title: Decreased [3H]ouabain binding sites in skeletal muscle of rats with chronic heart failure.
abstract: Abnormalities intrinsic to skeletal muscle are thought to contribute to decrements in exercise capacity found in individuals with chronic heart failure (CHF). Na+-K+-adenosinetriphosphatase (the Na+ pump) is essential for maintaining muscle excitability and contractility. Therefore, we investigated the possibility that the number and affinity of Na+ pumps in locomotor muscles of rats with CHF are decreased. Myocardial infarction (MI) was induced in 8 rats, and a sham operation was performed in 12 rats. The degree of CHF was assessed approximately 180 days after surgery. Soleus and plantaris muscles were harvested, and Na+ pumps were quantified by using a [3H]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 sham-operated counterparts, MI rats had a significant amount of heart failure, right ventricular-to-body weight ratio was greater (48%), and the presence of pulmonary congestion was suggested by an elevated lung-to-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 counterparts. [3H]ouabain binding sites were reduced 18% in soleus muscle (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 [3H]ouabain binding sites was similar for the two groups. The relationship between the reduction in Na+ pump number and the reduced exercise capacity in individuals with CHF remains to be determined.
authors.affiliation: Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506, USA.
authors.forename: J G
authors.initials: JG
authors.lastname: Pickar
authors.forename: J P
authors.initials: JP
authors.lastname: Mattson
authors.forename: S
authors.initials: S
authors.lastname: Lloyd
authors.forename: T I
authors.initials: TI
authors.lastname: Musch
mesh_terms: D000818:Animals; D001665:Binding Sites; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000378:metabolism*; D008124:Locomotion / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000737:chemistry / Q000378:metabolism*; D009203:Myocardial Infarction / Q000503:physiopathology; D010042:Ouabain / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015222:Sodium Channels / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D015222:Sodium Channels; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase