Hemorrhage and
resuscitation has been recognized as an exclusively destructive process which results in multiple organ dysfunction. Although it is well established that endogenous adaptation (preconditioning) mechanisms exist, it is unknown whether
hemorrhage and
resuscitation induces endogenous adaptive/protective mechanisms in the heart. Furthermore, alpha 1-adrenoceptors and
nuclear factor kappa B (
NF kappa B) have each been implicated in stress-induced signal transduction; however, whether they might be involved in
hemorrhage-induced adaptive signal transduction remains unknown. This study tests the hypothesis that H/R activates myocardial
NF kappa B and results in myocardial adaptation via alpha 1-adrenoceptors. Rats were briefly (10 min) hemorrhaged to 35 mmHg and resuscitated,
sham operated, or neither, with and without prior alpha 1-adrenoceptor inhibition (
prazosin). Hearts were then isolated and either probed for
NF kappa B activation or subjected to a second insult consisting of global normothermic I/R (20 min/40 min). Antecedent
hemorrhage and
resuscitation activated myocardial
NF kappa B and improved left ventricular developed pressure, coronary flow, and end diastolic pressure following
ischemia-reperfusion (P < 0.05, ANOVA with Bonferroni-Dunn).
Hemorrhage-induced adaptation was abolished by prior alpha 1-adrenoceptor blockade. This study constitutes the initial demonstration that H/R activates myocardial
NF kappa B and induces adaptive signal transduction against
ischemia-reperfusion injury.