Abstract
Henderson 1 described the depression of blood pressure in acapnia, advanced the hypothesis of a venopressor mechanism, and still believes that the decrease of the venous return to the right heart is a principal factor in the production of this effect. 2 Dale and Evans 3 showed by cardiometer experiments that the cardiac output is not significantly altered in hyperventilation, and thought the effect due to depression of the vasomotor centres of the bulb and spinal cord. Voluntary over-breathing in man results inconstantly in a reduction of the blood pressure; and McDowell 4 reported that in some dogs anesthetized with chloralose no fall, or even a rise, of blood pressure occurred with acapnia, while in all animals anesthetized with ether a fall occurred. These observations were explained by the hypothesis that acapnia has a dual effect on the circulation, (a) vasodilatation due to a central action, and (b) constriction of smaller and more peripheral vessels due to a local action.
In studying the effects of acapnia, it was desired to measure by the Fick method the cardiac output before and during hyperventilation, and to compare the effect on the output with the effect of partial obstruction of the venous return to the heart.
Dogs of 5 to 8 kgm. body weight, anesthetized with sodium-barbital, were used in all experiments. Ventilation of increased rate and volume was obtained by alternate positive and negative air pressure applied to the entire body except the head, in the manner of the Drinker respirator. A cylindrical metal chamber, 35 cm. x 15 cm. in diam., was used; its open end was closed by a thick rubber cuff, sealed about the dog's neck by several layers of adhesive tape.
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