CARDIAC MUSCLE CONTRACTILITY 



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FIG. 7. Stroke volumes as a function of the 

 diastolic volume in the course of the reaction 

 to changes in input pressure. Between the lower 

 pair of vertical arrows (starting at A) the input 

 pressure was raised. The arrowheads on the 

 curves indicate the sequence of changes ; an 

 increase in stroke volume, accompanied by an 

 increase (-'1 to B) and then a decrease (B to C) 

 in end-diastolic volume. Between the upper 

 pair of vertical arrows (starting at C) the input 

 pressure was lowered and the ensuing changes 

 are represented by path CD A. [From Rosen- 

 blueth et al. (248).] 



FIG. 8. Relation between membrane po- 

 tential and concentration of potassium in 

 bathing medium, frog ventricle. [From Liittgau 

 & Niedergerke (200).] 



workers (248), recently reported, calls attention to a 

 serious pitfall which may occur in such an approach. 

 Working with an isolated heart perfused with blood 

 from a donor dog for good maintenance of function 

 [see (248) and also (85) for details of the method], 

 they obtained pressure and volume data for a cycle 

 such as that outlined in figure 6.-1. They then raised 

 input pressure to level w, as shown in figure 65. As 

 expected, the diastolic volume increased, say from 

 OA to OB. Now, if the ventricle volume reaches equi- 

 librium with the output pressure during systole, the 

 stroke volume should be D'C. (In fact, isotonic short- 

 ening may fall short of point C in the first few beats.) 

 The interesting point, illustrated by figure 6C', is that 

 after a short period of time the end diastolic volume 

 decreases, so that it may end up back at the original 

 level OA characteristic of input pressure m. Further- 

 more, this is associated with more complete systolic 

 emptying so that systolic shortening may now proceed 

 further than C to point C . Comparison of figures 6.4 

 and 6C shows that the heart is operating from the same 

 diastolic \olume, but the stroke volume DC is greater 

 than the original stroke volume DC, and stroke work 

 (the area enclosed by the arrows) is likewise greater.' 

 The dynamic pressure-volume curves of the heart in 

 figure 6C are now shifted from UV and RS to U'V 

 and R'S' and the work capacity or contractility is 

 increased. In other words, the mere attempt to meas- 

 ure the pressure-volume curves by stepwise increase 

 in input pressure caused a change in those curves. A 

 discussion of the possible cause and significance of this 

 compensatory change, which allows the heart to work 

 at greater input or output pressures without excessive 



' Fig. 7, taken from the paper of Rosenblucth et al. (248), 

 shows the results of such an experiment in which stroke volume 

 is plotted as a function of diastolic volume. 



increase in volume, is not within the scope of this sec- 



tion. 



n. SODIUM AND POT.\SSIUM 



In\estigations of sodium and potassium in living 

 tissues ha\e occupied a central place in modern cellu- 

 lar physiology. The results ha\e included information 

 about the asymmetry of ion distributions across cell 

 membranes, elucidation of \'arious types of transport 

 of ions in and out of cells, and a basis for understand- 

 ing bioelectric phenomena in terms of the distribution 

 and movement of sodium and potassium. A brief 

 summary of some of the.se points will be presented, 

 since they bear on heart muscle as well as on other 

 tissues. The effects of alterations in the extracellular 

 concentration of sodium and potassium on cardiac 

 contractility will be discussed in more detail, since 

 the response of cardiac tissue is different in some re- 

 spects from that of skeletal muscle. A detailed 

 presentation of the effects of sodium and potassium on 

 bioelectric phenomena in the heart can be found in 

 Chapters 1 1 and 12. Alterations in cellular potassium 

 effected by \arious drugs or by changes in stimulation 

 frequencv are discu.ssed in sections vi, vii, viii, and ix. 



* Rosenblueth et al. believe that the work curves plotted in 

 fig. 6, which are based on instantaneous pressures and volumes 

 measured in a cardiac cycle, do not touch at any point the 

 pressure-volume curves of the resting and isometrically con- 

 tracted ventricle, but always remain inside the area bounded by 

 these curves. For this reason we are inclined to use the term 

 dynamic pressure-volume curve to refer to the values obtained 

 during the cardiac cycle. This leaves open the question as to 

 what extent the shift in the dynamic pressure-volume curve 

 represents a shift in the "equilibrium" pressure-volume curve 

 and to what extent it might represent a closer approach of the 

 dynamic pressure-volume curve to the equilibrium value. 



