Background. We explored the ability of increased oxygen pressure to mo
dify necrosis in an open-chest rabbit model of myocardial ischemia and
reperfusion. Methods and Results. A branch of the left coronary arter
y was occluded for 30 minutes followed by 3 hours of reperfusion. Infa
rction 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 deve
loped 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 con
trol animals (15.2+/-2.9%, 14.5+/-3.7%, and 9.8%+/-2.7%, respectively;
P less-than-or-equal-to .01), indicating that they had been protected
by the procedure. When hyperbaric oxygen was begun 30 minutes after t
he onset of reperfusion, no protection was seen (35.8+/-3.8%). Conclus
ions. We conclude that hyperbaric oxygen limits infarct size in the re
perfused rabbit heart and that the effect can be achieved when hyperba
ric oxygen is begun at reperfusion.