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心脏传入神经在兔容量扩张引起的肾神经抑制中起主导作用。

Cardiac afferents play the dominant role in renal nerve inhibition elicited by volume expansion in the rabbit.

作者信息

Badoer E, Moguilevski V, McGrath B P

机构信息

Department of Medicine, Monash Medical Centre, Melbourne, Victoria, Australia.

出版信息

Am J Physiol. 1998 Feb;274(2):R383-8. doi: 10.1152/ajpregu.1998.274.2.R383.

DOI:10.1152/ajpregu.1998.274.2.R383
PMID:9486295
Abstract

In the rabbit, vagotomy combined with arterial baroreceptor denervation abolishes the renal sympathoinhibition elicited by volume expansion. However, the effect of removing cardiopulmonary afferents alone has not been investigated. The aim of the present study was to determine the role of the cardiac afferents in the renal sympathetic response elicited by volume expansion in the normal conscious rabbit. Four experimental groups were used in which rabbits were administered 1) volume expansion (Haemaccel, 1.9 ml/min for 60 min), 2) volume expansion + bolus intrapericardial procaine (20 mg) to block cardiac afferents, 3) volume expansion + intravenous procaine (20 mg bolus), and 4) intrapericardial procaine alone (20 mg bolus). Volume expansion did not significantly affect mean arterial pressure or heart rate but produced a profound fall in renal sympathetic nerve activity (approximately 50%). Intrapericardial procaine administered 30 min after the start of volume expansion markedly reversed the renal sympathoinhibition to within 20% of the pre-volume expansion level, an effect that wore off over 25 min. In contrast, intravenous procaine lowered renal sympathetic nerve activity slightly further. The results suggest that cardiac afferents play the dominant role in the renal sympathoinhibition in response to volume expansion in the normal conscious rabbit.

摘要

在兔中,迷走神经切断术联合动脉压力感受器去神经支配可消除容量扩张引起的肾交感神经抑制。然而,单独去除心肺传入神经的作用尚未得到研究。本研究的目的是确定在正常清醒兔中,心脏传入神经在容量扩张引起的肾交感反应中的作用。使用了四个实验组,分别对兔进行以下处理:1)容量扩张(贺斯,1.9 ml/分钟,持续60分钟);2)容量扩张+心包内注射普鲁卡因推注(20毫克)以阻断心脏传入神经;3)容量扩张+静脉注射普鲁卡因(20毫克推注);4)单独心包内注射普鲁卡因(20毫克推注)。容量扩张对平均动脉压或心率无显著影响,但可使肾交感神经活动显著下降(约50%)。在容量扩张开始30分钟后心包内注射普鲁卡因,可使肾交感神经抑制明显逆转,降至容量扩张前水平的20%以内,该效应在25分钟后逐渐消失。相比之下,静脉注射普鲁卡因可使肾交感神经活动进一步轻微降低。结果表明,在正常清醒兔中,心脏传入神经在容量扩张引起的肾交感神经抑制中起主导作用。

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