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

نویسندگان

  • HIROSHI ENDOH
  • TAKAHO KANEKO
  • HIRO NAKAMURA
  • KATSUHIKO DOI
  • EIJI TAKAHASHI
  • Takaho Kaneko
  • Hiro Nakamura
  • Katsuhiko Doi
چکیده

Endoh, Hiroshi, Takaho Kaneko, Hiro Nakamura, Katsuhiko Doi, and Eiji Takahashi. Improved cardiac contractile functions in hypoxia-reoxygenation in rats treated with low concentration Co. Am J Physiol Heart Circ Physiol 279: H2713–H2719, 2000.—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 in normoxia. Thus we investigated the effects of prior chronic oral CoCl2 on mechanical functions of isolated, perfused rat hearts in hypoxia-reoxygenation. In normoxic rats, 43 days of Co administration increased hematocrit from 45 6 0.3% (control, n 5 18) to 51 6 0.6% (n 5 19). In hypoxia and reoxygenation, Co-pretreated hearts exhibited a significantly higher ratepressure 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 administration significantly raised myocardial Co 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-treated myocardium. We conclude that cardiac contractile functions would gain hypoxic tolerance when the endogenous cellular oxygen-sensing mechanism is activated.

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تاریخ انتشار 2000