CARDIAC EXCITABILITY— BROOKS 289 



neurochemical reactions. Section of the cardiac nerves and denervation of the 

 adrenals greatly lessens this response. As the heart itself is cooled the rate falls. 

 Within certain critical ranges a direct relationship is found between rate and heart 

 temperature but outside these limits expression of relationships are curvilinear 

 (Knowlton and Starling, 1912; Badeer, 1951; Hegnauer, 1952; Kao et ai, 1955). 

 Asystole may occur when the heart is cooled to 20° C. in some instances but 

 usually the rate falls to about 20 per minute at 15°-17° C. and the heart stops 

 beating regularly below 13° C, although a few sporadic beats may occur down to 

 8° C. Spontaneous arrhythmias are a common consequence of cooling (Brooks 

 et al., 1955) and fibrillation may occur before asystole. 



Changes in cardiac output tend to parallel those in rate. Following a brief initial 

 augmentation, probably due to shivering and autonomic compensatory activity, 

 there is a progressive drop in output with cooling. In large dogs the output remains 

 at approximately 1.5 to 1.23 liters per minute between heart temperatures of 38° to 

 28° C. but below that level it falls sharply and at 23.5° C. is only 0.65 liters per 

 minute (Kao et al., 1955). At these low temperatures, however, the heart pumps 

 more blood in relation to O2 consumption of the body. It can be concluded there- 

 fore, that unless the oxygen requirements of brain or other special tissues remain 

 higher and do not change proportionately with those of the rest of the body, the 

 drops in heart rate and output do not cause a serious hypoxia until arrhythmias or 

 irregularities of beat occur at very low heart temperatures (Brooks et al, 1955). 

 The effect of cooling on pacemaker action. In early studies of the locus of 

 the pacemaker (Eyster and Meek, 1921) it was found that cooling the SA node so 

 depressed its activity that pacemaker action was assumed by the uncooled regions 

 of the heart. Furthermore it was shown that localized heating of regions other 

 than the sinus tended to establish an ectopic pacemaker (Eyster and Meek, 1921 ; 

 Scott and Reed, 1951). Thus temperature changes definitely can influence origin 

 of the excitatory process. 



Recent studies indicate that the pacemaker is that region of the heart which 

 possesses the most unstable membrane. As soon as pacemaker cells repolarize a 

 gradual spontaneous depolarization begins as indicated by the presence of a pre- 

 potential (Erlanger, 1913; Rijlant, 1928; Draper and Weidmann, 1951). Little is 

 known about the nature of the processes involved ; slow depolarization might be 

 due to positive actions tending to depolarize or to a deficiency of stabilizing or 

 polarizing forces (Brooks et al., 1955). One thing is certain and that is that in 

 non-pacemaker tissues normal excitability is recovered long before initiation of a 

 beat begins and in non-pacemaker tissues no potential change similar to that 

 occurring in pacemakers is seen preliminary to the propagated action potential. 



One of the best methods of studying events in the pacemaker which produce a 

 propagated response is that of intracellular recording (Draper and Weidmann, 

 1951 ; Brady and Hecht, 1954; Hutter and Trautwein, 1955). The Oio of the slow 

 diastolic depolarization of the pacemaker which originates a beat is 5. The Qio of 

 other phases of the action potential have been found to be much lower (Trautwein, 

 1953; Coraboeuf and Weidmann, 1954). In the subsequent paper on cellular po- 

 tentials the effects of cold will be more adequately discussed. 



Hypothermia and the propagation of excitation. Conduction of an impulse 



