论在缺血前还是缺血后注射SOD,均不能有效影响DPH。得出结论,中性粒细胞在脑DPH的发生中起作用,而自由基机制似乎不太相关。