Abstract
The circulatory responses to hemorrhage involve a pattern of selective vasoconstriction and vasodilatation which produces a redistribution of the diminished cardiac output (Blalock and Levy 1937, Frank et al. 1956, Corday and Williams 1960, Sapirstein et al. 1960, Gregg 1962, Takács et al. 1962, Smith et al. 1965, Fell 1966, Neutze et al. 1968, Kovách et al. 1968, Kovách 1970). Hinshaw et al. (1961) observed in the dog that loss of 10 per cent of the blood volume produced a 21 per cent fall in cardiac output, but a decline of only 7 per cent in the arterial pressure. A 20 per cent hemorrhage caused a 45 per cent fall in cardiac output, but only 15 per cent drop in arterial blood pressure. The physiologic compensatory mechanisms activated by acute volume deficit favor the maintenance of pressure at the expense of flow.
These studies were supported by the Hungarian Medical Research Council and partly by the John A. Hartford Foundation.
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Kovách, A.G.B., Mitsányi, A., Monos, E., Nyáry, I., Sulyok, A. (1973). Control of Organ Blood Flow Following Hemorrhage. In: Kovách, A.G.B., Stoner, H.B., Spitzer, J.J. (eds) Neurohumoral and Metabolic Aspects of Injury. Advances in Experimental Medicine and Biology, vol 33. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3228-2_1
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