Myocardial sodium pump activity in endotoxin shock.
The effect of endotoxin administration on the integrity of sodium pump was studied in canine heart myocardium. Sodium pump activity was determined based on the 86Rb+ uptake by ventricular muscle strips. The results show that 4 hr following endotoxin administration the ouabain-sensitive 86Rb+ uptake was inhibited by 44-70%, and the inhibition was noncompetitive with 86Rb+ ions and was independent of Na+ concentrations. The sensitivity of sodium pump toward verapamil inhibition was unaffected by endotoxin administration, suggesting that the endotoxin-induced decrease in sodium pump activity is not mediated through alteration in either calcium or slow sodium channel. The sensitivity of 86Rb+ uptake to ouabain inhibition was decreased approximately sixfold in endotoxin-injected dogs. These data suggest that sodium pump is greatly impaired in dog hearts 4 hr after endotoxin administration. The impairment in sodium pump might have physiological significance in the development of myocardial dysfunction during endotoxic shock.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004285:Dogs; D005260:Female; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D010766:Phosphorylation; D012413:Rubidium / Q000378:metabolism; D012772:Shock, Septic / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014700:Verapamil / Q000494:pharmacology
D010042:Ouabain; D012964:Sodium; D014700:Verapamil; D000254:Sodium-Potassium-Exchanging ATPase; D012413:Rubidium; D002118:Calcium