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Mechanisms Regulating the Cardiac Output Response to Cyanide Infusion, a Model of Hypoxia
Chang-seng Liang, William E. Huckabee
Chang-seng Liang, William E. Huckabee
Published December 1, 1973
Citation Information: J Clin Invest. 1973;52(12):3115-3128. https://doi.org/10.1172/JCI107511.
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Research Article

Mechanisms Regulating the Cardiac Output Response to Cyanide Infusion, a Model of Hypoxia

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Abstract

When tissue metabolic changes like those of hypoxia were induced by intra-aortic infusion of cyanide in dogs, cardiac output began to increase after 3 to 5 min, reached a peak (220% of the control value) at 15 min, and returned to control in 40 min. This pattern of cardiac output rise was not altered by vagotomy with or without atropine pretreatment. However, this cardiac output response could be differentiated into three phases by pretreating the animals with agents that block specific activities of the sympatho-adrenal system. First, ganglionic blockade produced by mecamylamine or sympathetic nerve blockade by bretylium abolished the middle phase of the cardiac output seen in the untreated animal, but early and late phases still could be discerned. Second, beta-adrenergic receptor blockade produced by propranolol shortened the total duration of the cardiac output rise by abolishing the late phase. Third, when given together, propranolol and mecamylamine (or bretylium) prevented most of the cardiac output rise that follows the early phase.

Authors

Chang-seng Liang, William E. Huckabee

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