孤束核组胺能受体参与应激大鼠颈动脉窦压力感受性反射的重调定

Histaminergic receptors in the NTS involved in carotid sinus baroreceptor reflex resetting in stressed rats

目的 探讨孤束核 (NTS)组胺 (HA)能受体是否影响应激对颈动脉窦压力感受性反射(CSR)的重调定。方法 应激一周的大鼠 ,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五参数曲线拟合 ,求得ISP MAP关系曲线及特征参数 ,观察NTS注射不同HA受体拮抗剂对CSR的影响。结果 应激导致ISP MAP关系曲线显著全面上移 ,反射参数中阈压、饱和压、调定点和最大增益时ISP值增大 ,MAP反射变动范围及最大增益减小 ;NTS内注射H1或H2 受体拮抗剂 (氯苯吡胺 ,CHL ,0 5 μg或西咪替丁 ,CIM ,1 5 μg) 2 0min内均可明显减弱应激对CSR的上述改变 ,CIM减弱作用不如CHL ;NTS内注射CHL或CIM后 ,均不能使应激的CSR水平完全恢复到相应的非应激对照水平。结论 应激引起CSR重调定 ,反射敏感性下降 ;部分机制可能是激活中枢HA能系统 ,NTS的H1和H2 尤其H1受体在应激引起CSR重调定的机制中发挥重要作用 ;下丘脑

Objective To explore the effects of histaminergic receptors in the nucleus of solitary tract (NTS)on carotid sinus baroreceptor reflex(CSR) resetting resulted from stress.Methods 18 Wistar Rats were subjected to electric foot-shock twice daily for a week.The left and right carotid sinus regions were isolated from the systemic circulation under anesthesia with pentobarbital sodium.The intracarotid sinus pressure (ISP) was altered in a stepwise manner.ISP-mean arterial pressure (MAP)relationship curve and its characteristic parameters were constructed by fitting to the logistic function with five parameters.We observed the changes in CSR performance induced by stress and the effects of microinjection with histaminergic receptors antagonists into the NTS on the responses of CSR to stress.Results Stress made the ISP-MAP relationship curve significantly shift upwards and obviously decreased the value of the MAP range and maximum gain(G max),but increased the threshold pressure (TP),saturation pressure (SP),set point and ISP at G max (ISP Gmax).Microinjection of H 1 or H 2 receptors antagonist,chlorpheniramine (CHL,0.5μg)or cimetidine (CIM,1.5μg)into the NTS,significantly diminished the above-mentioned changes in CSR performance induced by stress and the alleviative effect of CIM was less remarkable than that of CHL.The responses of CSR under stress to H 1 or H 2 receptor antagonist generally occurred 20 min after the administration and lasted approximately for 16min.However,microinjection of CHL or CIM into the NTS could not completely abolish the stress-induced changes in CSR.Conclusion The stress results in a resetting of CSR and a decrease in reflex sensitivity.The stress-induced changes in CSR may be mediated,at least in part,by activating the brain histaminergic system.The H 1 and H 2 receptors in the NTS,especially,H 1 receptors may play an important role in the resetting of CSR under stress.The descending histaminergic pathway from the hypothalamus to NTS may be involved in these effects.