Remifentanil is a commonly used opioid in anesthesia with
cardioprotective effect in ischemia-reperfused (I/R) heart. We
evaluated the influence of remifentanil on myocardial infarct size
and expressions of proteins involved in apoptosis in I/R rat heart
following various time protocols of remifentanil administration.
Artificially ventilated anesthetized Sprague-Dawley rats were
subjected to a 30 min of left anterior descending coronary artery
occlusion followed by 2 h of reperfusion. Rats were randomly
assigned to one of five groups; Sham, I/R only, remifentanil
preconditioning, postconditioning and continuous infusion group.
Myocardial infarct size, the phosphorylation of ERK1/2, Bcl2, Bax
and cytochrome c and the expression of genes influencing Ca2+
homeostasis were assessed. In remifentanil-administered rat
hearts, regardless of the timing and duration of administration,
infarct size was consistently reduced compared to I/R only rats.
Remifentanil improved expression of ERK 1/2 and anti-apoptotic
protein Bcl2, and expression of sarcoplasmic reticulum genes
which were significantly reduced in the I/R rats only.
Remifentanil reduced expression of pro-apoptotic protein, Bax
and cytochrome c. These suggested that remifentanil produced
cardioprotective effect by preserving the expression of proteins
involved in anti-apoptotic pathways, and the expression of
sarcoplasmic reticulum genes in I/R rat heart, regardless of the
timing of administration.