Tsukahara T, Hongo K, Kassell N F, Ogawa H
Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville.
Neurosurgery. 1989 May;24(5):731-5. doi: 10.1227/00006123-198905000-00012.
The influence of subarachnoid hemorrhage (SAH) on vasodilatation induced by vasoactive intestinal polypeptide (VIP) was investigated in rabbit basilar arteries. VIP-induced relaxation was measured in ring sections of the basilar arteries precontracted by 10(-5) M serotonin using an isometric tension recording method. The cyclic adenosine monophosphate (cAMP) content was measured using radioimmunoassay as an indicator of the intracellular mechanism in the arterial smooth muscle cells. VIP (10(-11)-10(-6) M) evoked dose-dependent relaxation of the basilar arteries. The relaxation achieved with 10(-6) M VIP was 85 +/- 4% (n = 7) of the initial contractile tone in control arteries and 47 +/- 5% (n = 8) in the arteries evaluated 2 days after SAH, suggesting that VIP-induced relaxation was suppressed significantly after SAH (P less than 0.01). The cAMP content was significantly higher in the basilar arteries 2 days after SAH (425 +/- 48 pmol/g of tissue, n = 7) than in the control basilar arteries (194 +/- 57 pmol/g of tissue, n = 7). In normal arteries, the cAMP content was increased to a significant degree by VIP (10(-6) M) (325 +/- 60% of control cAMP content, n = 5), whereas the increase was less in the arteries evaluated 2 days after SAH (112 +/- 16% of control cAMP content, n = 5). These results suggest that SAH has an influence on cAMP metabolism in the arteries and that SAH impairs the postsynaptic mechanism of VIP-induced dilatation of the arteries.
在兔基底动脉中研究了蛛网膜下腔出血（SAH）对血管活性肠肽（VIP）诱导的血管舒张的影响。使用等长张力记录法，在由10⁻⁵M血清素预收缩的基底动脉环段中测量VIP诱导的舒张。使用放射免疫测定法测量环磷酸腺苷（cAMP）含量，作为动脉平滑肌细胞内机制的指标。VIP（10⁻¹¹ - 10⁻⁶M）引起基底动脉剂量依赖性舒张。10⁻⁶M VIP实现的舒张在对照动脉中为初始收缩张力的85±4%（n = 7），在SAH后2天评估的动脉中为47±5%（n = 8），表明SAH后VIP诱导的舒张显著受到抑制（P < 0.01）。SAH后2天基底动脉中的cAMP含量（425±48 pmol/g组织，n = 7）显著高于对照基底动脉（194±57 pmol/g组织，n = 7）。在正常动脉中，VIP（10⁻⁶M）使cAMP含量显著增加（为对照cAMP含量的325±60%，n = 5），而在SAH后2天评估的动脉中增加较少（为对照cAMP含量的112±16%，n = 5）。这些结果表明，SAH对动脉中的cAMP代谢有影响，并且SAH损害了VIP诱导的动脉扩张的突触后机制。
