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during in vivo myocardial
ischemia
Departments of 1 Surgery and 2 Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614
We have demonstrated that in vitro brief ischemia
activates nuclear factor (NF)-
B in rat myocardium. We report in vivo
ischemia-reperfusion (I/R)-induced NF-B activation, IB
kinase -
(IKK) activity, and IB
phosphorylation and
degradation in rat myocardium. Rat hearts were subjected to occlusion
of the coronary artery for up to 45 min or occlusion for 15 min
followed by reperfusion for up to 3 h. Cytoplasmic and nuclear
proteins were isolated from ischemic and nonischemic
areas of each heart. NF-B activation was increased in the
ischemic area (680%) after 10 min of ischemia and in
the nonischemic area (350%) after 15 min of ischemia
and remained elevated during prolonged ischemia and
reperfusion. IKK activity was markedly increased in ischemic
(1,800%) and nonischemic (860%) areas, and phosphorylated
IB levels were significantly elevated in ischemic (180%)
and nonischemic (280%) areas at 5 min of ischemia and
further increased after reperfusion. IB levels were decreased in
the ischemic (45%) and nonischemic (36%) areas after
10 min of ischemia and remained low in the ischemic area during prolonged ischemia and reperfusion. The results
suggest that in vivo I/R rapidly induces IKK activity and increases
IB phosphorylation and degradation, resulting in NF-B
activation in the myocardium.
IB phosphorylation; nuclear factor-B; reperfusion
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