1. In closed‐chest dogs anaesthetized with trichlorethylene, the inhalation of carbon dioxide sufficient to increase the arterial PCO2 from 40 to about 100 mm Hg, increased myocardial blood flow (measured using a 133Xe clearance technique) and right atrial pressure. There were no consistent changes in mean arterial blood pressure, heart rate or cardiac output. 2. The effect of hypercapnia on myocardial blood flow was not influenced by the previous administration of atropine and propranolol or of bretylium. It can be concluded, therefore, that the elevated arterial PCO2 has a direct vasodilator effect on the myocardial microcirculation. 3. During hypercapnia the coronary sinus PO2 was increased and the coronary arteriovenous oxygen content difference, and calculated myocardial oxygen consumption, reduced. It is suggested that this latter effect may be the result of myocardial depression produced by the decrease in arterial blood pH. 4. There was no evidence of myocardial glucose uptake either before or during hypercapnia. The myocardial extraction of lactate and pyruvate at rest varied between 0 and 55%. During acute hypercapnia the extraction of lactate usually fell. 5. When the arterial PCO2 was maintained at 100 mm Hg for a period of 1 hr the effects on myocardial blood flow and on oxygen consumption were not sustained. 6. Stepwise increments and decrements in arterial PCO2 of 10–20 mm Hg produced corresponding increases and decreases in myocardial blood flow and demonstrated that changes in arterial PCO2 of 20–30 mm Hg can markedly affect blood flow in the myocardium.
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