5o8 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



in addition to extensibility. The term extensibility 

 refers to the change in length of a segment of myo- 

 cardium when subjected to stress (uniform distend- 

 ing pressure). It is concerned with a static property 

 of the tissue under examination and does not vary 

 with the rate of application of stress (i i8). If diastole 

 is abbreviated, the relation between pressure and 

 segment length may also be determined by whether 

 full relaxation has taken place and the extent to 

 which inertial and viscous factors have been dissi- 

 pated. Thus, when diastole is curtailed, the myocar- 

 dial segment length may be shorter for any given 

 ventricular end diastolic pressure even though no 

 change in the extensibility of relaxed ventricular 

 myocardium has taken place. 



It was consistently observed that, at any given 

 heart rate, stellate stimulation provided for the earlier 

 onset of ventricular relaxation as the result of a 

 shortened systole. Such sympathetic activity thus 

 allowed a longer interval for ventricular relaxation 

 to become complete before the onset of the ensuing 

 systole. Figure 15 (right) shows data from an experi- 

 ment which emphasizes the importance of this phe- 

 nomena. In panel A the relation between left ventricu- 

 lar end diastolic pressure and changes in myocardial 

 segment length was not altered by stellate gang- 

 lion stimulation. In the absence of stellate stimula- 

 tion (panel B), 50 msec prior to systole the myo- 

 cardial segment was substantially shorter at any 

 given pressure and this effect was even more marked 

 at 70 msec prior to the onset of systole. During 

 stellate stimulation (panel C), 50 msec prior to the 

 onset of systole, there was no change in the pressure- 

 length relation and at 70 msec prior to systole the 

 myocardial segment was only slightly diminished in 

 length at any given pressure. It can be assumed that, 

 in this experiment, had the heart rate or stroke vol- 

 ume been increased or the heart further depressed 

 (14) to a point where diastole was shortened, by as 

 little as 50 msec, the relation between pressure and 

 segment length at the end of diastole would have 

 shifted to the left (as shown in panel B). Subsequent 

 stellate stimulation would have appeared to produce 

 an increased ventricular diastolic extensibility where- 

 as, in fact, by shortening systole, it would simply 

 have permitted time for inertial and viscous factors 

 to be dissipated and for relaxation to be complete. 

 That this is an important operative consideration is 

 indicated by the tracing in figure 16. In this study 

 both stellate ganglia were isolated, and the atrium 

 was paced at 210 per min throughout. In the left 

 panel, with the heart deprived of s\mpalhetic effer- 



IM 



■.'.5 



~i 



m 



FIG. 1 6 



ents from both stellate ganglia, the mean aortic 

 pressure was 138 mm Hg, stroke volume 9.2 ml, and 

 left ventricular stroke work 17.3 g-m. Diastole was 

 limited to 69 msec out of a total cycle time of 296 

 msec. In the right panel during left stellate ganglion 

 stimulation the mean aortic pressure was 155 mm 

 Hg, stroke volume 12.4 ml, and left ventricular stroke 

 work 26.1 g-m. Thus, left stellate ganglion stimulation 

 not only increased the force of contraction from a 

 lower end diastolic pressure but doubled diastolic 

 time, thereby increasing the time available for a 

 more complete ventricular relaxation. This problem 

 has been well formulated by Buckley el nl. (18-20), 

 who described the observed phenomena in terms of 

 mechanical impedance (ratio of ventricular pressure 

 to \entricular inflow). In the isolated mammalian 

 ventricle, norepinephrine was found to decrease 

 mid-filling impedance and to provide a lengthened 

 time available for filling when impedance was at 

 its lowest. The data shown in figures 15 and 16, 

 wherein the observed changes were induced by 

 stellate stimulation, arc compatible with the findings 

 of Buckley and indicate that sympathetic pathways 

 are capable of producing the same type of change in 

 the in situ heart. 



These findings are also consonant with the studies 

 of Lundin (62) on isolated frog muscle bundles, with 

 those of Ullrich (119), who used the isometrically 

 contracting canine left ventricle, and with the more 

 recent studies of Rosenbleuth el al. (81) on the canine 

 right ventricle. They are also in agreement with the 

 observations of Blinks (loa), who found no change in 

 the pressure-volume relation of isolated mammalian 

 atria when exposed to concentrations of epinephrine 

 which produced a marked positive inotropic effect. 

 The results shown above appear to be at variance 

 with the experiments of Rushmer el al. (84, 87), who 

 found an increased "distensibility" during epi- 



