1. Myocardial blood flow was measured by using a 133xenon clearance technique in closed-chest dogs anaesthetized with trichlorethylene. A gradual decrease in the inspired oxygen tension resulted in an increase in myocardial blood flow only when the Pa,o2 fell to between 30 and 35 mmHg.

2. When hypoxia was rapidly induced and sustained for a mean period of 18.3 min, myocardial blood flow markedly increased (from a mean of 118 ± 5 to 162±6 ml 100 g−1 min−1). There was a critical mean arterial oxygen tension (35 mmHg) above which increases in myocardial blood flow did not occur. This corresponded to a mean coronary sinus Po2 of 18 mmHg or an oxygen content of 50 ml/100 ml. These flow increases were not dependent on changes in arterial or coronary sinus pH or carbon dioxide tension, nor were they dependent on changes in perfusion pressure or heart rate.

3. Despite the fact that oxygen availability was substantially decreased, myocardial oxygen consumption was maintained throughout the period of hypoxia by means of increased oxygen extraction.

4. Towards the end of the hypoxic period, Pa,co2 rose significantly from 40 ± 1 to 48 ± 1.5 mmHg. There was no significant change in the non-respiratory component of acid-base balance.

5. During prolonged hypoxia (more than 30 min) myocardial blood flow remained consistently elevated, but oxygen consumption tended to fall progressively and this was associated with an increasingly severe metabolic acidosis. The haemodynamic and oxygen consumption changes returned to normal within a short time (15 min) after the resumption of a normal inspired oxygen concentration, as did the frequently observed electrocardiographic disturbances.

6. The responses to hypoxia were unaffected by a combination of atropine and propranolol. There was no evidence either that hypoxia-induced coronary vasodilatation was mediated through vascular β-adrenoreceptors or that propranolol interfered with the self-regulating control of myocardial blood flow.

It has been recognized for some time that hypoxia is capable of producing considerable increases in blood flow in the myocardium (Hilton & Eichholtz, 1925; Eckenhoff, Haf kenschiel, Landmesser & Harmel, 1947; Berne, Blackmon & Gardner, 1957; Feinberg, Gerola & Katz, 1958; Aukland, Kiil, Kjekshus & Semb, 1967). Little is known, however, about the exact relationship between arterial oxygen tension and myocardial blood flow. Further, although several factors associated with hypoxia are known to influence myocardial blood flow, the relative importance of each is uncertain; such factors include a direct effect of hypoxia on coronary vascular smooth muscle and indirect effects relating to changes in perfusion pressure, heart rate, extravascular support and associated metabolic disturbances. Likewise, the influence of neurogenic factors on myocardial vascular tone during hypoxia has not been systematically examined.

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