Okabe E, Oyama M, Kadoya K, Kohno H, Ito H
Pharmacology. 1983;27(3):160-8. doi: 10.1159/000137865.
Plasma cyclic AMP levels during anaphylactic shock in rats was studied in 7 groups of animals: (1) control rats; (2) rats with adrenomedullectomy; (3) rats treated with propranolol; (4) rats with reserpinization; (5) rats with 6-hydroxydopamine-induced chemical sympathectomy; (6) rats treated with hexamethonium, and (7) rats treated with cocaine (catecholamine uptake inhibitor). All experiments were carried out in ovalbumin-sensitized rats. Plasma cyclic AMP showed a rapid increase during anaphylactic shock in control rats. Adrenomedullectomy abolished the anaphylaxis-induced increase in plasma cyclic AMP, while hexamethonium had no effect. Propranolol caused a dose-dependent abolition of the increase. The treatment of rats with reserpine, 6-hydroxydopamine or cocaine partially inhibited the increase in plasma cyclic AMP. The results show that the adrenal medulla is the major source of catecholamines during anaphylactic shock, and that catecholamines in the adrenergic neuronal terminals may be partly responsible for the anaphylaxis-induced increase in plasma cyclic AMP.
在7组动物中研究了大鼠过敏性休克期间的血浆环磷酸腺苷（cAMP）水平：（1）对照大鼠；（2）肾上腺髓质切除的大鼠；（3）用普萘洛尔治疗的大鼠；（4）利血平化的大鼠；（5）用6-羟基多巴胺诱导化学性交感神经切除的大鼠；（6）用六甲铵治疗的大鼠，以及（7）用可卡因（儿茶酚胺摄取抑制剂）治疗的大鼠。所有实验均在卵清蛋白致敏的大鼠中进行。对照大鼠在过敏性休克期间血浆cAMP迅速升高。肾上腺髓质切除消除了过敏反应诱导的血浆cAMP升高，而六甲铵则无作用。普萘洛尔导致该升高呈剂量依赖性消除。用利血平、6-羟基多巴胺或可卡因处理大鼠部分抑制了血浆cAMP的升高。结果表明，肾上腺髓质是过敏性休克期间儿茶酚胺的主要来源，并且肾上腺素能神经末梢中的儿茶酚胺可能部分导致过敏反应诱导的血浆cAMP升高。
