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清醒犬低频血压变异性的起源

On the origin of low-frequency blood pressure variability in the conscious dog.

作者信息

Just A, Wagner C D, Ehmke H, Kirchheim H R, Persson P B

机构信息

I. Physiologisches Institut, Ruprecht-Karls-Universität, Heidelberg, Germany.

出版信息

J Physiol. 1995 Nov 15;489 ( Pt 1)(Pt 1):215-23. doi: 10.1113/jphysiol.1995.sp021043.

Abstract
  1. Baroreceptor denervation increases blood pressure variability below 0.1 Hz. This study was undertaken to determine to what extent these fluctuations originate from the central nervous system or from cardiovascular sources. 2. Blood pressure was recorded at a rate of 10 Hz for approximately 3.5 h in conscious, resting dogs. Power density spectra were calculated from all 2(17) points of each recording session and integrated between 0.0002 and 0.1 Hz. 3. Blockade of the afferent limb of the baroreceptor reflex by surgical denervation of sinoaortic and cardiopulmonary afferents (Den; n = 6) significantly increased integrated power more than sixfold compared with a control group (n = 11). 4. Impairment of the efferent limb in non-deafferented dogs by either alpha 1-adrenergic blockade with prazosin (Praz; n = 7) or ganglionic blockade with hexamethonium (Hex; n = 6) failed to raise variability. 5. Both prazosin (n = 6) and hexamethonium (n = 3) reduced the increased variability in denervated dogs. 6. In non-deafferented dogs receiving hexamethonium, elevation of mean blood pressure to the hypertensive level of the Den group, by a continuous infusion of noradrenaline (n = 4), did not change the variability. 7. It is concluded that in the absence of changes in posture, most of the increased blood pressure variability after baroreceptor denervation is derived from the central nervous system. 8. Direct comparison of power spectra of the Den (total variability) and Hex groups (variability derived from the cardiovascular system only) suggests that the central nervous system is also the prevalent source of low-frequency blood pressure variability in intact animals.
摘要
  1. 压力感受器去神经支配会增加低于0.1赫兹的血压变异性。本研究旨在确定这些波动在多大程度上源自中枢神经系统或心血管系统。2. 在清醒、静息的犬类中,以10赫兹的速率记录血压约3.5小时。从每个记录时段的所有2(17)个点计算功率密度谱,并在0.0002至0.1赫兹之间积分。3. 通过对窦主动脉和心肺传入神经进行手术去神经支配(Den;n = 6)来阻断压力感受器反射的传入支,与对照组(n = 11)相比,显著增加了积分功率超过六倍。4. 用哌唑嗪进行α1肾上腺素能阻断(Praz;n = 7)或用六甲铵进行神经节阻断(Hex;n = 6),在未去传入神经的犬类中损害传出支未能提高变异性。5. 哌唑嗪(n = 6)和六甲铵(n = 3)均降低了去神经支配犬类中增加的变异性。6. 在接受六甲铵的未去传入神经的犬类中,通过持续输注去甲肾上腺素(n = 4)将平均血压升高至Den组的高血压水平,并未改变变异性。7. 得出的结论是,在姿势无变化的情况下,压力感受器去神经支配后血压变异性增加的大部分源自中枢神经系统。8. Den组(总变异性)和Hex组(仅源自心血管系统的变异性)功率谱的直接比较表明,中枢神经系统也是完整动物中低频血压变异性的主要来源。

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