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

Figure 6

Effects of CB1R and CB2R signaling on propofol-induced cardioprotection in vivo. (a) Representative figures of cardiac ventricle slices showing myocardium infarct size among groups. (b) Histograms showing the relative infarct size among groups. Propofol was perfused from 1.5 hours before ischemia until the end of ischemia. Selective CB1R antagonist AM251 (1 mg/kg) or selective CB2R antagonist AM630 (1 mg/kg) was injected intravenously 30 minutes before propofol exposure. Infarct size was detected using TTC staining after 24-hour reperfusion. The results showed that propofol and AM251 pretreatment could reduce infarct size compared with pure ischemia/reperfusion. Pretreatment with AM630 fully antagonized the effects of propofol conditioning. (c) Histograms showing serum cTnI concentrations among groups. Propofol tended to reduce cardiac cTnI release at hours after ischemia, and selective CB2R antagonist AM630 (1 mg/kg) reversed the effect of propofol. per group. : versus sham. ##: versus I/R. ††: versus propofol + I/R. ‡‡: versus AM251 + I/R. §§: versus AM251 + propofol + I/R.

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(c) Serum cTnl