BACKGROUND: We explored the ability of increased oxygen pressure to modify necrosis in an open-chest rabbit model of myocardial ischemia and reperfusion. METHODS AND RESULTS: A branch of the left coronary artery was occluded for 30 minutes followed by 3 hours of reperfusion. Infarction was measured by triphenyl tetrazolium staining and expressed as a percentage of the ischemic zone. Untreated rabbits were ventilated with 100% oxygen at 1 atm absolute. Treatment animals were exposed to hyperbaric oxygen at 2.5 atm absolute. The 1.0-atm control hearts developed 41.5 +/- 4.6% infarction of the ischemic zone. Animals exposed to hyperbaric oxygen during ischemia only, reperfusion only, or ischemia and reperfusion had significantly smaller infarcts with respect to control animals (16.2 +/- 2.9%, 14.5 +/- 3.7%, and 9.8 +/- 2.7%, respectively; P < or = .01), indicating that they had been protected by the procedure. When hyperbaric oxygen was begun 30 minutes after the onset of reperfusion, no protection was seen (35.8 +/- 3.8%). CONCLUSIONS: We conclude that hyperbaric oxygen limits infarct size in the reperfused rabbit heart and that the effect can be achieved when hyperbaric oxygen is begun at reperfusion.
BACKGROUND: We explored the ability of increased oxygen pressure to modify necrosis in an open-chest rabbit model of myocardial ischemia and reperfusion. METHODS AND RESULTS: A branch of the left coronary artery was occluded for 30 minutes followed by 3 hours of reperfusion. Infarction was measured by triphenyl tetrazolium staining and expressed as a percentage of the ischemic zone. Untreated rabbits were ventilated with 100% oxygen at 1 atm absolute. Treatment animals were exposed to hyperbaric oxygen at 2.5 atm absolute. The 1.0-atm control hearts developed 41.5 +/- 4.6% infarction of the ischemic zone. Animals exposed to hyperbaric oxygen during ischemia only, reperfusion only, or ischemia and reperfusion had significantly smaller infarcts with respect to control animals (16.2 +/- 2.9%, 14.5 +/- 3.7%, and 9.8 +/- 2.7%, respectively; P < or = .01), indicating that they had been protected by the procedure. When hyperbaric oxygen was begun 30 minutes after the onset of reperfusion, no protection was seen (35.8 +/- 3.8%). CONCLUSIONS: We conclude that hyperbaric oxygen limits infarct size in the reperfused rabbit heart and that the effect can be achieved when hyperbaric oxygen is begun at reperfusion.
Authors: Hans Erik Bøtker; Derek Hausenloy; Ioanna Andreadou; Salvatore Antonucci; Kerstin Boengler; Sean M Davidson; Soni Deshwal; Yvan Devaux; Fabio Di Lisa; Moises Di Sante; Panagiotis Efentakis; Saveria Femminò; David García-Dorado; Zoltán Giricz; Borja Ibanez; Efstathios Iliodromitis; Nina Kaludercic; Petra Kleinbongard; Markus Neuhäuser; Michel Ovize; Pasquale Pagliaro; Michael Rahbek-Schmidt; Marisol Ruiz-Meana; Klaus-Dieter Schlüter; Rainer Schulz; Andreas Skyschally; Catherine Wilder; Derek M Yellon; Peter Ferdinandy; Gerd Heusch Journal: Basic Res Cardiol Date: 2018-08-17 Impact factor: 17.165
Authors: Orhan Tezcan; Oguz Karahan; Mustafa Alan; Cenap Ekinci; Celal Yavuz; Sinan Demirtas; Aysun Ekinci; Ahmet Caliskan Journal: Acta Cardiol Sin Date: 2017-03 Impact factor: 2.672