大鼠后肢舒张血管神经的研究

目的　研究大鼠后肢血管床是否存在血管舒张神经及其性质。方法　用营养液灌流利血平预处理毁脑脊髓大鼠后肢血管床并施以脊髓内电刺激。结果　电刺激可诱发后肢血管床灌流压下降。河豚毒、格列本脲能明显取消之；阿托品、普萘洛尔、氨茶碱及Ｎω 硝基 Ｌ 精氨酸甲基酯等药物无明显影响。结论　大鼠后肢血管床存在血管舒张神经，其神经递质通过开放Ｋ＋ＡＴＰ通道发挥舒张血管作用，可能是以ＣＧＲＰ为神经递质的肽能神经。

Study on vasodilator nerve in rat hind limb

AIM To investigate whether there is vasodilator nerve innervation in rat hind limb and what the nature of vasodilator nerve is. METHODS Wistar rats were treated with reserpine 1 mg·kg -1 ip at 24 h before experiment. The rats were pithed and the hind limb vascular bed was perfused with Krebs-Henseleite solution containing 1 mmol·L -1 phenylephrine at 2 ml·min -1 speed. The hind limb perfused pressure (HPP) as a main index was continuously recorded. Spinal cord electrical stimulation (SES) was repeatedly applied via an electrode at L 1～2 level of lumber vertebra. The various tool drugs were administered by iv or infusion by added to persusion solution. The data is expressed as decrease percentages of HPP increased by continuous infusion of phenylephrine. RESULTS HPP was increased from (5 7±1 5) to (21 6±3 7) kPa ( n =37) after phenylephrine perfusion. SES caused a fall of HPP in frequency dependent and voltage dependent manner. An optimum parameters of SES (10 Hz, 50 V and 1 msec) was selected to observe effects of various tool drugs on depressor response of HPP to SES. Tetrotodoxin (0 3 μmol·L -1 ) abolished the effect completely. L NAME (10 μmol·L -1 ), a NO synthase inhibitor, had no effect. Ganglion blocker arfonad (110 mg·kg -1 , iv, M R blocker atropine (10 μmol·L -1 ), β receptor blocker propranolol (1 μmol·L -1 ) and P 1 receptor blocker aminophylline (10 μmol·L -1 ) had also no effect. Glibenclamide (0 1 mmol·L -1 ), an ATP sensitive K + channel blocker, markedly abolished and slightly reversed the effect. CONCLUTION The nonadrenergic noncholinergic vasodilator nerve exists in rat hind limb and is not nitroxidergic or purinergic nerve. This nerve may be peptidergic nerve which releases some peptide such as CGRP and the major mechanism of vasodilatation probably activates the ATP sensitive K + channel.