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脑内血管加压素V1受体在心肌梗死大鼠对应激的心血管反应中的作用增强。

Enhanced involvement of brain vasopressin V1 receptors in cardiovascular responses to stress in rats with myocardial infarction.

作者信息

Dobruch Jakub, Cudnoch-Jedrzejewska Agnieszka, Szczepanska-Sadowska Ewa

机构信息

Medical University of Warsaw, Department of Experimental and Clinical Physiology, Krakowskie Przedmieście 26/28, Warsaw, 00-927, Poland.

出版信息

Stress. 2005 Dec;8(4):273-84. doi: 10.1080/10253890500456287.

DOI:10.1080/10253890500456287
PMID:16423716
Abstract

Stress is one of the factors provoking cardiovascular complications. The purpose of the study was to explore the role of vasopressin (VP) in central control of arterial blood pressure and heart rate under resting conditions and during stimulation by an alarming stress (air jet stress) in myocardial infarct-induced cardiac failure. Six groups of male Sprague Dawley (SD) rats were subjected either to sham surgery (sham rats) or to ligation of a left coronary artery (infarcted rats). After 5 weeks both infarcted and sham rats were subjected either to intracerebroventricular infusion of artificial cerebrospinal fluid (aCSF) (sham aCSF and infarcted aCSF), [Arg8]-VP (sham VP and infarcted VP) or VP V1a receptor antagonist (d(CH2)5[Tyr(Me)2Ala-]VP, sham V1ANT and infarcted V1ANT). Air jet stress elicited significantly greater increases in mean arterial blood pressure (MABP) and heart rate in the infarcted aCSF than in the sham aCSF rats. Intracerebroventricular infusion of V1ANT significantly reduced resting MABP and MABP and heart rate increases in response to stress in the infarcted but not in the sham rats. Intracerebroventricular infusion of VP elicited a significant increase in resting MABP in the infarcted VP but not in the sham VP rats. The results provide evidence for enhanced engagement of the brain V1 VP receptors in regulation of resting MABP and in generation of exaggerated cardiovascular responses to air jet stress during the post-infarct state.

摘要

应激是引发心血管并发症的因素之一。本研究的目的是探讨在心肌梗死诱发的心力衰竭中,血管加压素(VP)在静息状态下以及在警报应激(喷气应激)刺激期间对动脉血压和心率的中枢控制中的作用。将六组雄性斯普拉格-道利(SD)大鼠分别进行假手术(假手术大鼠)或左冠状动脉结扎(梗死大鼠)。5周后,梗死大鼠和假手术大鼠均接受脑室内注入人工脑脊液(aCSF)(假手术aCSF组和梗死aCSF组)、[精氨酸8]-VP(假手术VP组和梗死VP组)或VP V1a受体拮抗剂(d(CH2)5[Tyr(Me)2Ala-]VP,假手术V1ANT组和梗死V1ANT组)。与假手术aCSF组大鼠相比,喷气应激使梗死aCSF组大鼠的平均动脉血压(MABP)和心率显著升高。脑室内注入V1ANT可显著降低梗死大鼠而非假手术大鼠的静息MABP以及应激时MABP和心率的升高。脑室内注入VP可使梗死VP组大鼠的静息MABP显著升高,而假手术VP组大鼠则无此现象。这些结果为梗死状态后脑V1 VP受体在调节静息MABP以及对喷气应激产生过度心血管反应中的作用增强提供了证据。

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