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1Zentrum Anaesthesiologie, Abteilung Anaesthesiologische Forschung, 2Zentrum Pharmakologie und Toxikologie, and 3Zentrum Anatomie, Abteilung Elektronenmikroskopie, University Göttingen, D-37075 Göttingen, Germany
Submitted 28 March 2002 ; accepted in final form 23 April 2003
To investigate the localization of the earliest damage in ischemic and ischemic-reperfused myocardium, anesthetized rats were subjected to coronary occlusion for 15, 30, 45, or 90 min. One-half of the animals in each group had no reperfusion, whereas the other half was reperfused for 14 min. With the use of histological methods, preferentially in the periphery of the area at risk, localized zones were detected that lacked the hypoxia-specific increase in NADH fluorescence. The extent of these areas displaying injured tissue was found to be significantly smaller in the ischemic-nonreperfused hearts than in the ischemic-reperfused organs (15-min ischemia: 0.22 ± 0.12% vs. 43.0 ± 5.0%; 30-min ischemia: 5.7 ± 2.7% vs. 64.6 ± 2.9%; 45-min ischemia: 5.6 ± 1.2% vs. 66.0 ± 7.5%; 90-min ischemia: 39.3 ± 5.5% vs. 86.7 ± 1.8% of the area at risk). The results point to a localized initiation of the damage close to the surrounding oxygen-supplied tissue during ischemia and an expansion of this injury by intercellular actions into yet-intact areas upon reperfusion.
mapping of tissue reduced nicotinamide adenine nucleotide fluorescence; lethal reperfusion injury; propidium iodide
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