THE CONTROL OF THE FUNCTION OF THE HEART 



501 



reveals certain similarities. Both the increased aortic 

 resistance and the norepinephrine made the rise and 

 decline of ventricular pressure steeper, shortened the 

 total period of systole (from beginning of rise of ven- 

 tricular pressure to the incisura) and shortened the 

 period required for the systolic ejection of comparable 

 v^olumes. It is further found that when a ventricle is 

 able to meet an increased aortic resistance without 

 increasing L\'ED pressure (fig. 8B, left), the sub- 

 sequent administration of norepinephrine may enable 

 it to meet the same or e\en a greater resistance in- 

 crease from a lower L\'ED pressure. Such an in- 

 stance is shown in figure 85 (right). Figure 8C shows 

 a similar phenomenon and also shows particularly 

 clearly the accentuation of the ventricular pressure 

 dip in early diastole that was frequently encountered 

 when an increased aortic resistance was imposed. 



Slow speed tracings of the type shown in figure 9 

 are also informative. It shows the same imposed aor- 

 tic resistance increase with and without norepineph- 

 rine infusion in the same experiment. Without the 

 norepinephrine infusion (right panel), the pattern 

 was as previously described. During the norepineph- 

 rine (left panel), the L\'ED pressure transients were 

 less well defined. In experiments of this type it was 

 found that by increasing or decreasing the norepi- 

 nephrine infusion rate, the left \-entricle could be 

 made to vary the rapidity with which it passed 

 through phase 2 and arrived at the new equilibrium 

 level in phase 3. 



These findings on the effect of norepinephrine 

 confirm those of Anrep (3 ) but are not in agreement 

 with those of Rosenblueth et al. (82) in that the level 

 of catecholamine present appeared to be of impor- 

 tance to the exhibition of homeometric autoregula- 

 tion by the ventricle. First, in some instances a heart 

 which was in relatively poor condition, as indicated 

 by its LVED pressure, would show little or sometimes 

 no apparent homeometric autoregulation; when 

 norepinephrine was infused a response could then be 

 obtained. .Second, the higher the level of circulating 

 norepinephrine, the greater was the increased re- 

 sistance against which the \entricle could eject a 

 comparable stroke volume without an elevated end 

 diastolic pressure (fig. 8). Third, norepinephrine in- 

 fluenced the myocardium in a manner such that it 

 would respond to a sudden increase in pressure not 

 only more adequately but also more rapidly (fig. 9). 

 Such findings are not only consonant with the ob- 

 servation that norepinephrine shifts the ventricular 

 function curve to the left and makes it steeper (fig. 2), 

 but also invites consideration of the possibility that 



250 



increased \-entricular activity either increases the 

 locally available myocardial norepinephrine or facili- 

 tates its utilization during homeometric autoregula- 

 tion. 



Significance of homeometric autoregidalion, \\'hate\-er 

 the mechanism or mechanisms by which homeo- 

 metric autoregulation is accomplished, the resulting 

 increase in contractility has two important conse- 

 quences. The first is that it permits the ventricle 

 beating at any given rate to eject the same stroke 

 volume against a wide range of resistances without 

 requiring an increa.sed LVED pressure or fiber length. 

 Thus, over certain ranges, it acts in such a manner as 

 to conserve heterometric autoregulation for changes 

 in stroke volume (fig. 4). Second, the increase in con- 

 tracility, especially that aspect of it which is exhibited 

 as a more rapidly developed ventricular pressure, 

 diminishes the proportion of the total cardiac cycle 

 that systole would otherwise require. This is a par- 

 ticular advantage when heart rate is increased since, 

 if such a phenomenon did not occur, the diastolic 

 interval would be so constrained that ventricular 

 relaxation would be incomplete before the next 

 .systole (67), ventricular filling impaired, and coro- 

 nary flow limited. In this connection, it was of par- 

 ticular interest to note the frequency with which the 

 heart, when its rate was suddenly increased, ex- 

 hibited pulsus alternans in the first few beats but be- 

 came regular again as the increase in contractility 

 became manifest (fig. 6). 



INFLUENCE OF OXYGEN .W.-ML-ABILITY ON VENTRICULAR 



PERFORM.ANCE. The vcntriclc will produce less ex- 

 ternal stroke work from any given filling pressure 

 when the blood flow to the myocardium is unduly 

 restricted (shift of \TCla to the right). Under these 

 circumstances, when mean atrial pressure rises. 



