312 



PHYSIOLOGY OF INDUCED HYPOTHERMIA 



and show a decreased rate of rise, diminished reversal, and lowered conduction 

 velocity. In addition, the duration of the premature action potential is decreased 

 and the plateau is less prominent. 



No irregularity in the repolarization limb of the action potential is recorded 

 which might be associated with the dips found in the curve depicting the recovery 

 of excitability of the intact ventricle and auricle. On the other hand, studies of 

 single isolated Purkinje fibers have revealed a definite period of supernormality 

 just prior to the end of repolarization.^^ 



When the membrane potential is only slightly higher than the critical threshold 

 value, the stimulus current required to elicit a response is minimal (fig. 8). Subse- 

 quently, as repolarization progresses, the current required to produce a threshold 

 depolarization is increased. This phenomenon is easily explained in terms of the 

 relationship between critical threshold potential and resting potential (fig. 4) 

 described above, and suggests that in this particular tissue recovery of excitability 

 actually precedes recovery of normal polarization. The converse situation — com- 



+ 30- 



-60 



-90- 



Fig. 8. — Tracing of transmembrane potentials of an isolated Purkinje fiber showing the 

 occurrence of supernormality. Compare with figures 3 and 4. At A, a small depolarization re- 

 sulting from stimulus (arrow) lowers the membrane potential to the critical threshold level 

 and an action potential (a) ensues. After the end of repolarization (B) or during slow 

 diastolic depolarization (C) stimuli stronger than A are re(|uircd to depolarize tlie membrane 

 to the critical threshold level at wliich firing of actinn potentials b and c occurs. 



