Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats

Figure 1

Effects of propofol conditioning on endocannabinoid release in vivo. (a) Serum AEA concentrations among groups. (b) Serum 2-AG concentrations among groups. In the rat myocardial ischemia/reperfusion (I/R) injury model, propofol conditioning was achieved by an intravenous bolus of 10 mg/kg followed by continuous infusion at a rate of 39 mg/kg·h from one hour before ischemia until the end of ischemia. Peripheral blood was collected at 10 minutes after the beginning of propofol conditioning and at 0, 1, 2, and 4 hours after ischemia. Endocannabinoids including AEA and 2-AG were detected by LC/LC-MS. The results showed that propofol conditioning and I/R enhanced cardiac endocannabinoid release in vivo. per group for each time point. : ; : versus sham. ; ##: versus propofol. †: versus I/R. ; ‡‡: versus baseline. &: ; &&: versus 10 mins after the beginning of propofol exposure. §: ; §§: versus the end of ischemia. ; ¶¶: versus 1 hr after ischemia. ; ££: versus 2 hr after ischemia. I/R, ischemia/reperfusion.

(a) Serum AEA

(b) Serum 2-AG