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去压力神经大鼠中血管加压素诱导的心动过缓

Vasopressin-induced bradycardia in barodenervated rats.

作者信息

Brizzee B L, Adams E M, Walker B R

机构信息

Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112.

出版信息

Am J Physiol. 1991 Oct;261(4 Pt 2):R957-64. doi: 10.1152/ajpregu.1991.261.4.R957.

DOI:10.1152/ajpregu.1991.261.4.R957
PMID:1928442
Abstract

Experiments were performed on conscious chronically instrumented rats to determine the contribution of baroreceptor reflex (BRR)-independent mechanisms in the bradycardia associated with intravenous administration of arginine vasopressin (AVP). At least 2 wk prior to experimentation, the aortic and carotid baroreceptors were denervated in six rats. Following recovery, the maximum bradycardic responses to pressor doses of phenylephrine (PE) or AVP were determined on separate days in each animal. Pulse interval (PI) was calculated from heart rate (HR), and the slopes of PI vs. mean arterial blood pressure (MABP) and PI vs. dose were determined for each experiment by linear regression. There was no significant correlation of PI vs. MABP in response to bolus PE in these barodenervated rats. However, there was a significant correlation of PI vs. MABP and PI vs. dose in response to AVP in five of the six barodenervated rats. These data suggest that pressor levels of AVP may elicit bradycardia independent of the BRR. Another group of experiments was performed in the Langendorff-isolated rat heart preparation to assess the direct chronotropic effect of AVP. Hearts were not paced, and the coronary arteries were perfused at a constant flow. HR was determined at various concentrations of AVP (n = 4 at each dose). In addition, because unpaced hearts exhibited low intrinsic rates, the same protocol was performed in hearts receiving isoproterenol to elevate basal HR (n = 4 at each AVP dose). There was no chronotropic effect of AVP in isolated hearts with or without isoproterenol administration.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

对清醒的慢性植入仪器的大鼠进行实验,以确定压力感受器反射(BRR)非依赖性机制在静脉注射精氨酸加压素(AVP)相关的心动过缓中的作用。在实验前至少2周,对6只大鼠进行主动脉和颈动脉压力感受器去神经支配。恢复后,在每只动物的不同日子里分别测定对升压剂量的去氧肾上腺素(PE)或AVP的最大心动过缓反应。根据心率(HR)计算脉搏间期(PI),并通过线性回归确定每个实验中PI与平均动脉血压(MABP)以及PI与剂量的斜率。在这些压力感受器去神经支配的大鼠中,对推注PE的反应中PI与MABP无显著相关性。然而,在6只压力感受器去神经支配的大鼠中的5只中,对AVP的反应中PI与MABP以及PI与剂量存在显著相关性。这些数据表明,AVP的升压水平可能引发与BRR无关的心动过缓。另一组实验在Langendorff离体大鼠心脏标本中进行,以评估AVP的直接变时作用。心脏未起搏,冠状动脉以恒定流量灌注。在不同浓度的AVP下测定HR(每个剂量n = 4)。此外,由于未起搏的心脏固有心率较低,在接受异丙肾上腺素以提高基础HR的心脏中进行相同方案的实验(每个AVP剂量n = 4)。无论是否给予异丙肾上腺素,AVP在离体心脏中均无变时作用。(摘要截断于250字)

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