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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Blood Pressure, Heart Rate, Hyperoxia, Male, Myocardial Infarction, Myocardial Reperfusion, Myocardial Reperfusion Injury, Oxygen, Oxygen Inhalation Therapy, Partial Pressure, Rats, Rats, Wistar.
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Does hyperoxia during early reperfusion increase ischemia/reperfusion injury? Context: Oxygen is routinely administered to patients undergoing acute myocardial infarction as well as during revascularization procedures and cardiac surgery. Because reactive oxygen species are mediators of ischemia/reperfusion injury, increased oxygen availability might theoretically aggravate myocardial injury during reperfusion. We hypothesized that ventilation with a hyperoxic gas at start of reperfusion might increase ischemia/reperfusion injury. Rats were anesthetized with isoflurane and ventilated with 40% oxygen. The animals were subjected to 40 min of regional myocardial ischemia and 120 min of reperfusion. In the test group, rats (n=11) were ventilated with a normobaric hyperoxic gas (95% O2) during the last 10 min of ischemia and the first 10 min of reperfusion. Control rats (n=14) were ventilated with 40% O2 throughout the experiments. Due to irreversible reperfusion arrhythmias, one animal in the hyperoxia group and six animals in the control group were excluded. Hearts (n=8 in the control group and n=10 in the test group) were harvested for measurement of infarct size. The incidence of lethal arrhythmias was 1/11 in the test group and 6/14 in the control group (p=0.06). Reperfusion with normobaric hyperoxia did not influence infarct size (20±8% of area at risk) compared with the normoxia group (24±8% and of area at risk), respectively (mean±SD, p>0.2).
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Normobaric hyperoxia during early reperfusion did not increase ischemia/reperfusion injury. Final Decision: no