Iwai R, Endo S, Kamiyama K, Otsuji T, Sugita T, Takaku A
Department of Neurosurgery, Toyama Medical and Pharmaceutical University, Japan.
No To Shinkei. 1988 Jul;40(7):603-8.
The pathological mechanism of cerebral vasospasm following subarachnoid hemorrhage has not been well clarified until now. There have been reports that denervation supersensitivity in cerebral vessels occurring after subarachnoid hemorrhage may possible play a role in the appearance of cerebral vasospasm. On the other hand, we have accepted that oxyhemoglobin (Oxy-Hb) is an important spasmogenic substance. In the present study, we investigated the effect of chemical denervation (reserpine or 6-hydroxydopamine: 6-OHDA) and surgical denervation (bilateral superior cervical ganglionectomy: SCG) on the constrictive sensitivity of cat basilar arteries to noradrenaline (Nor) and oxyhemoglobin (Oxy-Hb) in situ.
Adult cats were anesthetized with intramuscular pentobarbital and maintained on a respirator through a tracheostomy. By the transclival approach, the basilar artery was exposed. A cannula was then inserted into the subarachnoid space, and through it, Oxy-Hb and Nor were injected. The sequential changes in caliber of the basilar artery were measured using photography. SCG was done 7 days before the application of Nor or Oxy-Hb and 14 days before application of Oxy-Hb. Pretreatment with reserpine was done as follows: 1 mg/kg of reserpine was injected subcutaneously once each day for 2 days. On the following day, the sensitivity of the basilar arteries to Nor or Oxy-Hb was assessed. Pretreatment with 6-OHDA was done as follows: 5 mg of 6-OHDA was dissolved in 1.0 ml of artificial CSF, and then injected into the cisterna magna. Seven days later, Nor or Oxy-Hb was applied.
Pretreatment with reserpine tended to increase the vasoconstriction induced by 10(-7)-10(-4) M of Nor and the constriction induced by 10(-3) M of Nor was increased statistically (P less than 0.05). Cisterna magna injection of 6-OHDA tended to increase the vasoconstriction induced by Nor. SGG tended to increase the vasoconstriction induced by 10(-7)-10(-4) M of Nor and at a dose of 10(-3) M of Nor, the constriction of the basilar arteries was increased statistically (P less than 0.05). However, pretreatment with reserpine, 6-OHDA and SCG did not increase the vasoconstriction induced by Oxy-Hb. These results lead us to suggest that denervation supersensitivity does not participate in the vasoconstriction induced by Oxy-Hb.
迄今为止,蛛网膜下腔出血后脑血管痉挛的病理机制尚未完全阐明。有报道称,蛛网膜下腔出血后脑血管发生的去神经超敏反应可能在脑血管痉挛的出现中起作用。另一方面,我们已经认识到氧合血红蛋白(Oxy-Hb)是一种重要的致痉物质。在本研究中,我们研究了化学去神经(利血平或6-羟基多巴胺:6-OHDA)和手术去神经(双侧颈上交感神经节切除术:SCG)对猫基底动脉原位对去甲肾上腺素(Nor)和氧合血红蛋白(Oxy-Hb)的收缩敏感性的影响。
成年猫用肌肉注射戊巴比妥麻醉,并通过气管切开术在呼吸机上维持呼吸。通过经斜坡入路暴露基底动脉。然后将套管插入蛛网膜下腔,并通过它注射Oxy-Hb和Nor。使用摄影测量基底动脉管径的连续变化。在应用Nor或Oxy-Hb前7天进行SCG,在应用Oxy-Hb前14天进行SCG。利血平预处理如下:每天皮下注射1mg/kg利血平,共2天。在接下来的一天,评估基底动脉对Nor或Oxy-Hb的敏感性。6-OHDA预处理如下:将5mg 6-OHDA溶解在1.0ml人工脑脊液中,然后注入小脑延髓池。7天后,应用Nor或Oxy-Hb。
利血平预处理倾向于增加由10^(-7)-10^(-4)M Nor诱导的血管收缩,并且由10^(-3)M Nor诱导的收缩在统计学上增加(P小于0.05)。小脑延髓池注射6-OHDA倾向于增加由Nor诱导的血管收缩。SCG倾向于增加由10^(-7)-10^(-4)M Nor诱导的血管收缩,并且在10^(-3)M Nor的剂量下,基底动脉的收缩在统计学上增加(P小于0.05)。然而,利血平、6-OHDA和SCG预处理并未增加由Oxy-Hb诱导的血管收缩。这些结果使我们认为去神经超敏反应不参与由Oxy-Hb诱导的血管收缩。