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慢性肾性高血压患者动脉压力感受器反射的中枢调节受损。

Impaired central mediation of the arterial baroreflex in chronic renal hypertension.

作者信息

Guo G B, Abboud F M

出版信息

Am J Physiol. 1984 May;246(5 Pt 2):H720-7. doi: 10.1152/ajpheart.1984.246.5.H720.

Abstract

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

摘要

在兔肾性高血压6周后,动脉压力感受器对心率(HR)的反射控制受损,但对腰交感神经活动(LSNA)的压力感受器反射控制仍保留。这种选择性损伤可能反映了压力感受器的主要异常。在本研究中,我们检验了以下假设:持续时间更长的肾性高血压可能通过反射的中枢神经系统介导缺陷而损害对LSNA的压力感受器反射控制。在肾性高血压诱导4个月后,在水合氯醛-乌拉坦麻醉下,通过静脉注射去氧肾上腺素使动脉压升高或通过腔静脉闭塞使压力降低期间,测定压力感受器反射反应。高血压兔对LSNA和HR的反射控制明显受损。与正常血压兔相比,高血压兔对左主动脉减压神经(所有动脉压力感受器传入纤维均切断)的传入电刺激的LSNA和HR反射抑制减弱。当仅刺激有髓纤维或同时刺激有髓和无髓纤维时,均观察到这种减弱。我们得出结论,高血压6周后仍保留的对LSNA的压力感受器反射控制在高血压4个月后受损。这种损伤反映了反射的中枢神经系统介导异常。

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