Effects Of Propofol On Calcium Homeostasis Of Rabbit Hearts Subjected To Ischemia-Reperfusion

Objective To study the effect of propofol on calcium homeostasis of rabbit hearts subjected to ischemia-reperfusion under the protection of cardioplegic solution. Material and methods 24 Newzealand rabbits were anaesthesized with thiopental. Hearts were isolated and perfused by Langendorff technique. Hearts were divided into four groups(n=6): Hearts in group C were perfused with K-H buffer which were saturated with oxygen and were beating for 90 minutes. Hearts in group I, P and PH group were experienced global ischemia for 60 minutes under the protection of cardioplegic solution and than reperfused for 30minutes. The K-H buffer in group P and group PH cotained propofol 50 ii M and 200 t M. At the end of perfusion, used electron microscope to observe the change of mitochondrial structure and isolated heart mitochondria then used fura2-AM as the indicator of matrix concentration of calcium([Ca Im) to measure [Ca2+]m, [Ca2+]m when mitochondria was in high calcium concentration liquid and in high sodium concentration liquid. The content of malondia(MDA) in heart mitochondria were measured by the method of thiobarbituric acid( TBA). Using phosphorum titration method to measure the activity of Ca-ATPase in heart mitochondria. Results [Ca2+]m in group I, group P and group PH were significantly higher than that in group C. There is no significant difference among the three groups. The ability of uptaking calcium among four groups had no significant difference but the mitochondria in group I, P and PH released more calcium than that in group C under the induction of sodium. Propofol under two concentration had no effect on mitochondria calcium homeostasis. In group I, P and PH, damage mitochondria could be seen by electron microscope . Mitochondria in group I were damaged most severily in three groups. There were higher content of MDA in the mitochondria of group I, P and PH than that of group C. But MDA in the mitochondria of group P and group PH were lower than that in group I. The activity of Ca-ATPase of mitochondria in three groups were lower than group C but there was no difference among three groups. Conclusion Propofol can relieve the mitochondrial permeability transition pore opening at reperfusion stage at clinic concentration. But the mechanism is not through inhibit mitochondrial calcium overload, probably as a result of diminished oxidative stress.