Objective      To investigate the protective effect of propofol postconditioning on myocardial ischemia-reperfusion (I/R) injury in renal hypertensive rats (RHR) and possible mechanism.       Methods      Renal hypertensive model was induced in adult male Sprague-Dawley (SD) rats with two-kidney one-clip method

and cardiac I/R injury was established by ligaturing left anterior descending (LAD) coronary artery for 30 min and then reperfusing for 60 min. Twenty-four RHR were randomly divided into 3 groups (n=8): I/R group

propofol group (P group) and propofol+atractyloside group (PA group). Normal saline 1.5 mL (I/R group)

propofol 2 mg/kg (P group)

and propofol 2 mg/kg and atractyloside 5 mg/kg (PA group) were intravenously infused at the beginning of reperfusion (propofol and atractyloside diluted to 1.5 mL with normal saline equally). Systolic blood pressure (SBP)

diastolic blood pressure (DBP) and heart rate (HR) were recorded before ligaturing LAD coronary artery (T0)

at 15 min (T1) and 30 min (T2) after ligaturing LAD coronary artery

and at 15 min (T3)

30 min (T4) and 60 min (T5) of reperfusion

respectively. Morphologic change of myocardial cells was observed with an electron microscope at 60 min of reperfusion. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay at 60 min of reperfusion.       Results      SBP and DBP of the P group were higher than those of the PA group and I/R group (P0.05) at T3 and T4. Microscopic observation showed the majority of myocardial cells were intact and mitochondria were moderately swollen at 60 min of reperfusion in the P group. The I/R group and PA group showed obvious mitochondrial swelling

disorganized cristae

and vacuolation at 60 min of reperfusion. The apoptosis index [(16±4)%] of myocardial cells in the P group was decreased compared with that [(48±5)%] of the I/R group and that [(38±8)%] of the PA group (P0.05).       Conclusion      Propofol postconditioning effectively protects the RHR against I/R injury by inhibition of mitochondrial permeability transition pore during the early reperfusion.