Influence of endotoxin on myocardial calcium transport and the effect of augmented venous return.
The influence of endotoxin shock and of experimentally increased venous return during endotoxin shock on myocardial vesicular calcium uptake and calcium stimulated ATPase activity was investigated. Vesicular calcium uptake was depressed (p less than 0.01) from 0.9 mumoles/mg protein/min to 0.3 mumoles/mg/min after 5 hr of endotoxin shock. Control ATPase did not differ between endocardial surface and epicardial surface. This was accompanied by a depressed (p less than 0.01) ATPase activity from 1.2 mumoles Pi/mg/min at the endocardial surface, and to 0.9 mumoles Pi/mg/min at the epicardial surface. A femoral arteriovenous shunt was used to increase venous return by 313 +/- 71 ml/min (approximately 17 ml/kg) during the shock period. Vesicles from AV shunted animals after endotoxin were capable of normal calcium uptake and normal ATPase activity. Results suggest that myocardial depression during endotoxin shock is more severe on the endocardial surface and is caused by depressed vesicular calcium uptake secondary to depressed ATPase activity. Furthermore, this depression may be avoided by maintenance of an adequate venous return.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001166:Arteriovenous Shunt, Surgical; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism*; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D009201:Myocardial Depressant Factor / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D012772:Shock, Septic / Q000503:physiopathology*; D014680:Veins / Q000503:physiopathology
D009201:Myocardial Depressant Factor; D000251:Adenosine Triphosphatases; D002118:Calcium