We have previously reported the mechanism behind the myocardial injury and the activation of autonomic nervous system during the
ischemia-reperfusion (IR) of the rat brain. This study was planned to investigate the effect of
carvedilol, a β-blocker, in improving the myocardial injury caused by IR of the rat brain. We have used a whole cerebral IR model in rats by clamping both the right and left common carotid arteries. Rats were divided into five groups;
Sham surgery group (Group-
Sham),
carvedilol treatment before
ischemia group (Group-Is+C), vehicle control group (Group-Is+V),
carvedilol treatment before reperfusion group (Group-Re+C) and the vehicle control group (Group-Re+V). We have measured the blood pressure and heart rate via a
catheter, myocardial tissue β1-adrenaline receptor (β1-AR) levels, phosphor-p38
mitogen-activated protein kinase (p-p38 MAPK) signaling factor,
malondialdehyde (MDA), and apoptosis (TUNEL assay and expression of
caspase-7 protein). The results indicated that the increased expressions of β1-AR, p-p38 MAPK,
caspase-7, apoptotic cells and MDA level in the myocardial tissue due to
brain ischemia-reperfusion were significantly reduced by
carvedilol treatment. From these observations we can suggest that, with the advantage of its
antioxidant and β blocking action,
carvedilol had played the improvement of myocardial injury in
ischemia-reperfusion of the brain.