Hypoxic Conditioning Suppresses Nitric Oxide Production upon Myocardial Reperfusion

Exp. Biol. Med. 2008;233:766-774
doi:10.3181/0710-RM-282
© 2008 Society for Experimental Biology and Medicine

 

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Hypoxic Conditioning Suppresses Nitric Oxide Production upon Myocardial Reperfusion

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Myoung-Gwi Ryou*,
Jie Sun*,
Kevin N. Oguayo*,
Eugenia B. Manukhina,
H. Fred Downey* and
Robert T. Mallet*1


* Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas; and Institute of General Pathology and Pathophysiology, Moscow, Russian Federation



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Figure 1. IHC did not alter activities of hypoxia-inducible myocardial enzymes. Lactate dehydrogenase (LDH), glucose-6-phophate dehydrogenase (G6PDH), creatine kinase (CK), and phosphofructokinase (PFK) activities were measured in transmural biopsies taken from left ventricular myocardium perfused by the left anterior descending (LAD) and left circumflex (LCX) coronary arteries, and from right ventricular myocardium (RV) of non-hypoxic controls (filled bars) and dogs conditioned by 20 d IHC (open bars). Values are means ± SEM from 4 control and 8 IHC dogs. No statistically significant between-group differences were detected.



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Figure 2. Nitrite release during reperfusion reactive hyperemia. NO2 release peaked within 2 min reperfusion in non-hypoxic control dogs (Panel A). IHC dampened this reperfusion NO2 burst, and lowered cumulative NO2 release during the first 5 min reperfusion by 56% (Panel B). Means ± SEM from 6 IHC and 5 control experiments. * P < 0.05 vs. non-hypoxic control, P < 0.05 vs. pre-occlusion baseline (BL).



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Figure 3. LAD blood flow during reperfusion. No significant differences were detected in LAD flow during pre-occlusion baseline or following reperfusion (Panel A). Cumulative LAD flow during the first 5 min reperfusion did not differ in non-hypoxic vs. IHC dogs (Panel B). Means ± SEM from the same experiments as in Figure 2. P < 0.05 vs. baseline (BL).



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Figure 4. IHC suppressed nitric oxide synthase activities in left and right ventricular myocardium. NOS activities were measured in the same myocardial biopsies as in Figure 1. Abbreviations as in Figure 1. * P < 0.05 vs. non-hypoxic control.



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Figure 5. Immunoblot of eNOS in left ventricular myocardium of non-hypoxic and IHC dogs. Densities of the bands for total eNOS, P-1177S eNOS, and P-495T eNOS are normalized to densities of the actin bands, which served as loading controls. Values in panel B are means ± SEM from 8 IHC and 4 non-hypoxic control experiments. * P < 0.05 vs. control.

Hypoxic Conditioning Suppresses Nitric Oxide Production upon Myocardial Reperfusion
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