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Influence of endotoxin on myocardial calcium transport and the effect of augmented venous return
Insights
Endotoxin shock severely impairs myocardial calcium uptake and ATPase activity, particularly on the endocardial surface. Maintaining adequate venous return can prevent this cardiac depression during endotoxin shock.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Shock Pathophysiology
Background:
- Endotoxin shock leads to myocardial depression, affecting cardiac function.
- The role of vesicular calcium handling in this process requires further elucidation.
Purpose of the Study:
- To investigate the impact of endotoxin shock on myocardial vesicular calcium uptake and ATPase activity.
- To determine if increased venous return can mitigate these effects.
Main Methods:
- Induction of endotoxin shock in animal models.
- Measurement of myocardial vesicular calcium uptake and calcium-stimulated ATPase activity.
- Experimental increase of venous return using an arteriovenous shunt.
Main Results:
- Endotoxin shock significantly depressed myocardial vesicular calcium uptake and ATPase activity (p < 0.01).
- Myocardial depression was more pronounced on the endocardial surface.
- Increased venous return via an arteriovenous shunt normalized calcium uptake and ATPase activity.
Conclusions:
- Myocardial depression in endotoxin shock is linked to reduced vesicular calcium uptake, secondary to decreased ATPase activity.
- Adequate venous return is crucial for maintaining myocardial function during endotoxin shock.
- Therapeutic strategies aimed at improving venous return may be beneficial in managing endotoxin shock.
Abstract:
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.