Natelson B H, Tapp W N, Drastal S, Suarez R, Ottenweller J E
Neurobehavioral Unit, VA Medical Center, East Orange, New Jersey.
Psychosom Med. 1991 May-Jun;53(3):322-31. doi: 10.1097/00006842-199105000-00006.
Results of earlier experiments suggested that hamsters with inherited heart disease were at a higher risk of succumbing to stress during the vasospastic, lesion-forming period of their lives rather than later when the process of congestive heart failure had begun. To test this hypothesis, we stressed cardiomyopathic hamsters (CMH) whose ages differed by about 3 months; the younger of the two groups of stressed hamsters was in the vasospastic phase of the disease. The stressor was cold immobilization in which stressor intensity was manipulated using two durations of cold exposure. Log rank survival curves revealed no difference in mortality with the more intense stressor. However, significantly fewer of the older hamsters succumbed to the less intense stressor (46% as compared with 85% of the younger CMHs). Examination of the hearts in the experiment where mortality rate was the same for both groups revealed evidence of cardiac dilatation, indicative of heart failure, only in the older hamsters following stress. Since the younger hamsters did not show these changes and since they, but not the older animals, have coronary microvascular spasm and an increased susceptibility to stress, it would appear that the process of coronary vasospasm should be viewed as an independent and additional risk factor in determining the consequences of stress. Because of the effects of stress in the younger cardiomyopathic hamster, we believe that a neural link--which can be activated by stress--may be involved in the pathogenetic process of coronary vasospasm.
早期实验结果表明,患有遗传性心脏病的仓鼠在其生命中的血管痉挛、病变形成期比在充血性心力衰竭过程开始的后期更容易因应激而死亡。为了验证这一假设,我们对年龄相差约3个月的心肌病仓鼠(CMH)施加应激;两组受应激的仓鼠中较年轻的处于疾病的血管痉挛阶段。应激源是冷束缚,通过两种冷暴露时长来控制应激源强度。对数秩生存曲线显示,在较强应激源作用下死亡率没有差异。然而,在较弱应激源作用下,老年仓鼠死亡的数量明显较少(46%,而年轻的CMH为85%)。在两组死亡率相同的实验中对心脏进行检查发现,仅在应激后的老年仓鼠中出现了心脏扩张的迹象,这表明存在心力衰竭。由于年轻仓鼠没有出现这些变化,且它们(而非老年动物)存在冠状动脉微血管痉挛且对应激的易感性增加,因此冠状动脉痉挛过程似乎应被视为决定应激后果的一个独立且额外的风险因素。由于应激对年轻的心肌病仓鼠有影响,我们认为一种可被应激激活的神经联系可能参与了冠状动脉痉挛的发病过程。