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Stress triggers different pathophysiological mechanisms in younger and older cardiomyopathic hamsters
Q Chang1, B H Natelson, J E Ottenweller
1Neurobehavioral Unit (127A), VA Medical Center, East Orange, NJ 07018-1095, USA.
Insights
Stress affects cardiomyopathic hamsters (CMHs) differently based on age. Younger CMHs experience coronary vasospasm, while older CMHs develop worsening congestive heart failure (CHF).
Area of Science:
- Cardiology
- Pathophysiology
- Animal Models
Background:
- Cardiomyopathic hamsters (CMHs) exhibit increased susceptibility to stress during the lesion-forming stage of their disease.
- Previous studies suggest age-dependent responses to stress in CMHs.
Purpose of the Study:
- To test the hypothesis that stress induces distinct pathophysiological effects in younger versus older CMHs.
- To investigate whether stress causes coronary vasospasm in younger CMHs and congestive heart failure (CHF) exacerbation in older CMHs.
Main Methods:
- CMHs aged 2.5 and 6.5 months underwent a 5-day stress protocol (cold immobilization).
- Cardiac function (dP/dt, developed pressure, Tau) and coronary vascular resistance (CVR) were assessed post-stress using Langendorff perfusion.
- CVR was also measured after arginine vasopressin (AVP) infusion.
Main Results:
- Stress induced ventricular dysfunction in older CMHs but not in younger CMHs.
- Younger CMHs had higher baseline CVR, and stress led to a greater AVP-induced CVR increase compared to controls.
- These findings suggest stress-induced coronary vasoconstriction in younger CMHs and exacerbated CHF in older CMHs.
Conclusions:
- Younger CMH hearts show increased vascular tone, with stress triggering coronary vasoconstriction consistent with vasospasm.
- Older CMHs exhibit persistent cardiac dysfunction post-stress, indicating worsened CHF.
- Differential stress-induced pathological pathways may explain the lethal effects of stress in CMHs of varying ages.
Objectives:
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.
Methods:
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).
Results:
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).
Conclusion:
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.