Chang Q, Natelson B H, Ottenweller J E, Conway R S
Neurobehavioral Unit (127A), VA Medical Center, East Orange, NJ 07018-1095, USA.
Cardiovasc Res. 1995 Dec;30(6):985-91.
Because cardiomyopathic hamsters (CMHs) in the lesion-forming period of their disease are more susceptible to the lethal effects of stress than older CMHs, we tested the hypothesis that different pathophysiological effects of stress may occur: coronary vasospasm in younger CMHs and congestive heart failure in older ones.
CMHs aged 2.5 and 6.5 months were stressed with 2 h supine cold immobilization for 5 consecutive days. Three, 5 and 7 days after stress, the hearts were excised and perfused using a modified Langendorff system. Maximum +/- dP/dt, developed pressure, ventricular relaxation time (Tau) and coronary vascular resistance (CVR) were recorded and CVR was also measured following coronary infusion of arginine vasopressin (AVP).
Stress produced ventricular dysfunction (decreased maximum +/- dP/dt, developed pressure, and increased Tau) in older CMHs (P < 0.05) but not in younger CMHs. Baseline CVR in younger CMHs was significantly higher than in older CMHs (P < 0.01) and AVP infusion produced a bigger increase in CVR in younger stressed CMHs than in either younger nonstressed or older stressed CMHs (P < 0.05).
The younger CMH heart exhibits greater resting vascular tone and stress produces coronary vasoconstriction that is consistent with coronary spasm. In contrast, the older CMH experiences a decrease in cardiac function which remains 7 days after stress and indicates an exacerbation of CHF from the mild form existing prior to stress. The lethal effects of stress may occur because of the activation of different pathological processes in younger and older CMHs.
由于处于疾病病变形成期的心肌病仓鼠(CMH)比年龄较大的CMH更容易受到应激的致死效应影响,我们检验了以下假设:应激可能会产生不同的病理生理效应,即年轻CMH出现冠状动脉痉挛,而老年CMH出现充血性心力衰竭。
对2.5个月和6.5个月大的CMH连续5天进行2小时仰卧冷束缚应激。应激后3、5和7天,取出心脏并使用改良的Langendorff系统进行灌注。记录最大±dP/dt、舒张末压力、心室舒张时间(Tau)和冠状动脉血管阻力(CVR),并在冠状动脉输注精氨酸加压素(AVP)后测量CVR。
应激在老年CMH中导致心室功能障碍(最大±dP/dt、舒张末压力降低,Tau增加)(P < 0.05),但在年轻CMH中未出现。年轻CMH的基线CVR显著高于老年CMH(P < 0.01),并且AVP输注在年轻应激CMH中导致的CVR升高幅度大于年轻非应激CMH或老年应激CMH(P < 0.05)。
年轻CMH心脏表现出更高的静息血管张力,应激会导致冠状动脉收缩,这与冠状动脉痉挛一致。相比之下,老年CMH的心脏功能下降,应激7天后仍存在,这表明应激前存在的轻度心力衰竭加重。应激的致死效应可能是由于年轻和老年CMH中不同病理过程的激活所致。