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- W2313905592 abstract "Henderson1 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 Evans3 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 McDowell4 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 acap..." @default.
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- W2313905592 date "1931-06-01" @default.
- W2313905592 modified "2023-09-24" @default.
- W2313905592 title "The Cardiac Output in Hyperventilation." @default.
- W2313905592 doi "https://doi.org/10.3181/00379727-28-5607" @default.
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