220 



1. lODOACETATE AND lODOACETAMIDE 



of the membrane changes, and this may be a result of the intracelhilar de- 

 pletion of high-energy phosphate. It is interesting that an initial stimulation 

 of contractility is usually seen (with iodoacetamide it is more pronounced), 

 and this is accompanied by a slowing of repolarization and a lengthening 

 of the duration of the action potential. Changes in the other parameters 

 are in general those expected on the basis of the above effects on the ac- 

 tion potential. 



The changes observed in amphibian ventricle are quite similar, in that 

 there are relatively minor depressions of the resting and action potential 

 magnitudes, while the repolarization rate is markedly accelerated (Kleinfeld 

 et al, 1955; Kossmann, 1957; Carmeliet and Petit, 1957; Boulpaep, 1959). 



Fig. 1-23. Effects of 0.05 n\M iodoacetate on the various 

 characteristics of frog ventricle. AP-RT = action potential 

 rise time (duration of depolarization), RP = resting po- 

 tential; AP = action potential magnitude; AP-D = action 

 potential duration; and SV = stroke volume. (From Klein- 

 feld et al, 1955.) 



The data of Kleinfeld et al. have been plotted in Fig. 1-23 so that the se- 

 quence of changes can be visualized. The authors postulated that early 

 effects of iodoacetate may be due to a direct effect on the membrane, per- 

 haps unassociated with metabolism, but quite possibly there are metabolic 

 systems within the membrane. One can conclude that the cellular membrane 

 changes brought about by iodoacetate are very similar in atria and ventri- 

 cles and that these can to a great extent explain the functional responses 



