Lars Henrik Mariero1, Arkady Rutkovskiy, Kåre-Olav Stensløkken, Jarle Vaage. 1. Faculty of Medicine, Department of Molecular Biosciences, University of Oslo, and Institute for Experimental Medical Research, Department of Surgery, Oslo University Hospital, Oslo, Norway. l.h.mariero@medisin.uio.no
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSION: Normobaric hyperoxia during early reperfusion did not increase ischemia/reperfusion injury.
OBJECTIVE: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. METHODS: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. RESULTS: 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). CONCLUSION: Normobaric hyperoxia during early reperfusion did not increase ischemia/reperfusion injury.
Authors: Mervyn Singer; Paul J Young; John G Laffey; Pierre Asfar; Fabio Silvio Taccone; Markus B Skrifvars; Christian S Meyhoff; Peter Radermacher Journal: Crit Care Date: 2021-12-19 Impact factor: 9.097