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• W2224414911 abstract "An intracellular mechanism that senses decreases in tissue oxygen level and stimulates hypoxia-related gene expression has been reported in various cell types including the cardiac cell. The mechanism can also be activated by Co 2+ in normoxia. Thus we investigated the effects of prior chronic oral CoCl 2 on mechanical functions of isolated, perfused rat hearts in hypoxia-reoxygenation. In normoxic rats, 43 days of Co 2+ administration increased hematocrit from 45 ± 0.3% (control, n = 18) to 51 ± 0.6% ( n = 19). In hypoxia and reoxygenation, Co 2+ -pretreated hearts exhibited a significantly higher rate-pressure product (267 and 163%, respectively) and coronary flow (127 and 118%, respectively) and lower end-diastolic pressure (72 and 60%, respectively) compared with the control hearts. Although the oral Co 2+ administration significantly raised myocardial Co 2+ concentration, it did not affect mitochondrial respiration, tissue glycogen concentration, or myocardial tissue histology. The levels of vascular endothelial growth factor, aldolase-A, and glucose transporter-1 mRNA were significantly elevated in the Co 2+ -treated myocardium. We conclude that cardiac contractile functions would gain hypoxic tolerance when the endogenous cellular oxygen-sensing mechanism is activated." @default.
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• W2224414911 date "2000-12-01" @default.
• W2224414911 modified "2023-09-23" @default.
• W2224414911 title "Improved cardiac contractile functions in hypoxia-reoxygenation in rats treated with low concentration Co²⁺" @default.
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• W2224414911 doi "https://doi.org/10.1152/ajpheart.2000.279.6.h2713" @default.
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