Patel K P, Schmid P G
Department of Physiology and Pharmacology, USD School of Medicine, University of South Dakota, Vermillion.
J Auton Nerv Syst. 1988 Apr;22(3):211-9. doi: 10.1016/0165-1838(88)90109-9.
Electrophysiological and neuroanatomical studies indicate that reciprocal connections between the paraventricular nucleus (PVH) and medullary sites are involved in cardiovascular regulation. To determine whether the PVH is involved in the regulation of baroreflex responses, lumbar sympathetic nerve activity (LSNA) and heart rate (HR) changes were recorded in response to increases in arterial pressure (produced by bolus doses of phenylephrine i.v.) prior to, during, and 60 min following the injection of lidocaine (2% lidocaine, 200 nl) bilaterally in the PVH of chloralose-anesthetized rabbits. Baseline blood pressure, HR, and LSNA did not change in response to the administration of lidocaine in the PVH. The magnitude of 'baroreflex responses' in HR and LSNA were expressed as the ratios of maximal changes in these parameters divided by the corresponding maximal changes in blood pressure. Application of lidocaine to the PVH produced a significantly greater decrease in LSNA (greater than 50%) compared to prelidocaine responses to baroreceptor stimulation. This increase in baroreflex response returned to the normal level during the recovery phase. In contrast, there was no significant change in the response of the HR to baroreceptor stimulation. Administration of norepinephrine into the PVH, intended to simulate possible changes in noradrenergic function, did not affect either LSNA or HR responses to baroreceptor stimulation. Interruption of neural activity in the PVH, augmented the inhibitory response of LSNA but not HR to baroreceptor stimulation. These results indicate that changes in peripheral sympathetic nerve activity and HR in response to baroreceptor activation may be affected differentially by specific forebrain structures such as PVH.
电生理和神经解剖学研究表明，室旁核（PVH）与延髓部位之间的相互连接参与心血管调节。为了确定PVH是否参与压力反射反应的调节，在给氯醛糖麻醉的家兔双侧PVH注射利多卡因（2%利多卡因，200 nl）之前、期间和之后60分钟，记录了对动脉压升高（静脉注射大剂量去氧肾上腺素所致）的反应中腰交感神经活动（LSNA）和心率（HR）的变化。PVH注射利多卡因后，基线血压、HR和LSNA未发生变化。HR和LSNA中“压力反射反应”的幅度表示为这些参数的最大变化率除以相应的血压最大变化率。与利多卡因注射前对压力感受器刺激的反应相比，向PVH应用利多卡因使LSNA显著降低（超过50%）。在恢复阶段，这种压力反射反应的增强恢复到正常水平。相反，HR对压力感受器刺激的反应没有显著变化。向PVH注射去甲肾上腺素以模拟去甲肾上腺素能功能的可能变化，对LSNA或HR对压力感受器刺激的反应均无影响。PVH神经活动的中断增强了LSNA而非HR对压力感受器刺激的抑制反应。这些结果表明，特定的前脑结构如PVH可能会对压力感受器激活后外周交感神经活动和HR的变化产生不同影响。
