Simpson R E, Phillis J W
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Brain Res. 1991 Jul 12;553(2):305-8. doi: 10.1016/0006-8993(91)90839-n.
Rat pial arteries were observed through a closed cranial window during hypercapnic and hypoxic episodes whilst the cerebral cortex was superfused at 37 degrees C first with artificial cerebrospinal fluid (CSF) and subsequently with adenosine deaminase (ADA, 0.5-2.0 U/ml) in CSF. The results indicate that ADA attenuated hypercapnic and hypoxic dilatatory arteriolar responses by 64% and 56% respectively. Recovery was obtained by superfusing with ADA-free CSF for 1 h. We conclude that adenosine is involved in hypercapnia- and hypoxia-evoked dilation of pial arteries.
在高碳酸血症和低氧发作期间,通过闭合的颅骨视窗观察大鼠软脑膜动脉,同时在37℃下先用人工脑脊液(CSF)然后用含腺苷脱氨酶(ADA,0.5 - 2.0 U/ml)的CSF对大脑皮层进行表面灌注。结果表明,ADA分别使高碳酸血症和低氧引起的小动脉扩张反应减弱了64%和56%。通过用不含ADA的CSF表面灌注1小时可实现恢复。我们得出结论,腺苷参与了高碳酸血症和低氧引起的软脑膜动脉扩张。