Montano N, Gnecchi-Ruscone T, Contini M, Finocchiaro M L, Lombardi F, Malliani A
Centro Ricerche Cardiovascolari, Università di Milano, Italy.
Am J Physiol. 1993 Feb;264(2 Pt 2):H345-51. doi: 10.1152/ajpheart.1993.264.2.H345.
In 13 decerebrate cats, we studied the effects of captopril (10 mg/kg iv bolus) on the background discharge of thoracic preganglionic sympathetic fibers. After drug administration there was an initial reduction in systolic arterial pressure (SAP), which was followed by a later inhibition of sympathetic discharge (from 2.7 +/- 0.5 to 0.79 +/- 0.1 imp/0.1 s; P < 0.01). Captopril significantly reduced the excitatory response of sympathetic fibers to premature ventricular contraction (70 +/- 17 vs. 257 +/- 30%), inferior vena cava obstruction (176 +/- 56 vs. 315 +/- 85%) and asphyxia (143 +/- 20 vs. 245 +/- 51%). Vice versa the sympathetic response to aortic occlusion was unaffected (-58 +/- 8 vs. -62 +/- 6%). A similar reduction in sympathetic discharge was observed after captopril administration in anesthetized cats (n = 3). On the contrary, no changes in background neural discharge were noticed in decerebrate-spinalized cats (n = 5), despite comparable hemodynamic effects. These data indicate that captopril reduces sympathetic efferent activity and its responsiveness to excitatory stimuli. The lack of neural effects in decerebrate-spinalized cats is consistent with a brain stem site of action of captopril.
在13只去大脑猫中，我们研究了卡托普利（静脉推注10mg/kg）对胸段节前交感神经纤维自发放电的影响。给药后，收缩压（SAP）最初下降，随后交感神经放电受到抑制（从2.7±0.5降至0.79±0.1次/0.1秒；P<0.01）。卡托普利显著降低了交感神经纤维对室性早搏（70±17对257±30%）、下腔静脉阻塞（176±56对315±85%）和窒息（143±20对245±51%）的兴奋性反应。反之，对主动脉阻断的交感反应未受影响（-58±8对-62±6%）。在麻醉猫（n=3）中给予卡托普利后也观察到类似的交感神经放电减少。相反，在去大脑脊髓猫（n=5）中，尽管有类似的血流动力学效应，但未发现自发放电有变化。这些数据表明，卡托普利降低了交感传出活动及其对兴奋性刺激的反应性。在去大脑脊髓猫中缺乏神经效应与卡托普利的脑干作用部位一致。
