Marín J, Rivilla F, Salaices M, Lobato R D, Burgos J, Sánchez-Ferrer C F, Fernández A
Rev Esp Fisiol. 1985 Dec;41(4):381-6.
The effect of experimental subarachnoid hemorrhage (SAH) on the adrenergic innervation and on the 45Ca2+ uptake of cat cerebral arteries was analyzed. Intracisternal injections of autologous blood reduced the noradrenaline content of perivascular nerve endings and 3H-noradrenaline uptake. These values returned to normal levels in a period of two weeks after SAH. The activity of dopamine-beta-hydroxylase was also reduced 3 and 7 days after SAH. Superior cervical gangliectomy and intracisternal injection of 6-hydroxydopamine also reduced these three parameters. The uptake of 45Ca2+ by arteries from animals submitted to SAH was greater than if the blood vessels were from untreated cats. Lantanum brought about a less 45Ca2+ displacement in the arterial segments from untreated animals than in those from cats after SAH. These results suggest that SAH induces a transient adrenergic denervation as well as changes in the membrane of smooth muscle cell which increase the quantity of Ca2+ bound to it. All these modifications might be involved in the cause of chronic cerebral vasospasm that appears after SAH.
分析了实验性蛛网膜下腔出血(SAH)对猫脑动脉肾上腺素能神经支配及45Ca2+摄取的影响。脑池内注入自体血可降低血管周围神经末梢的去甲肾上腺素含量及3H-去甲肾上腺素摄取。这些值在SAH后两周内恢复至正常水平。SAH后3天和7天,多巴胺-β-羟化酶的活性也降低。颈上神经节切除术及脑池内注射6-羟基多巴胺也降低了这三个参数。与未处理猫的血管相比,SAH动物动脉对45Ca2+的摄取更大。与未处理动物的动脉段相比,拉坦前列素在SAH后猫的动脉段中引起的45Ca2+置换较少。这些结果表明,SAH诱导短暂的肾上腺素能去神经支配以及平滑肌细胞膜的变化,从而增加与其结合的Ca2+量。所有这些改变可能都与SAH后出现的慢性脑血管痉挛的病因有关。