摘要
目的探讨中枢胆碱能M_1受体在应激条件下对颈动脉窦压力感受器反射(CSR)的影响。方法健康雄性SD大鼠随机分成非应激组(n=12)和应激组(n=12),后者接受不可逃避的足底电击,每日2次,每次持续2h。应激1周的SD大鼠,经筛选、麻醉后孤离双侧颈动脉窦区,将不同窦内压(ISP)与其对应的平均动脉压(MAP)值进行Logistic曲线拟合,求得ISP-MAP、ISP-增益(Gain)关系曲线及其特征参数,观察侧脑室微量注射选择性胆碱能M_1受体拮抗剂哌仑西平(PRZ)对CSR的影响。结果侧脑室注射PRZ(1.0 mmol/L,5μl)导致应激大鼠ISP-MAP关系曲线后半程明显下移(P<0.05),ISP-Gain关系曲线中部明显上移(P<0.05),反射参数中饱和压和最大增益时的窦内压值减少(P<0.05),而反射最大Gain加大(P<0.05);侧脑室注射相同剂量、容积的PRZ对非应激大鼠CSR的各项指标均无明显影响(P>0.05);侧脑室注射PRZ不能使应激的CSR水平恢复到非应激水平(P<0.05)。结论中枢胆碱能M_1受体参与应激对CSR功能抑制性重调定;除此之外,应激调节中尚有其他神经机制因素的参与。
Objective To investigate the effects of central muscarinic M,cholinoceptor on the stress-induced carotid sinus baroreceptor reflex（CSR） resetting.Methods Male Sprague-Dawley rats were divided into two groups at random：the unstressed（n=12） and the stressed group（n=12）.The latter was subjected to unavoidable electric foot-shock twice daily for a week,each session of foot-shock lasted 2 hours.The left and right carotid sinus regions were isolated from the systemic circulation in all animals anesthetized with pentobarbital sodium.The intracarotid sinus pressure（ISP） was altered in a stepwise manner in vivo.ISP-mean arterial pressure（MAP）,ISP-Gain relationship curves and reflex characteristic parameters were constructed by fitting to the logistic function with five parameters.The changes in CSR performance induced by stress and the effects of microinjection with the selective muscarinic M,cholinoceptor antagonist pirenzepine（PRZ）,into the lateral ventricle on the responses of CSR to stress were observed. Results Microinjection of PRZ（1.0mmol/L,5μl） into the lateral ventricle in the stressed group,significantly shifted the posterior half range of ISP-MAP relationship curve downwards（P〈0.05）, remarkably shifted the middle parts of ISP-Gain relationship curve upwards（P 0.05） and obviously decreased the value of the reflex parameters such as saturation pressure and ISP at maximum gain（P〈0.05） but increased reflex maximum gain（P〈0.05）.Microinjection of PRZ into the lateral ventricle in the unstressed group with the same dose and volume did not change CSR performance significantly（P〈0.05）. The changes in the stressed CSR performance resulted from the administration of PRZ into the lateral ventricle did not recover to the levels of unstressed CSR after injection.Conclusion Central cholinergic M, receptor is involved in the stress-induced CSR inhibitory resetting,at the same time,the effects of stress on CSR also have other neuromechanisms.
出处
《苏州大学学报（医学版）》
CAS
北大核心
2011年第6期897-901,共5页
Suzhou University Journal of Medical Science
基金
苏州大学博士科研基金资助项目(Q4134808)
苏州市科技计划项目(应用基础研究计划SYS201010)
