干旱区生态环境知识资源中心(Arid): 大鼠蓝斑组胺受体在应激导致颈动脉窦反射重调定中的作用

Arid

	大鼠蓝斑组胺受体在应激导致颈动脉窦反射重调定中的作用
其他题名	ROLES OF THE HISTAMINERGIC RECEPTORS IN THE LOCUS CERULEUS IN STRESS-INDUCED CAROTID BAROREFLEX RESETTING IN RATS
	王国卿 1; 李建祥 2; 傅春玲 2; 孙万平 1; 童建 2
ISSN	1000-6834
出版年	2007
卷号	23 期号:2 页码:168-172
中文摘要	目的:揭示蓝斑(LC)的H1和H2受体在足底电击应激对颈动脉窦反射(CBR)重调定中的作用.方法:足底电击应激1周的SD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、ISP-增益(Gain)关系曲线及反射特征参数,观察LC微量注射选择性H1或H2受体拮抗剂氯苯吡胺(CHL)或西咪替丁(CIM)对应激状态下CBR的影响.结果:应激导致ISP-MAP关系曲线显著全面上移(P＜0.05),ISP-Gain关系曲线中部明显下移(P＜0.05),反射参数中阈压、饱和压、调定点和最大增益时的ISP值增大(P＜0.05),而MAP反射变动范围及反射最大增益减小(P＜0.05);LC内注射CHL(0.5mug/mul)或CIM(1.5mug/mul)20 min内均可明显减弱应激对CBR的上述改变(P＜0.05),CIM的减弱效应不如CHL的显著(P＜0.05);LC注射上述相同剂量的CHL或CIM对非应激大鼠的CBR无明显影响(P＞0.05);LC内注射CHL或CIM均不能使应激的CBR水平完全恢复到相应的非应激对照水平.结论:应激引起CBR重调定,反射敏感性下降;部分机制可能是激活中枢组胺能系统,LC的H_1和H_2受体无为H_1受体在应激对CBR的重调定机制中发挥重要作用,下丘脑-LC的组胺能通路可能是应激所致CBR重调定的下行通路之一;除此之外,应激作用中尚有其他因素的参与.
英文摘要	To explore the roles of H_1 and H_2 receptors in the locus ceruleus(LC) in the carotid baroreflex(CBR) resetting resulted from foot-shock stress. Methods: Mate SD rats were divided into two groups(n=18) at random: unstressed and stressed group. The latter were subjected to unavoidable electric foot-shock twice daily for a week and 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 CBR performance induced by stress and the effects of microinjection with histaminergic receptors antagonists into the LC on the responses of CBR to stress were examined, Results: Stress significantly shifted the ISP-MAP relationship curve upwards(P<0.05) and obviously moved the middle part of ISP-Gain relationship curve downwards (P<0.05), arid decreased the value of the MAP range and maximum gain (P<0.05), but increased the threshold pressure, Saturation pressure, set point and ISP at maximum gain (P<0.05). Microinjection of selective H_1 or H_2 receptor antagonist, chlorpheniramine (CHL, 0.5 mug/mul) or cimetidine(CIM, 1.5 mug/mul) into the LC, significantly attenuated the above-mentioned changes in CBR performance induced by stress and the alleviative effect of CIM was less remarkable than that of CHL (P<0.05) .The responses of CBR under stress to H_1 or H_2 receptor antagonist generally occurred 20 min after the administration and lasted approximately for 16 min. Microinjection with the same dose of CHL or CIM into the LC in the unstressed group did not change CBR performance significantly (P>0.05). However, microinjection of CHI or CIM into the LC could not completely abolish the stress-induced changes in CBR. Conclusion: The, stress results in a resetting of CBR and a decrease in reflex sensitivity. The stress-induced changes in CBR may be mediated, at least.in part, by activating the brain histaminergic system. The H_1 and H_2 receptors in the LC, especially, H_1 receptors may play an important role in the resetting of CBR under stress. The descending histaminergic pathway from the hypothalamus to LC, may be involved in these effects. Moreover, the effects of stress on CBR also have other mechanisms.
中文关键词	颈动脉窦反射重调定 ; 应激 ; 蓝斑H1受体 ; 蓝斑H2受体 ; 平均动脉压
英文关键词	carotid baroreflex resetting stress H_1 receptor in the loctis ceruleus H_2 recepilor in the focus ceruleus
语种	中文
国家	中国
收录类别	CSCD
WOS类目	CARDIAC CARDIOVASCULAR SYSTEMS
WOS研究方向	Cardiovascular System & Cardiology
CSCD记录号	CSCD:2820679
资源类型	期刊论文
条目标识符	http://119.78.100.177/qdio/handle/2XILL650/221894
作者单位	1.苏州大学医学院基础医学系生理学教研室, 苏州, 江苏 215123, 中国; 2.苏州大学放射医学与公共卫生学院卫生毒理学教研室, 州, 江苏 215123, 中国
推荐引用方式 GB/T 7714	王国卿,李建祥,傅春玲,等. 大鼠蓝斑组胺受体在应激导致颈动脉窦反射重调定中的作用[J],2007,23(2):168-172.
APA	王国卿,李建祥,傅春玲,孙万平,&童建.(2007).大鼠蓝斑组胺受体在应激导致颈动脉窦反射重调定中的作用.,23(2),168-172.
MLA	王国卿,et al."大鼠蓝斑组胺受体在应激导致颈动脉窦反射重调定中的作用".23.2(2007):168-172.