Leffler C W, Busija D W, Armstead W M, Mirro R, Beasley D G
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.
Pediatr Res. 1989 Feb;25(2):180-3. doi: 10.1203/00006450-198902000-00020.
Effects of ischemia (20 min) on cerebral cortical prostanoid synthesis and microvascular responses to hypercapnia and topical acetylcholine were examined in anesthetized newborn pigs. Pial arteriolar dilation in response to hypercapnia (10% CO2 ventilation, 10 min) was absent 2 h after ischemia and reversed toward constriction by 24 h postischemia. In sham control piglets, hypercapnia increased cortical periarachnoid fluid prostanoid concentrations. After ischemia, hypercapnia did not affect prostanoid concentrations on the brain surface. Acetylcholine (10(-3) M)-induced pial arteriolar constriction was reversed toward dilation 24 h after cerebral ischemia. Further, acetylcholine-induced prostanoid synthesis was markedly attenuated after ischemia. We conclude that cerebral ischemia-reperfusion alters cerebral prostanoid synthesis and microvascular control in newborn pigs. These abnormalities persist for at least 24 h.
在麻醉的新生猪中,研究了缺血(20分钟)对大脑皮质前列腺素合成以及对高碳酸血症和局部乙酰胆碱的微血管反应的影响。缺血2小时后,对高碳酸血症(10%二氧化碳通气,10分钟)的软脑膜小动脉扩张反应消失,缺血后24小时则转为收缩。在假手术对照仔猪中,高碳酸血症会增加皮质蛛网膜下腔液体前列腺素浓度。缺血后,高碳酸血症不影响脑表面的前列腺素浓度。脑缺血24小时后,乙酰胆碱(10⁻³ M)诱导的软脑膜小动脉收缩转为扩张。此外,缺血后乙酰胆碱诱导的前列腺素合成明显减弱。我们得出结论,脑缺血再灌注会改变新生猪的脑前列腺素合成和微血管控制。这些异常至少持续24小时。