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Previous studies have demonstrated that endogenous norepinephrine (NE) plays an important role in the mediation of ischemic preconditioning. The present study is designed to determine whether NE is also involved in mediation of the protective effects of postconditioning. Methods The rat hearts were rapidly excised under anesthesia and attached to a Langendorff apparatus via the aorta for retrograde perfusion with Krebs-Henseleit buffer solution. All hearts were subjected to 30 min of left coronary artery occlusion followed by 60 min of reperfusion, except the control group. Animals were randomly divided into 5 groups as follows: ① control group, the hearts were underwent same procedures without ischemic insult; ② ischemia reperfusion group, the left coronary artery was occluded for 30 min and followed by 60 min of reperfusion; ③ ischemic postconditioning (IPost) group, immediately at the onset of reperfusion, the heart was initiated with 1 min of full coronary flow, followed by 1 min of re-occlusion, repeated for a total of three cycles; ④ IPost plus prazosin group, the heart was perfused with prazosin for 10 min before ischemia; ⑤ IPost plus reserpine group, a single dose of reserpine was administered by i.m. injection, 24 hours before the experiment. Coronary flow was measured by timed collection of coronary effluent and sample of coronary effluent at 5 min of reperfusion were collected for the measurement of creatine kinase (CK). Infarct size and risk area were determined at the end of experiments. Results 30 min of ischemia and followed by 60 min of reperfusion caused a significant decrease in cardiac function and a significant increase in CK release and infarct size. Postconditioning with three cycles of 1-min ischemia and 1-min reperfusion markedly improved cardiac function and reduced CK release and infarct size. However, the cardioprotection afforded by postconditioning was abolished by prazosin (10-6M), a selective α1 adrenergic receptor antagonist, or by pretreatment with reserpine (0.45 mg·kg-1), which significantly reduced NE level in both plasma and coronary effluent. Conclusions These results suggest that the protective effects of ischemic postconditioning are related to stimulation of endogenous NE release in rat hearts.
Previous studies have demonstrated that endogenous norepinephrine (NE) plays an important role in the mediation of ischemic preconditioning. The Present study is designed to determine whether NE is also involved in mediation of the protective effects of postconditioning. Methods The rat hearts were rapidly excised under anesthesia and attached to a Langendorff apparatus via the aorta for retrograde perfusion with Krebs-Henseleit buffer solution. All hearts were subjected to 30 min of left coronary artery occlusion followed by 60 min of reperfusion, except the control group. Animals were randomly divided into 5 groups of follows: ① control group, the hearts were underwent the same procedures without ischemic insult; ② ischemia reperfusion group, the left coronary artery was occluded for 30 min and followed by 60 min of reperfusion; ③ ischemic postconditioning (IPost) group, immediately at the onset of reperfusion, the heart was initiated with 1 min of full coronary flow, followed by 1 IPost plus prazosin group, the heart was perfused with prazosin for 10 min before ischemia; ⑤ IPost plus reserpine group, a single dose of reserpine was administered by im injection, 24 hours before the experiment. Coronary flow was measured by timed collection of coronary effluent and sample of coronary effluent at 5 min of reperfusion were collected for the measurement of creatine kinase (CK). Infarct size and risk area were determined at the end of experiments. Results 30 min of ischemia and followed by 60 min of reperfusion caused a significant decrease in cardiac function and a significant increase in CK release and infarct size. Postconditioning with three cycles of 1-min ischemia and 1-min reperfusion markedly improved cardiac function and reduced However, the cardioprotection afforded by postconditioning was abolished by prazosin (10-6M), a selective α1 adrenergic receptor antagoni st, or by pretreatment with reserpine (0.45 mg · kg-1), which significantly reduced NE level in both plasma and coronary effluent. Conclusions These results suggest that the protective effects of ischemic postconditioning are related to stimulation of endogenous NE release in rat hearts.