Stimulation of dog urinary bladder muscle to the point of rigor and subjection of dog urinary bladder muscle to ischemia caused an increase in the effluent venous CPK activity. The technique of monitoring CPK activity employed in this study allows the detection of specific visceral muscle cellular compromise without the necessity of biopsy during ongoing physiologic experimentation. Lactate concentration in the venous blood of the vesical vein was unchanged by supramaximal stimulation or ischemia of the urinary bladder and suggests that anaerobic metabolism did not play a prominent role in energy metabolism during these experimental stresses. Bladder muscle glycogen was found to be about one-tenth the concentration found in skeletal muscle and was not depleted during the course of these experiments.
|Original language||English (US)|
|Number of pages||3|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - Feb 1969|