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  • Author or Editor: John H. Lumsden x
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SUMMARY

We tested the hypothesis that lymphocytes from swine with susceptibility to malignant hyperthermia (mh) had calcium extrusion activity higher than unaffected swine. Cytoplasmic concentration of ionized calcium was determined by use of dual emission spectrofluorometry and measurement of the ratio of free to calcium-bound form of the fluorescent calcium dye indo-1. Net calcium accumulation and unidirectional calcium extrusion rate were dependent on intracellular calcium concentration. Calcium extrusion from calcium-loaded lymphocytes was monitored while calcium influx was inhibited by suspending the cells in calcium-free medium with a calcium chelator. Net calcium accumulation of untreated lymphocytes was monitored in calcium-replete medium. A novel method of calculation of ionized calcium was used. This method confirmed our previous findings of lower ionized calcium concentration (86 ± 40 and 370 ± 216 nmol/L; P < 0.01) and slower rates of calcium accumulation 39 ± 16 and 127 ± 52 nmol/L/min) in untreated lymphocytes from mh-susceptible swine compared with controls. These changes were attributable to calcium extrusion activity two- to three-fold higher in lymphocytes of mh-susceptible swine (154 ± 36 and 408 ± 47 nmol/L/min at 175 nmol/L; 972 ± 111 and 1,690 ± 505 nmol/L/min at 425 nmol/L). These data were compatible with our model of higher calcium extrusion activity being a compensatory adaptation of mh-susceptible swine lymphocytes to their hypersensitivity to stimuli that increase cytoplasmic calcium concentration.

Free access
in American Journal of Veterinary Research

SUMMARY

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.

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in American Journal of Veterinary Research