DECREASED [H-3] OUABAIN BINDING-SITES IN SKELETAL-MUSCLE OF RATS WITHCHRONIC HEART-FAILURE

Abnormalities intrinsic to skeletal muscle are thought to contribute t o decrements in exercise capacity found in individuals with chronic he art failure (CHF). Na+-K+-adenosinetriphosphatase (the Na+ pump) is es sential for maintaining muscle excitability and contractility. Therefo re, we investigated the possibility that the number and affinity of Na + pumps in locomotor muscles of rats with CHF are decreased. Myocardia l infarction (MI) was induced in 8 rats, and a sham operation was perf ormed in 12 rats. The degree of CHF was assessed similar to 180 days a fter surgery. Soleus and plantaris muscles were harvested, and Na+ pum ps were quantified by using a [H-3]ouabain binding assay. At the time of muscle harvest, MI and sham-operated rats were similar in age (458 +/- 54 vs. 447 +/- 34 days old, respectively). Compared with their sha m-operated counterparts, MI rats had a significant amount of heart fai lure, right ventricular-to-body weight ratio was greater (48%), and th e presence of pulmonary congestion was suggested by an elevated lung-t o-body weight ratio (29%). Left ventricular end-diastolic pressure was significantly increased in the MI rats (11 +/- 1 mmHg) compared with the sham-operated controls (1 +/- 1 mmHg). In addition, mean arterial blood pressure was lower in the MI rats compared with their control co unterparts. [H-3]ouabain binding sites were reduced 18% in soleus musc le (136 +/- 12 vs. 175 +/- 13 pmol/g wet wt, MI vs. sham, respectively ) and 22% in plantaris muscle (119 +/- 12 vs. 147 +/- 8 pmol/g wet wt, MI vs. sham, respectively). The affinity of these [H-3]ouabain bindin g sites was similar for the two groups. The relationship between the r eduction in Na+ pump number and the reduced exercise capacity in indiv iduals with CHF remains to be determined.