The effect of hypocapnia on arterial blood pressure.

In man, hypocapnia induced by hyperventilation causes a drop in arterial pressure. The calculated peripheral resistance is decreased, indicating a net vasodilatation. The forearm blood flow is markedly increased, and the vascular resistance of the forearm is much reduced. Persons with impaired function of the sympathetic nervous system continue to show these effects. The increase in forearm flow is not prevented by brachial block. These results suggest that hypocapnia acts directly on blood vessels to produce a net overall vasodilatation and fall in blood pressure, and that this effect is not mediated through the nervous system, as usually supposed. B REATHING carbon dioxide raises the blood pressure and hyperventilation lowers it in man and experimental animals. Changes in blood carbon dioxide are supposed to affect vessels both directly and by way of the vasomotor centers.' These actions are thought to be opposite in direction, with the central effect being the stronger. That is, a high carbon dioxide level causes an overall vasoconstriction because of its effect on the vasomotor centers, even though the direct action is to dilate vessels. Loss of carbon dioxide has opposite effects, both centrally and locally. These conclusions are based on animal experiments. It is the purpose of this paper to describe the effects on vascular tone of lowering carbon dioxide by hyperventilation in (1) normal subjects and (2) patients in whom portions of the nervous system have been destroyed by disease or surgery or blocked by drugs. The results of this study do not support the conventional concept of the means by which carbon dioxide affects vascular tone. 89 one-minute periods of maximal voluntary forced breathing of either room air or a 5 per cent carbon dioxide, 21 per cent oxygen gas mixture. Procedures included simultaneous measurements of forearm blood flow by plethysmography, intraarterial pressure , pulse rate, cardiac output by dye dilution method2 and arterial blood pH and carbon dioxide content;3a4 from the latter blood carbon dioxide tension was calculated. Local forearm vascular resistance was calculated as mean blood pressvre (mm. Hg) forearm blood flow (cc./min./100 cc. tissue) and overall peripheral resistance as mean blood pressvre (mm. Hg) cardiac output (L/min.) Forearm blood flows at 37 C. with hand excluded,5 central venous pressure and intra-arterial pressures were measured with the use of strain gauges and a Sanborn Poly-Viso oscillograph. Single determina-tions of cardiac output were separated by 15-minute intervals, and the Evans blue dye …