Effect of shock on calcium accumulation by cardiac sarcoplasmic reticulum.
Earlier work has suggested that the decreased cardiac performance in shock is due to negative inotropic substances that alter the Ca++ metabolism of the myocardium. We investigated this possibility by examining the Ca++-dependent ATPase activity and the Ca++-uptake ability of cardiac sarcoplasmic reticulum (microsomes) from normal hearts and endotoxin-shocked hearts. Both the ATPase activity and the accumulation of Ca++ by microsomes from shocked hearts were lower than for microsomes from normal hearts. In the presence of serum from shocked dogs, the ATPase activities and Ca++-uptake of both microsome preparations were reduced from those measured in modified Krebs-Henseleit, but this was not considered significant because the same extent of depression was seen with serum from normal dogs. These findings could not attribute the depressed ATPase activities and Ca++-uptake abilities to a shock-induced circulating cardio-depressant material but did demonstrate that calcium metabolism in cardiac tissue was altered in the shock state.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004285:Dogs; D066298:In Vitro Techniques; D007930:Leucine / Q000494:pharmacology; D008861:Microsomes / Q000201:enzymology / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D010070:Oxalates / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D012769:Shock / Q000201:enzymology / Q000378:metabolism*
D010070:Oxalates; D000251:Adenosine Triphosphatases; D007930:Leucine; D002118:Calcium