Clinical pathologic profiles of dogs and turkeys with congestive heart failure, either noninduced or induced by rapid ventricular pacing, and turkeys with furazolidone toxicosis.
Characteristic alterations in the serum and urine biochemical profiles of Doberman Pinschers with congestive heart failure (CHF) resulting from idiopathic dilated cardiomyopathy were determined. We compared these alterations with those observed in 2 other models of CHF: rate overload induced by rapid ventricular pacing in dogs, and biventricular hypertrophy and dilatation induced in turkey poults by furazolidone toxicosis. Serum and urine biochemical changes in both models of CHF in dogs were mild to moderate in degree, and were moderately consistent. They could be attributed to secondary neurohumoral, hepatic, and renal effects of heart failure. The most marked and consistent changes observed were mildly decreased anion gap that developed, in part, because of decreased serum sodium concentration, moderately increased catecholamine concentrations, moderate lactaciduria, hyposthenuria, and mildly increased urea concentrations and liver enzyme activities. In birds with furazolidone cardiomyopathy, we observed mild increases in serum urate concentration, liver and muscle enzyme activities, but moderately increased sodium concentration with decreased chloride concentration. In the pacing and furazolidone models, in which CHF was rapidly induced, moderate to marked hypoproteinemia was attributable to decreases in albumin and globulin concentrations. Using the avian model we found that the hypoproteinemia could be largely attributed to blood volume expansion, and to a lesser extent, inanition. Development of hypoalbuminemia during rapid ventricular pacing and furazolidone treatment may contribute to the effects of rate overload or drug toxicity in the pathogenesis of CHF, because hypoalbuminemia may contribute to altered hemodynamics and neuroendocrine system activation. Our data indicate that clinical biochemical analysis of serum and urine may be useful for assessing progression of CHF.
O'Brien
P J
PJ
Department of Pathology, Ontario Veterinary College, University of Guelph, Canada.
O'Grady
M
M
Lumsden
J H
JH
Holmberg
D L
DL
Shen
H
H
Weiler
J E
JE
Horn
R D
RD
Mirsalimi
S M
SM
Julian
R J
RJ
D000818:Animals; D002304:Cardiac Pacing, Artificial / Q000662:veterinary; D004283:Dog Diseases / Q000097:blood / Q000378:metabolism* / Q000652:urine; D004285:Dogs; D005260:Female; D005664:Furazolidone / Q000633:toxicity*; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000662:veterinary*; D008297:Male; D011201:Poultry Diseases / Q000139:chemically induced / Q000378:metabolism*; D014422:Turkeys / Q000378:metabolism*
D005664:Furazolidone