Ma R, Zucker I H, Wang W
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575, USA.
Am J Physiol. 1997 Dec;273(6):H2664-71. doi: 10.1152/ajpheart.1997.273.6.H2664.
Previous studies from our laboratory have shown that the cardiac sympathetic afferent reflex is enhanced in dogs with experimental heart failure. The aim of the present study was to determine if the central gain of the cardiac sympathetic afferent reflex was also enhanced in dogs with heart failure. Fifteen dogs with pacing-induced heart failure were used in this study. Seventeen sham-operated dogs served as control. At the time of the acute experiment the dogs were anesthetized with alpha-chloralose. Arterial blood pressure, heart rate, and renal sympathetic nerve activity were recorded. After sinoaortic denervation and cervical vagotomy, a thoracotomy was performed in the second intercostal space. The left stellate ganglion was identified, and the left cardiac sympathetic nerves were cut. The central end of the left cardiac sympathetic nerves was placed on bipolar stimulating electrodes. The renal sympathetic nerve activity responses to electrical stimulation (30 Hz, 1 ms with varying voltages from 1 to 10 V; or 10 V, 1 ms with varying frequencies from 1 to 30 Hz) of the afferent cardiac sympathetic nerves were compared between sham and heart failure groups. Reflex renal sympathetic nerve activity responses to stimulation of the cardiac sympathetic nerves were significantly greater in the heart failure group compared with that in the sham group (21.4 +/- 3.2 vs. 9.8 +/- 2.9% at 10 V, 30 Hz and 27.7 +/- 4.5 vs. 9.9 +/- 3.4% at 30 Hz, 10 V, heart failure vs. sham group, respectively; for both relationships, P < 0.05). This enhanced central gain of the cardiac sympathetic afferent reflex in the heart failure group was significantly attenuated after intravenous and cerebroventricular injection of the angiotensin II receptor antagonist losartan (5 mg/kg i.v. and 0.125 mg/kg in 0.1 ml i.c.v.). These data suggest that the central gain of the cardiac sympathetic afferent reflex is enhanced in dogs with heart failure and central angiotensin II plays an important role in this enhanced response.
我们实验室之前的研究表明，在实验性心力衰竭的犬中，心脏交感传入反射增强。本研究的目的是确定心力衰竭犬的心脏交感传入反射的中枢增益是否也增强。本研究使用了15只起搏诱导性心力衰竭犬。17只假手术犬作为对照。在急性实验时，用α-氯醛糖麻醉犬。记录动脉血压、心率和肾交感神经活动。在进行主动脉弓去神经支配和颈迷走神经切断术后，在第二肋间间隙进行开胸手术。识别左星状神经节，并切断左心脏交感神经。将左心脏交感神经的中枢端置于双极刺激电极上。比较假手术组和心力衰竭组肾交感神经活动对心脏交感传入神经电刺激（30Hz，1ms，电压从1到10V变化；或10V，1ms，频率从1到30Hz变化）的反应。与假手术组相比，心力衰竭组对心脏交感神经刺激的反射性肾交感神经活动反应显著更大（在10V，30Hz时分别为21.4±3.2%对9.8±2.9%，在30Hz时为27.7±4.5%对9.9±3.4%，10V，心力衰竭组对假手术组；两种关系均P<0.05）。在静脉内和脑室内注射血管紧张素II受体拮抗剂氯沙坦（5mg/kg静脉注射和0.125mg/kg于0.1ml脑室内注射）后，心力衰竭组心脏交感传入反射的这种增强的中枢增益显著减弱。这些数据表明，心力衰竭犬的心脏交感传入反射的中枢增益增强，中枢血管紧张素II在这种增强的反应中起重要作用
