Meyrelles S S, Mauad H, Mathias S C, Cabral A M, Vasquez E C
Department of Physiological Sciences, Biomedical Center, UFES, Vitoria, ES, Brazil.
J Auton Nerv Syst. 1998 Nov 10;73(2-3):135-42. doi: 10.1016/s0165-1838(98)00129-5.
There are clinical and experimental evidences that the cardiopulmonary reflex function is impaired in chronic hypertension, but it could be due to myocardial hypertrophy rather than to hypertension itself. To test this hypothesis we evaluated the Bezold-Jarisch reflex in experimental conditions of myocardial hypertrophy and arterial normotension. Adult male Wistar rats were subjected to myocardial hypertrophy (MHR) treating them with the beta-adrenoceptor agonist isoproterenol (0.3 mg/kg/day, s.c.) for 15 days and compared with vehicle injected control rats (CR). No significant changes in body weight (283+/-14 vs. 299+/-9 g), resting mean arterial pressure (104+/-4 vs. 110+3 mm Hg) or heart rate (330+/-11 vs. 358+/-18 bpm) were observed in MHR compared to CR. As expected, MHR showed left and right ventricular and left atrial hypertrophy when compared to CR. The bradycardia and hypotension that characterizes the Bezold-Jarisch reflex, induced by the 5-HT3, agonist phenyldiguanide (1.5-24.0 microg/kg, i.v.), were significantly decreased in MHR compared to CR. Cardiac muscarinic responsiveness, which was assessed by electrical stimulation of the efferent vagus in anesthetized animals or by stimulation of muscarinic receptors in isolated hearts, was unchanged or increased, respectively, in MHR compared to CR. Additional studies showed that the baroreflex and chemoreflex were also attenuated in MHR compared to CR. These data indicate that cardiac hypertrophy impairs the Bezold-Jarisch reflex probably due to changes at central integrative areas of the reflex.
有临床和实验证据表明，慢性高血压患者的心肺反射功能受损，但这可能是由于心肌肥厚而非高血压本身所致。为了验证这一假设，我们在心肌肥厚和动脉血压正常的实验条件下评估了贝佐尔德 - 雅里什反射。成年雄性Wistar大鼠接受心肌肥厚处理（MHR组），用β - 肾上腺素能受体激动剂异丙肾上腺素（0.3 mg/kg/天，皮下注射）治疗15天，并与注射赋形剂的对照大鼠（CR组）进行比较。与CR组相比，MHR组大鼠的体重（283±14 vs. 299±9 g）、静息平均动脉压（104±4 vs. 110±3 mmHg）或心率（330±11 vs. 358±18 bpm）均无显著变化。正如预期的那样，与CR组相比，MHR组出现左、右心室及左心房肥厚。由5 - HT3激动剂苯二甲胍（1.5 - 24.0 μg/kg，静脉注射）诱导的、作为贝佐尔德 - 雅里什反射特征的心动过缓和低血压，在MHR组中与CR组相比显著降低。通过对麻醉动物的传出迷走神经进行电刺激或对离体心脏中的毒蕈碱受体进行刺激来评估的心脏毒蕈碱反应性，在MHR组中与CR组相比分别未改变或增加。进一步的研究表明，与CR组相比，MHR组的压力反射和化学反射也减弱。这些数据表明，心脏肥厚可能由于反射中枢整合区域的变化而损害贝佐尔德 - 雅里什反射。
