Mirro R, Lowery-Smith L, Armstead W M, Shibata M, Zuckerman S L, Leffler C W
Department of Pediatrics, University of Tennessee, Memphis 38163.
Stroke. 1992 Nov;23(11):1613-6. doi: 10.1161/01.str.23.11.1613.
Hypocapnic cerebral vasoconstriction is used therapeutically to reduce elevated intracranial pressure caused by cerebral edema. Because cerebral ischemia/reperfusion injury causes a selective loss of prostanoid-dependent responses, including vasodilation to hypercapnia, we designed these experiments to examine the effect of ischemia/reperfusion on hypocapnic cerebral vasoconstriction.
Microvascular responses were studied in 10 newborn pigs (closed cranial window) in response to hyperventilation-induced hypocapnia (PaCO2, 22 +/- 2 mm Hg) both before and 45 minutes after 20 minutes of global cerebral ischemia. Responses to hypercapnia (PaCO2, 63 +/- 3 mm Hg), topical isoproterenol (10(-7) M), and norepinephrine (10(-4) M) were also studied before and after ischemia in the same animals for comparison.
Before ischemia/reperfusion, pial arterioles vasoconstricted to hypocapnia (-17 +/- 2%) and norepinephrine (-35 +/- 4%) and vasodilated to CO2 (37 +/- 7%) and isoproterenol (25 +/- 2%). After ischemia/reperfusion, the constriction of pial arterioles to hypocapnia (-19 +/- 2%) was similar to that before ischemia. This is in contrast to the loss of dilation to hypercapnia. Dilation to isoproterenol and constriction to norepinephrine were not affected by ischemia.
Hypocapnic cerebral vasoconstriction is maintained after ischemia/reperfusion. Since prostanoid-dependent responses, such as hypercapnic dilation, are lost following cerebral ischemia, these data suggest that hypocapnic constriction is not dependent on an intact prostanoid system and that cerebral vascular responses to CO2 involve multiple mechanisms, depending on whether CO2 is increasing or decreasing from baseline.
低碳酸性脑血管收缩被用于治疗因脑水肿导致的颅内压升高。由于脑缺血/再灌注损伤会导致包括对高碳酸血症的血管舒张在内的前列腺素依赖性反应选择性丧失，我们设计了这些实验来研究缺血/再灌注对低碳酸性脑血管收缩的影响。
对10只新生猪（开颅窗）在全脑缺血20分钟之前和之后45分钟时对过度通气诱导的低碳酸血症（动脉血二氧化碳分压[PaCO2]，22±2mmHg）的微血管反应进行了研究。对同一批动物在缺血前后对高碳酸血症（PaCO2，63±3mmHg）、局部应用异丙肾上腺素（10⁻⁷M）和去甲肾上腺素（10⁻⁴M）的反应也进行了研究以作比较。
在缺血/再灌注之前，软脑膜小动脉对低碳酸血症（-17±2%）和去甲肾上腺素（-35±4%）发生收缩，对二氧化碳（37±7%）和异丙肾上腺素（25±2%）发生舒张。缺血/再灌注之后，软脑膜小动脉对低碳酸血症的收缩（-19±2%）与缺血前相似。这与对高碳酸血症的舒张丧失形成对比。对异丙肾上腺素的舒张和对去甲肾上腺素的收缩不受缺血影响。
缺血/再灌注后低碳酸性脑血管收缩得以维持。由于脑缺血后前列腺素依赖性反应如高碳酸血症性舒张丧失，这些数据提示低碳酸性收缩不依赖于完整的前列腺素系统，并且脑血管对二氧化碳的反应涉及多种机制，这取决于二氧化碳是从基线水平升高还是降低。
