Summary
The effects of acute systemic anoxia on heart rate were investigated in 46 anaesthetized, artificially ventilated and spontaneously breathing dogs. Severe anoxia produced by inhalation of 100 per cent nitrogen over a period of 1 to 3 min elicited in both groups of animals a biphasic response consisting of a primary tachycardia and secondary bradycardia. Whereas primary tachycardia was usually moderate, secondary bradycardia was very pronounced and amounted to a 45.8 per cent reduction of heart rate in artificially ventilated dogs, and to 67.2 per cent in dogs breathing spontaneously. Bilateral cervical vagotomy, atropinization and ganglionic blockade caused consistently a considerable reduction or abolition of anoxic bracycardia. On the contrary, elimination of the sympatho-adrenal system by means of spinal cord destruction and bilateral adrenalectomy was conducive to an evident enhancement of bradycardia. The intensity of bradycardia was not reduced following denervation of carotid and aortic baro- and chemoreceptors. On the contrary, denervation invariably resulted in a considerable increase of bradycardia. It is concluded that secondary anoxic bradycardia is mainly due to the increased tone of the vagal cardioinhibitory center, the local depressant action of anoxia on the heart itself being of minor importance. Increased vagal tone is opposed by the concomitant stimulation of the sympatho-adrenal system. Anoxic bradycardia cannot be regarded as resulting from stimulation of carotid and aortic receptors. It is, therefore, inferred that some other mechanism, reflex or central, is activated during acute systemic anoxia giving rise to the increased vagal discharge to the heart.
Similar content being viewed by others
References
Alveryd, A., and S. Brody: Cardiovascular and respiratory changes in man during oxygen breathing. Acta physiol. scand. 15, 140 (1948).
Bernthal, T., W. Greene jr., and A. M. Revzin: Role of carotid chemoreceptors in hypoxic cardiac acceleration. Proc. Soc. exp. Biol. (N. Y.) 76, 121–124 (1951).
Cross, C. E., P. A. Rieben, C. I. Barron, and P. F. Salisbury: Effects of arterial hypoxia on the heart and circulation: an integrative study. Amer. J. Physiol. 205, 963–970 (1963).
Daly De Burgh, M., and M. J. Scott: The effects of stimulation of the carotid body chemoreceptors on heart rate in the dog. J. Physiol. (Lond.) 144, 148–166 (1958).
—— —— The effect of hypoxia on the heart rate of the dog with special reference to the contributions of the carotid body chemoreceptors. J. Physiol. (Lond.) 145, 440–446 (1959).
—— —— An analysis of the primary cardiovascular reflex effects of stimulation of the carotid body chemoreceptors in the dog. J. Physiol. (Lond.) 162, 555 to 573 (1962).
—— —— The cardiovascular responses to stimulation of the carotid body chemoreceptors in the dog. J. Physiol. (Lond.) 165, 179–197 (1963).
—— —— The effects of changes in respiration on the cardiovascular responses to stimulation of the carotid body chemoreceptors. The regulation of human respiration. Haldane Centenary Volume p. 149–162. Oxford: Blackwell Scientific Publications 1963.
Downing, S. E., J. H. Mitchell and A. G. Wallace: Cardiovascular responses to ischemia, hypoxia, and hypercapnia of the central nervous system. Amer. J. Physiol. 204, 881–887 (1963).
——, and J. H. Mitchell: Cardiovascular responses to hypoxic stimulation of the carotid bodies. Circulat. Res. 10, 676–685 (1962).
——, and J. H. Siegel: Baroreceptor and chemoreceptor influences on sympathetic discharge to the heart. Amer. J. Physiol. 204, 471–479 (1963).
Dripps, R. D., and J. H. Comroe: The effect of the inhalation of high and low oxygen concentrations on respiration, pulse rate, ballistocardiogram and arterial oxygen saturation (oximeter) of normal individuals. Amer. J. Physiol. 149, 277–291 (1947).
Greene, C. W., and N. C. Gilbert: Studies of the response of the circulation to low oxygen tension. II. The electrocardiogram during extreme oxygen want. Amer. J. Physiol. 51, 181 (1920).
—— —— Studies of the response of the circulation to low oxygen tension. V. Stages in the loss of function of the rhythm producing and the conducting tissue of the human heart during anoxemia. Amer. J. Physiol. 56, 475–486 (1921).
Heymans, C., and E. Neil: Reflexogenic areas of the cardiovascular system. London: Churchill 1958.
Litwin, J.: Circulatory consequences of anoxia. Drugs and Respiration-Proceedings of the 2nd International Pharmacological Meeting, Prague, 20–23 August, 1963, Vol. 11, p. 49–57. Oxford: Pergamon Press 1964.
——, and D. M. Aviado: Effects of anoxia on the vascular resistance of the dog's hind limb. Circulat. Res. 8, 585–593 (1960).
Salem, H., M. Penna, and D. M. Aviado: Mechanism for bradycardia arising from stimulation of carotid body. Arch. int. Pharmacodyn. 150, 249–258 (1964).
Salisbury, P. F., C. E. Cross, and C. I. Barron: Circulatory effects of arterial hypoxia. Aerospace Med. 34, 935–938 (1963).
Sands, J., and A. C. De Graff: The effects of progressive anoxemia on the heart and circulation. Amer. J. Physiol. 74, 416–435 (1925).
Soma, L. R., M. Penna, and D. M. Aviado: Mechanism for cardiac stimulation during anoxemia in the modified heart-lung preparations. Pflügers Arch. ges. Physiol. 282, 209–224 (1965).
Strumza, M.-V., and J. M. Strumza-Poutonnet: Sur le mécanisme de la bradycardie anoxique préterminale. C. R. Soc. Biol. (Paris) 156, 1998–2000 (1962).
Van Liere, E. J., and J. C. Stickney: Hypoxia—a detailed review of the effects of oxygen want in the body. Chicago: The University of Chicago Press 1963.
Whitehorn, W. V., A. Edelmann, and F. A. Hitchcock: The cardiovascular responses to the breathing of 100 per cent oxygen at normal barometric pressure. Amer. J. Physiol. 146, 61–65 (1946).
Author information
Authors and Affiliations
Additional information
Shortly after completion of this study, Dr. Litwin died tragically while a visiting scientist at the University of Pennsylvania, leaving his wife, small daughter, and widowed mother in Warsaw. For the benefit of his family, a fund has been established, the proceeds of which will be transmitted entirely to them. All those in sympathy with this cause are invited to send checks made out to the “Jerzy Litwin Fund”, mailed c/o George B. Koelle, Chairman, Department of Pharmacology, Medical School, University of Pennsylvania, Philadelphia, Pa., 19104, U.S.A.
Rights and permissions
About this article
Cite this article
Litwin, J., Skolasińska, K. On the mechanism for bradycardia induced by acute systemic anoxia in the dog. Pflügers Archiv 289, 109–121 (1966). https://doi.org/10.1007/BF00380410
Received:
Issue Date:
DOI: https://doi.org/10.1007/BF00380410