Why the study?
Does physical and environmental stress alter heart rate and catecholamine levels in dogs with heart failure compared to healthy controls?
Does physical and environmental stress alter heart rate and catecholamine levels in dogs with heart failure compared to healthy controls?
Dogs with heart failure exhibit chronically activated sympathetic nervous system activity even in mild stages, which blunts further catecholamine responses to light stress.
Indicates chronic sympathetic activation in mild experimental mitral regurgitation; leaves open translation to clinical veterinary or human heart failure management.
To clarify heart rate modulation by the sympathetic nervous system, dogs with naturally acquired and experimentally induced heart failure were examined. Heart rate and plasma catecholamine concentrations were measured in clinically healthy dogs (control dogs) and dogs with mitral regurgitation (MR) during a resting period, a standing period, a period of standing in a medical examination room (to which the dogs were unaccustomed), a running period, and a period of recovery after running. The heart rate and plasma catecholamine concentration increased in control dogs during the standing period and the medical examination room period, relative to the resting period. However, dogs with MR did not exhibit any clear increase in heart rate or catecholamine concentration under these light stress conditions. Running stress increased plasma catecholamine levels in control dogs; however, dogs with MR did not exhibit any significant changes. Thirty-two dogs with naturally acquired heart disease were classified as grades I to III on the ISACHC scale. The degree of increase in heart rate and plasma catecholamine levels in dogs with naturally acquired heart failure depended on their degree of heart failure. In conclusion, an increased heart rate and an activated sympathetic nervous system were observed, even in mild heart failure. This chronically activated sympathetic activity is expected to increase myocardial oxygen consumption, myocardial hypertrophy, and fibrosis, and to portend a poorer prognosis in heart failure.
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Uechi et al. (2002) studied this question.
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