Abstract
At present there are two general theories that have been proposed to account for the autoregulatory vascular response to decreased coronary arterial flow. One holds that an increased concentration of vasoactive tissue metabolites which accumulate as a result of myocardial hypoxia, most notable among which is the nucleoside adenosine, directly causes vasodilation in the coronary resistance vessels (1, 2, 3, 4). The other states that the low pO2 incident to low coronary flow acts directly on vascular smooth muscles to cause vasodilation, possibly because of depletion of ATP and other oxygen dependent energy substrates necessary to maintain the contractile state (5, 6, 7, 8). Recently, a study of isolated coronary vascular smooth muscle strips has suggested another mechanism in which both the local oxygen tension and adenosine concentration may act in concert to effect coronary vasodilation in the presence of myocardial hypoxia: this in vitro study demonstrated an enhancement of adenosine induced relaxation of vascular smooth muscle when local oxygen tension was reduced to below 40 mm Hg (9).
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Berne, R.M., Blackmon, J.R., and Gardner, T.H.: Hypoxemia and coronary flow. J. Clin. Invest. 36:1101–1106, 1957.
Katori, M. and Berne, R.M.: Release of adenosine from anoxic hearts: relationship to coronary flow. Circ. Res. 19:420–425, 1966.
Rubio, R., Berne, R.M., and Katori, M.: Release of adenosine in reactive hyperemia of the dog heart. Am. J. Physiol. 216: 56–62, 1969.
Rubio, R, and Berne, R.M.: Release of adenosine by the normal myocardium in dogs and its relationship to the regulation of coronary resistance. Circ. Res. 25:407–415, 1969.
Guyton, A.C., Ross, J.M., Carrier, O., and Walker, J.R.: Evidence for tissue oxygen demand as the major factor causing autoregulation. Circ. Res. 15(Supp. I):60–69, 1964.
Carrier, O., Jr., Walker, J.R., and Guyton, A.C.: Role of oxygen in autoregulation of blood flow in isolated vessels. Am. J. Physiol. 206:951–954, 1964.
Fairchild, H.M., Ross, J., and Guyton, A.C.: Failure of recovery from reactive hyperemia in the absence of oxygen. Am. J. Physiol. 210:490–492, 1966.
Detar, R. and Bohr, D.F.: Oxygen and vascular smooth muscle contraction. Am. J. Physiol. 214:241–244, 1968.
Detar, R. and Gelai, M.: Oxygen, adenosine and isolated coronary arterial vascular smooth muscle. The Physiologist 14:132(abstract), 1971.
Dixon, W.J.: Biomedical Computer Programs (Ed.). Univ. of Calif. Press, Berkeley, 1971, pp543–557.
Case, R.B., Nasser, M.G., and Crampton, R.J.: Biochemical aspects of early myocardial ischemia. Am. J. Cardiol. 24:766–775, 1969.
Scott, J.B., and Radowski, D.: Role of hyperosmolarity in the genesis of active and reactive hyperemia. Circ. Res. 28(Supp. l):26–32, 1971.
Downing, S.E., Talner, N.S., and Gardner, T.H.: Influences of hypoxemia and acidemia on left ventricular function. Am. J. Physiol. 210:1327–1334, 1966.
Daugherty, R.M., Scott, J.B., Dabney, J.M., and Haddy, F.J.: Local effects of O2 and CO2 on limb, renal, and coronary vascular resistances. Am. J. Physiol. 213:1102–1110, 1967.
Ng, M.L., Levy, M.N., DeGeest, H., and Zieske, H.: Effects of myocardial hypoxia on left ventricular performance. Am. J. Physiol. 211:43–50, 1966.
Penna, M., Linares, F., and Caceres, L.: Mechanism for cardiac stimulation during hypoxia. Am. J. Physiol. 208:1237–1242, 1965.
Downing, S.E., Mitchell, J.H., and Wallace, A.G.: Cardiovascular response to ischemia, hypoxia and hypercapnia of the central nervous system. Am. J. Physiol. 204:881–887, 1963.
Sobol, B.J., Wanloss, S.A., Joseph, E.B., and Azarshahy, I.: Alterations of coronary blood flow in the dog by inhalation of 100 per cent oxygen. Circ. Res. 11:797–802, 1962.
Sarnoff, S.J., Braunwald, E., Welch, G.H., Jr., Case, R.B., Stainsby, W.N., and Marcruz, R.: Hemodynamic determinants of oxygen consumption of the heart with special reference to the tension-time index. Am. J. Physiol. 192:148–156, 1958.
Downing, S.E., Remensyder, J.P., and Mitchell, J.J.: Cardiovascular responses to hypoxic stimulation of carotid bodies. Circ. Res. 10:676–685, 1962.
Pool, P.E., Covell, J.W., Chidsey, C.A., and Braunwald, E.: Myocardial high energy phosphate stores in acutely induced hypoxic heart failure. Circ. Res. 19:221–229, 1966.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1973 Plenum Press, New York
About this chapter
Cite this chapter
Moir, T.W., Jones, P.K. (1973). Observations on the Effect of Changes in Arterial Oxygenation on Adenosine Induced Coronary Vasodilation. In: Bloor, C.M., Olsson, R.A. (eds) Current Topics in Coronary Research. Advances in Experimental Medicine and Biology, vol 39. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9020-0_2
Download citation
DOI: https://doi.org/10.1007/978-1-4615-9020-0_2
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4615-9022-4
Online ISBN: 978-1-4615-9020-0
eBook Packages: Springer Book Archive