Contribution of hypercapnia and hypoxia to the vascular response to ischaemia.

1. Hypoxia, induced by 7-12% oxygen breathing, produced vasodilatation in the intact or in the phenoxybenzamine and propranolol treated forearm of human volunteers when arterial blood POz decreased below 45 mmHg, or when deep forearm venous blood PO, decreased below 3540 mmHg. 2. Circulatory arrest of the forearm following alpha and beta adrenergic receptor blockade was followed by greater increases in blood flow and greater decreases in forearm vascular resistance during CO, breathing than during room air breathing. The increased flow following ischaemia was maintained at a high level until COz administration was stopped. 3. The vasodilator response following ischaemia of the human forearm, produced by digital occlusion of the brachial artery, was compared to that produced by hypercapnia or hypoxia or a combination of the two, produced by breathing the appropriate gas mixtures. The forearm was pre-treated with phenoxybenzamine and propranolol to produce alpha and beta adrenergic receptor blockade. For equal increases in deep forearm venous blood PCO, the vasodilator response to hypercapnia averaged 60% of that following ischaemia. For equal decreases in deep forearm venous blood PO, the vasodilator response to hypoxia averaged 26% of that produced by ischaemia. The vasodilator response to ischaemia was not modified by breathing 100% oxygen to maintain the deep forearm venous blood PO, at a level above that seen with the circulation free during room air breathing. Combined hypoxia and hypercapnia of equal severity as those produced by ischaemia resulted in a vasodilator response which averaged 64% of that produced by ischaemia.