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Brain and Nerve No to Shinkei Volume 40, Issue 6 （June 1988）

Brain and Nerve 脳と神経 40巻6号（1988年6月発行）

Japanese English

原著

Oxyhemoglobin誘発による脳血管攣縮と交感神経因子（第1報）—α-blockerよりの検討 EXPERIMENTAL CEREBRAL VASOSPASM INDUCED BY OXYHEMOGLOBIN AND THE SYMPATHETIC NERVOUS SYSTEM (PART 1): EFFECT OF ALPHA-ADRENERGIC RECEPTOR BLOCKERS 岩井良成 ¹ , 遠藤俊郎 ¹ , 神山和世 ¹ , 大辻常男 ¹ , 杉田毅 ¹ , 高久晃 ¹ Ryosei Iwai ¹ , Shunro Endo ¹ , Kazuyo Kamiyama ¹ , Tsuneo Otsuji ¹ , Takeshi Sugita ¹ , Akira Takaku ¹ ¹富山医科薬科大学脳神経外科 ¹Department of Neurosurgery, Toyama Medical and Pharmaceutical University pp.547-552

発行日 1988年6月1日 Published Date 1988/6/1

DOI https://doi.org/10.11477/mf.1406206119

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Abstract 文献概要
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　抄録　脳底動脈の変化を直視下で観察するネコ実験モデルを用い，oxyhemoglobin （Oxy-Hb）により誘発される脳血管収縮に対するα-blockerの影響を観察し，その病的意義を検討した。Oxy-Hbによる脳底動脈の収縮は，noradrenalinの収縮を有意に抑制する濃度のPOB （phenoxybenzamine chloride），pra-zosinの前投与により軽度抑制されるものの，有意の差は得られなかった。PGF_2αによる収縮もOxy-Hbの場合と同様に軽度の抑制傾向が認められた。以上の結果よりOxy-Hbはnoradrenalinのagonistとは考えられない。また，α-blockerによるOxy-Hb収縮の軽度抑制は，交感神経系の関与よりも，α—blockerの持つ，いわゆるgeneral suppressorの作用によるものと考えられる。

This study was performed as part of a series of investigations into the relation between cerebral vasospasm following subarachnoid hemorrhage and the sympathetic nervous system. We studied the effect of phenoxybenzamine chloride (POB) and prazosin hydrochloride (Prazosin) on the cerebral vasoconstriction in the basilar arteries of cats in-duced by application of oxyhemoglobin (Oxy-Hb), noradrenalin (Nor) and prostaglandin F_2α(PGF_2α).

Adult cats were anesthetized with intramuscular pentobarbital and maintained on a respirator through a tracheostomy. By the transclival ap-proach, a bone window was formed in the clivus, and the dura was opened, exposing the basilar artery. A cannule was inserted into the subarach-noid space, and through it, Oxy-Hb, Nor and PGF_2α were injected. The sequential changes in caliber of the basilar artery were measured using photography.

First, we determined the doses of POB and Prazosin necessory for decreasing the vasoconstric-tion induced by Nor, and 20 mg/kg of POB and 10 mg/kg of Prazosin were found to decrease the vasoconstriction induced by 10^-3M Nor, statistical-ly. Second, we investigated the effect of 20 mg/kg of POB and O. 5 mg/kg and 10 mg/kg of Prazosin on the cerebral vasoconstriction induced by Oxy-Hb or PGF_2α. POB (20 mg/kg) was infused for 2 hours before the application of Oxy-Hb or PGF_2α. Prazosin was given intravenously. In the first group, 0.02% Prazosin (0.5 mg/kg) was adminis-tered intravenously for 1. 5 hours before the ap-plication of Oxy-Hb or PGF_2α. In the second group, 1.5 hours elapsed between the biginning of Prazosin (10mg/kg) infusion and the application of Oxy-Hb or PGF_2α. The same doses of POB and Prazosin which decreased the vasoconstriction induced by Nor also slightly inhibited the con-striction induced by Oxy-Hb but not to a statisti-cally significant extent. However, POB and Prazosin, like Oxy-Hb, tended to decrease the vasoconstriction induced by PGF_2α. It is thus pos-sible that alpha-adrenergic receptor blockers work as so-called generalized suppressors.

We conclude that Oxy-Hb does not act as an adrenergic receptor agonist, i. e., the relation between the vasospasm induced by Oxy-Hb and the sympathetic nervous system is not significant.