Ponchon P, Elghozi J L
Laboratory of Pharmacology, Centre National de la Recherche Scientifique URA 1482, Faculty of Medicine Necker, Paris, France.
Am J Physiol. 1997 Jul;273(1 Pt 2):R58-69. doi: 10.1152/ajpregu.1997.273.1.R58.
The aim of this study was to generate hemorrhage-triggered fluctuations in blood pressure (BP) at low frequency (LF, < 0.2 Hz) in conscious rats and investigate with spectral analysis the relative roles of hemorrhage-activated catecholamines, the renin-angiotensin system (RAS), and arginine vasopressin (AVP) on the generation of these fluctuations. The individual contribution of these factors was assessed using a combination of the selective antagonists, prazosin, losartan, and Manning compound (AVPX). At rest, systolic BP (SBP) LF fluctuations were slightly increased by losartan. The mid-frequency (MF; 0.2-0.6 Hz) oscillations of SBP and diastolic BP (DBP) were decreased by prazosin alone or associated with AVPX or losartan. The high-frequency (HF; respiratory) oscillations of SBP were increased by prazosin, prazosin plus losartan, and prazosin plus AVPX. After severe hemorrhage (20 ml/kg), the spontaneous BP recovery was characterized by the occurrence of slow fluctuations of SBP and DBP, centered approximately 0.065 Hz, and by increases of MF (89%) oscillations of SBP. The HF component of SBP variability tended to be increased by blood loss. The occurrence of the SBP LF fluctuations was prevented when alpha 1-adrenergic activity was blocked by prazosin. These oscillations were always present, despite inhibition of angiotensin II, and were increased after inhibition of the AVP activity. Pretreatment with the specific inhibitors used in these studies favored the amplifying effect of hemorrhage on HF fluctuations while they prevented the postbleeding increase in MF oscillations. In conclusion, the present results show an association between the dependence of the postbleeding blood pressure level on catecholamines and the occurrence of slow fluctuations of BP. The buffering role of AVP suggests the establishment of a hierarchy between humoral systems in the genesis of the LF oscillations of BP, with the slow oscillations being generated by the main pressor system and being dampened by the other systems. The postbleeding rise in the MF component of SBP variability could be considered a reflection of the activations of both the sympathetic vasomotor drive and the RAS. The postbleeding increase in the HF component of BP variability was dampened by the activation of the humoral systems. These effects may reflect the low preload state due to hypovolemia.
本研究的目的是在清醒大鼠中引发低频（LF，<0.2 Hz）的出血触发血压（BP）波动，并通过频谱分析研究出血激活的儿茶酚胺、肾素-血管紧张素系统（RAS）和精氨酸加压素（AVP）在这些波动产生中的相对作用。使用选择性拮抗剂哌唑嗪、氯沙坦和曼宁化合物（AVPX）的组合评估这些因素的个体贡献。静息时，氯沙坦使收缩压（SBP）的低频波动略有增加。单独使用哌唑嗪或与AVPX或氯沙坦联合使用可降低SBP和舒张压（DBP）的中频（MF；0.2 - 0.6 Hz）振荡。哌唑嗪、哌唑嗪加氯沙坦以及哌唑嗪加AVPX可增加SBP的高频（HF；呼吸性）振荡。严重出血（20 ml/kg）后，自发性血压恢复的特征是SBP和DBP出现缓慢波动，中心频率约为0.065 Hz，以及SBP的MF振荡增加（89%）。失血使SBP变异性的HF成分趋于增加。当哌唑嗪阻断α1 - 肾上腺素能活性时，可防止SBP低频波动的出现。尽管抑制了血管紧张素II，这些振荡仍始终存在，并且在抑制AVP活性后增加。本研究中使用的特异性抑制剂预处理有利于出血对HF波动的放大作用，同时它们可防止出血后MF振荡的增加。总之，目前的结果表明出血后血压水平对儿茶酚胺的依赖性与血压缓慢波动的发生之间存在关联。AVP的缓冲作用表明在BP低频振荡的发生过程中体液系统之间建立了层次结构，缓慢振荡由主要升压系统产生并被其他系统抑制。出血后SBP变异性MF成分的升高可被视为交感血管运动驱动和RAS激活的反映。出血后BP变异性HF成分的增加因体液系统的激活而受到抑制。这些效应可能反映了由于血容量不足导致的低前负荷状态。
