Cardiac sympathetic afferent reflex in dogs with congestive heart failure
Cardiac sympathetic afferent reflex in dogs with congestive heart failure
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DOI：
10.1152/ajpregu.1996.271.3.r751
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发表时间：
1996-09-01
影响因子：
2.8
通讯作者：
Zucker, IH
中科院分区：
文献类型：
--
作者：
Wang, W;Zucker, IH
众所周知，慢性心力衰竭（HF）时交感神经张力升高，心脏交感神经传入反射是一种交感神经兴奋性反射。目前还没有研究设计来检查这种反射在HF状态下控制交感神经流出中的作用。在这项研究中，我们测试的假设，心脏交感神经传入反射增强HF，因此，能够有助于增加交感神经流出在这种疾病状态。在14只狗中进行心室起搏，直到HF迹象明显。14只假手术犬作为对照。在急性实验时，用α-氯醛糖麻醉犬。在去窦房结神经和切断迷走神经状态下，测定了两种剂量的缓激肽（BK）和辣椒素（Cap）对左心室心外膜血流动力学[动脉压和心率（HR）]和肾交感神经活动（RSNA）的反应。HF组的MAP、RSNA和HR对BK的反应均高于假手术组。HF组中对BK（50 μ g）的RSNA反应显著增加（34.0 ± 5.9vs.11.5 ± 4.2%，P < 0.05）。HF组对Cap的MAP、RSNA和HR反应与BK相似，HF组对Cap的RSNA反应显著增加（10 μ g为29.8 +/- 11.3 vs. 13.8 +/- 2.3%，P < 0.05; 100 μ g为46.5 +/- 10.7 vs. 18.7 +/- 3.1%，P < 0.05）。环氧化酶阻断剂吲哚美辛（5 mg/kg iv）可减弱HF组对BK的反射反应。这些数据表明，增强心脏交感神经传入反射心外膜BK在HF似乎是介导的前列腺素合成水平的改变。局部使用利多卡因阻断心脏交感神经传入在HF状态下比在正常状态下显著更多地降低RSNA的基线（-24.2 +/-3.6vs.-4.3 +/-4.5%，P < 0.05）。我们得出结论，从这些数据中，心脏交感神经传入反射是敏感的HF状态，并推测，这种增强的心脏交感神经传入反射可能有助于持续较高的交感神经张力在慢性HF。
It is well accepted that sympathetic tone is elevated in chronic heart failure (HF) and that the cardiac sympathetic afferent reflex is a sympathoexcitatory reflex. There have been no studies designed to examine the role of this reflex in control of sympathetic outflow in the HF state. In this study we tested the hypothesis that cardiac sympathetic afferent reflexes are enhanced in HF and are, therefore, capable of contributing to the increase in sympathetic outflow in this disease state. Ventricular pacing was carried out in 14 dogs until signs of HF were evident. Fourteen sham dogs served as controls. At the time of the acute experiment the dogs were anesthetized with alpha-chloralose. The hemodynamic [arterial pressure and heart rate (HR)] and renal sympathetic nerve activity (RSNA) responses to left ventricular epicardial application of two doses of bradykinin (BK) and capsaicin (Cap) were determined in the sinoaortic-denervated and vagotomized state. The MAP, RSNA, and HR responses to BK were greater in the HF group compared with the sham group. The RSNA response to BK (50 mu g) in the HF group was significantly increased (34.0 +/- 5.9 vs. 11.5 +/- 4.2%, P < 0.05). The MAP, RSNA, and HR responses to Cap in the HF group were similar to the responses to BK. The RSNA response to Cap in the HF group was significantly increased (29.8 +/- 11.3 vs. 13.8 +/- 2.3% for 10 mu g, P < 0.05 and 46.5 +/- 10.7 vs. 18.7 +/- 3.1% for 100 mu g, P < 0.05). The cyclooxygenase blocker indomethacin (5 mg/kg iv) attenuated the reflex responses to BK in the HF group. These data suggest that the enhanced cardiac sympathetic afferent reflex to epicardial BK in HF appears to be mediated by altered levels of prostaglandin synthesis. Blockade of cardiac sympathetic afferents with topical lidocaine reduced baseline of RSNA significantly more in the HF state than in the normal state (-24.2 +/- 3.6 vs. -4.3 +/- 4.5%, P < 0.05). We conclude from these data that the cardiac sympathetic afferent reflex is sensitized in the HF state and speculate that this enhanced cardiac sympathetic afferent reflex may contribute to the sustained higher sympathetic tone in chronic HF.