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Improved cardiac contractile functions in hypoxia-reoxygenation in rats treated with low concentration Co 2+

2000; American Physical Society; Volume: 279; Issue: 6 Linguagem: Inglês

10.1152/ajpheart.2000.279.6.h2713

1522-1539

Hiroshi Endoh, Takaho Kaneko, Hiro Nakamura, Katsuhiko Doi, Eiji Takahashi,

High Altitude and Hypoxia

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.