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- W2213441421 abstract "Reperfused hypertrophic hearts are prone to develop reflow abnormalities, which are likely to impair O 2 return to the myocardium. Yet, reflow deficit may not be the only factor determining postischemic oxygenation in the hypertrophic heart. Altered O 2 demand may also contribute to hypoxia. In addition, the extent to which myocardial Po 2 dictates energy and functional recovery in the reperfused heart remains uncertain. In the present study, moderately hypertrophied hearts from spontaneously hypertensive rats were subjected to ischemia-reperfusion, and the recovery time courses of pH and high-energy phosphates were followed by 31 P NMR. 1 H NMR measurement of intracellular myoglobin assessed tissue O 2 levels. The present study found that the exacerbation of hypoxia in the postischemic spontaneously hypertensive rat heart arises mostly from impaired microvascular supply of O 2 . However, postischemic myocardial Po 2 , at least when it exceeds ∼18% of the preischemic level, does not limit mitochondrial respiration and high-energy phosphate resynthesis. It only passively reflects changes in the O 2 supply-demand balance." @default.
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- W2213441421 date "2016-01-15" @default.
- W2213441421 modified "2023-10-17" @default.
- W2213441421 title "Myocardial Po2 does not limit aerobic metabolism in the postischemic heart" @default.
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- W2213441421 doi "https://doi.org/10.1152/ajpheart.00335.2015" @default.
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