EFFECTS OF NERVE STIMULATION AND HORMONES ON THE HEART 



549 



"myocardial contractility" will be an important 

 contribution of the future and will involve analysis 

 at the cellular and molecular levels. The mechanisms 

 by which autonomic transmitter substances can 

 promote these changes in myocardial function will also 

 require extensive investigation. Since the normal 

 cardiovascular adjustments involve changes in heart 

 rate even more prominently than changes in stroke 

 volume, the mechanisms by which the pacemaker 

 activity is accelerated deserve e.xtensi\e investigation. 

 The autonomic nerve impulses which ultimately reach 

 the heart to influence heart rate and "contractility" 

 must be traced to their origins in the central nervous 

 system. The factors which induce changes in myo- 

 cardial fiber length (ventricular distention) must also 

 be more explicitly determined. 



The integrative functions of the nervous system in 

 normal animals tend to overshadow the peripheral or 

 secondary mechanisms which are revealed in the 

 standard physiological preparations — anesthetized, 

 thoracotomized animals. The extensive investigation 

 of such preparations over the past 50 years has 

 provided a clear understanding of the peripheral 

 mechanisms of cardiac control. Such studies are no 

 more efficient in elucidating the central integrative 



mechanisms than isolated nerve-muscle preparations 

 are suitable for an analysis of the central control of 

 fine movements of the extremities. Full blown patterns 

 of cardiac, peripheral \'ascular, and respiratory 

 responses, like those encountered during .spontaneous 

 exercise, can be elicited by electrical stimulation of 

 discrete areas in the diencephalon. This particular 

 region in the diencephalon serves as a pathway for 

 nerve fibers from many different regions in the brain. 

 Thus, the central nervous system contains anatomical 

 provisions for the development of integrated re- 

 sponses involving combinations of autonomic and 

 somatic discharges. 



Eliciting these responses by electrical stimulation 

 does not give positive assurance that these regions are 

 involved in normal cardiac control, but does indicate 

 that this is a possibility. A great deal of additional 

 investigation will be required to determine the origins 

 of the impuLses and to learn the neural pathways by 

 which they reach the effector organs of the cardio- 

 vascular system. It is equally important to determine 

 if the observations on dogs are sufficiently applicable 

 to human responses to warrant extrapolation of these 

 data from one species to the other. 



REFERENCES 



1. Anzol.a, J., .AND R. F. RusHMER. Cardiac responses to 

 sympathetic stimulation. Circulation Res. 4: 302, 1956. 



2. Baker, D. W., R. M. Ellis, D. L. Fr.anklin, and R. F. 

 RusHMER. Some engineering aspects of modern cardiac 

 research. Proc. Inst. Radio Engrs. 47: 191 7, 1959. 



3. Berglund, E. Ventricular function VI. Balance of left and 

 right ventricular output: relation between left and right 

 atrial pressures. .4m. J. Physiol. 178: 381, 1954. 



4. Bishop, J. M., K. W. Donald, and O. L. Wade. Circula- 

 tory dynamics at rest and on exercise in the hyperkinetic 

 states. Clin. Sc. 14: 329, 1955. 



5. Brecher, G. a. Venous Return. New York : Grune & 

 Stratton, 1956. 



6. Gotten, M. DeV. Circulatory changes affecting measure- 

 ment of heart force in situ with strain gauge arches. Am. J. 

 Physiol. 174: 365, 1953. 



7. Dorland, W. a. N. American Illustrated .Medical Dictionary, 

 i6th ed. Philadelphia: W. B. Saunders, 1934. 



8. DuoMARco, J. L., R. Rimini, and J. P. S.wkiz.k. Intento de 

 apreciacion de la presion venosa efectiva por medio de la 

 angiocardiografia. Rev. Argent. Cardiol. 17: 15, 1 950. 



9. Fisher, J. N., C. B. Chapman, and B. J. Sproule. Effect 

 of exercise on stroke volume in human subjects. Clin. Res. 

 8: 73. i960. 



10. Folkow, B. Ner\ous control of the blood vessels. Physiol. 

 Rev. 35 : 629, 1 955. 



1 1 . Fr.\nk, O. On the dynamics of cardiac muscle. Translated 

 by C. B. Chapman and Eugene Wasserman. Am. Heart J. 

 58: 282; 467, 1959. 



12. Franklin, D. L., D. \V. B.aker, R. M. Ellis, .and R. F. 

 Rushmer. a pulsed ultrasonic flowmeter. IRE Trans, on 

 Med. Electronics. ME 6: 204, 1959. 



13. Fr.anklin, D. L., R. M. Ellis, and R. F. Rushmer. Aortic 

 blood flow in dogs during treadmill exercise. J. Appl. 

 Physiol. 14; 809, 1959. 



1 4 G.AUER, O. H. Volume changes of the left ventricle during 

 blood pooling and exercise in the intact animal. Their 

 effects on left \ entricular performance. Physiol. Rev. 35 : 



143. '955- 



15. Green, H. D. Analysis of cardiovascular activity. .Methods 

 in Med. Research I : 241, 1948. 



16. GrrNTHEROTH, W. G. Fimction of liver and spleen as 

 venous reservoirs. Fed. Proc. 17: 63, 1958. 



17. Hawthorne, E. W., M. Caspar, and W. G. Pogue. 

 Instantaneous dimensional changes of the left ventricle in 

 awake dogs. Fed Proc. ig: 106, i960. 



18. Holmgren, .\. Circulatory changes during muscular 

 work in man ; with special reference to arterial and central 

 venous pressures in the systemic circulation. Scandinav. J. 

 Clin. & Lab. Invest. 8 (Suppl. 24); i, 1956. 



19. Howell, W. H., and F. Donaldson, Jr. Experiments upon 

 the heart of the dog with reference to the maximum volume 

 of blood sent out by the left \entricle in a single beat, and 

 the influence of variations in venous pressure, arterial 

 pressure, and pulse rate upon work done by the heart. 

 Phil. Trans. Roy. Soc. London (Pt. l) 175: 139, 1884. 



20. Howell, \V. H. An American Textbook of Physiology. Phila- 

 delphia : Saunders, 1896. 



