The etiology of left ventricular dysfunction can effect the catecholamine response to heart failure Catecholamines in Heart Failure

Activation of the sympathetic nervous system in congestive heart failure (CHF) is manifest in part by depletion of myocardial norepinephrine (NE). We tested the hypothesis that this neuroadrenergic response to CHF occurs independent of the etiology of LV dysfunction by studying several models of CHF occurring in the same species. CHF was induced in Nicholas strain turkeys by providing furazolidone (FZD) in a dose of 0.5mg per kg of feed. Myocardial and kidney norepinephrine were assayed, and compared to normal turkeys (NL), turkeys with CHF induced by 5% alcohol in drinking water (ETOH), and turkeys with inbred dilated cardiomyopathy (DCM). Cardiac NE in 16 NL turkeys at age 1 month was 388 ± 184 ng/gm (mean ± S.E.M.). In 16 FZD turkeys, cardiac NE was much more variable (678 ± 161 ng/gm), but not statistically different from NL. In contrast, cardiac NE was 236 ± 82 ng/gm in 16 ETOH (p<0.01 vs NL) birds, and 834 ± 299 (p<0.001 vs NL) in 16 DCM birds. Thus cardiac NE was depleted in ETOH turkeys, quite variable (but no different from control) in FZD, and higher than normal in DCM. Kidney NE at 1 month was unchanged in all 3 groups Results at age 2 months were similar, but differences in myocardial NE between groups smaller. In all 3 CHF groups heart weight to body weight ratio was higher, echocardiographic diastolic diameter larger, and mean arterial pressure lower than normals. When all groups were combined, cardiac NE did not correlate with indices of CHF. Thus the etiology of LV dysfunction can alter the neuroadrenergic response to CHF.