The protective effect of propofol on erythrocytes during cardiopulmonary bypass

Abstract

To evaluate the relationship between erythrocyte injury and intracellular calcium ion overload, and the protective effect of propofol on erythrocytes during cardiopulmonary bypass (CPB). 40 children with congenital heart diseases who underwent surgical repair under CPB were included. The patients were randomly divided into two groups: control group (group C) and propofol group (group P). Anesthesia was maintained in the patients with 6 mg/kg/h propofol in Group P, and those in the Group C inhaled 1%–2% isoflurane. The blood samples were taken before CPB, 30 min after CPB, at the end of CPB, and 2 h and 24 h after CPB to measure the content of erythrocyte intracellular calcium ion (E−Ca²⁺), Ca²⁺−Mg²⁺-ATPase and Na⁺−K⁺-ATPase activities, index filtration of erythrocytes (IF), mean corpuscular volume (MCV) and the concentration of plasma free hemoglobin (F−Hb). Results showed that in the control group, E−Ca²⁺, IF, MCV and F−Hb were gradually increased and Ca²⁺−Mg²⁺-ATPase and Na⁺−K⁺-ATPase activities were decreased. The increase of E−Ca²⁺ was linearly paralleled to IF, MCV and F−Hb. In propofol group, all the above-mentioned parameters were significantly improved (P<0.05). This study suggests that erythrocyte injury is related to elevation of intracellular calcium during CPB and propofol has a protective effect on erythrocyte injury.

Keywords

erythrocyte / cardiopulmonary bypass / propofol

References

[1] AbeH, KatadaK, OritaM, et al. . Effects of calcium antagonists on the erythrocyte membrane. J Pharm Pharmacol, 1991, 4322-26

[2] NakaeY, FujitaS, NamikiA. Propofol inhibits Ca²⁺ transients but not contraction in intact beating guinea pig hearts. Anaesth Analg, 2000, 901286-1286

[3] ShenM X, ShenW T, LinC, et al. . Simulataneous measurement of erythrocyte Ca²⁺, Mg²⁺—ATPase and Na⁺, K⁺-ATPase. J Shanghai Med Lab, 1990, 5211-211

[4] ReinhartW H, BallmarP E, RohnerF, et al. . The influence of extracorporeal circulation on erythrocytes and flow properties of blood. J Thorac Cardiovasc Surg, 1990, 100538-538

[5] TsienR W, TsienR Y. Calcium channels, stores, and oscillations. Ann Rev Cell Biol, 1990, 6715-715

[6] HalperinJ, BrugnaraC, TostesonM, et al. . Voltage-activated cation transportion human erythrocytes. Am J Physiol, 1991, 257C986-C986

[7] MurphyP G, BennettJ R, MeyersD S, et al. . The effect of propofol anaesthesia on free radical-induced lipid peroxidation in rat liver microsomes. Eur J Anaesthesiol, 1993, 10261-261

[8] StewartJ R, BlackwellW H, CruteS L, et al. . Inhibition of surgically induced ischemia/reperfusion injury by oxygen free radical scavengers. J Thorac Cardiovasc Surg, 1983, 86262-262

[9] CavarocchiN C, EnglandM D, SchaffH V, et al. . Oxygen free radical generation during cardiopulmonary bypass: correlation, with complement activation. Circulation, 1986, 74(suppl): III130-III130

[10] MurphyP G, MyersD S, DaviesM J, et al. . The antioxidant potential of propofol (2,6-diisopropylphenol). Br J Anaesth, 1992, 68613-613

[11] GreenT R, BennettS R, NelsonV M. Specificity and properties of propofol as an antioxidant free radical scavenger. Toxicol Appl Pharmacol, 1994, 129163-163

[12] MurphyP G, BennettJ R, MeyersD S, et al. . The effect of propofol anaesthesia on free radical-induced lipid peroxidation in rat liver microsomes. Eur J Anaesthesiol, 1993, 10261-261

[13] CookD J, HousmansP R. Mechanism of the negative inotropic effect of propofol in isolated ferret ventricular myocardium. Anesthesiology, 1994, 80859-859