摘要
目的 探讨胆碱能机制在 p H降低时颈动脉体 (CB)功能活动变化中的作用 .方法 在离体灌流条件下 ,记录颈动脉窦神经 (CSN)传入纤维的化学感受性单位放电 .结果 乙酰胆碱 (ACh)抑制单位放电 (n=16 ,P<0 .0 5 ) ,阿托品阻断 ACh的作用 ;尼古丁呈剂量依赖性增加单位放电 (n=10 ,r= 0 .94,P<0 .0 1) ;箭毒可阻断尼古丁的作用 ,对自发放电无显著影响 ;尼古丁并不增加化学感受性单位对 p H降低的放电反应 (n=19) ;p H降低时筒箭毒对化学感受性单位放电变化无显著影响 (n=17) ;硝苯吡啶 (5 mmol· L- 1 )对自发的基础单位放电 (n=8)和刺激诱导的电活动 (n=9)均无明显影响 .结论 胆碱能机制与 p H降低时
AIM To elucidate the physiological significance of N cholinergic receptor in CB chemosensory processes under low pH conditions. METHODS The unit discharges of carotid chemosensory afferent fibers were recorded in the in vitro carotid body (CB) sinus nerve preparations from 41 rabbits ( n =86 ). RESULTS Exogenous ACh (20 mg·L -1 ) inhibited unit discharges recorded on sinus nerve ( n =16, P <0.05), while atropine only blocked the effect of ACh; Addition of nicotine in the different concentrations led to dose dependent increases ( r =0.94, P <0.01, n =10). Nicotinic stimulation was antagonized by D tubocurarine but the basal discharge was not significantly affected. Superfusion of the CB with acid solution increased the discharge from (0.95±0 34) to (1.84±0.55) imp·s -1 ( n =19). After the addition of 5 mg·L -1 nicotine to acidic perfusate, the unit discharge still showed an increase from (0.96±0.25) to (1.53±0.24) imp·s -1 ( P <0.05), but nicotine did not augment the discharge response of the units to acidification; D tubocurarine did not alter the action of acid solution on chemosensory discharge ( n =17); Nifedipine (5 mmol·L -1 ) did not significantly affect both of the spontaneous basal discharge ( n =8) and acid evoked electric activity ( n =9). CONCLUSION The present results suggest that ACh might act only as a physiological modulator on carotid chemosensory activity without direct involvement in cholinergic mechanisms as done by low pH perfusion of CB.
出处
《第四军医大学学报》
2000年第10期1219-1222,共4页
Journal of the Fourth Military Medical University
关键词
胆碱能受体
颈动脉体化学感受器
pH降低
cholinergic receptors
acetylecholine
carotid body chemoreceptor
unit discharge
low pH
