RESTRAINT STRESS CHANGES HEART SENSITIVITY TO ARRHYTHMOGENIC DRUGS

AIM: To study the effects of acute restraint stress on ventricular ele ctric stability (VES) and its mechanisms of action. METHODS: VES was e valuated both in vivo and in vitro by the changes of arrhythmogenic re sponses to icv or ip aconitine in rats and iv BaCl2 or adrenaline in r abbits following restraint stress for different durations. Pretreatmen ts and the assay of heart-specific enzymes were made. RESULTS: The hea rt sensitivity to these drugs was promoted after stress for 2 h, but o btunded after stress for 8 h (the latency of ventricular arrhythmia to icy aconitine was shortened from 4.1 +/- 0.9 min in control rats to 2 .9 +/- 0.9 min after stress for 2 h, P < 0.05; but prolonged to 9.3 +/ - 3.8 min after stress for 8 h, P < 0.05). In Langendorff heart, the c hanges of VES induced by stress were similar to those in vivo, but to lesser degree. Pretreatment with adrenalectomy inhibited the descendin g phase of VES, while pretreatment with both aminophylline and vagotom y remarkably depressed the ascending phase at 8 h. In addition, the se rum activities of lactate dehydrogenase (LDH), creatine kinase (CK), a nd aspartate aminotransferase and their isozymes, LDH(1) and CK-MB, we re elevated at 2 h, and rose continuously at 8 h. CONCLUSION: Acute re straint stress causes biphasic changes of VES. The initial decrease of VES was related to adrenal catecholamine release, whereas the followi ng increase of VES was ascribed to adaptive decrease of cAMP and vagal activation. The changes of VES did not always parallel the injury of heart.