Effects of glycyrrhizin on mitochondrial ATPase and membrane fluidity in canine brain following cardiac arrest and resuscitation / 中华麻醉学杂志

ABSTRACT

Objective To study the effects of glycyrrhizin on cerebral mitochondrial ATPase and membrane fluidity and malondialdehyde (MDA) and water content and brain function after cardiac arrest and resuscitation.Methods Eighteen dogs weighing 10-14 kg were randomly divided into 3 groups ( n = 6 each) group A control; group B cardiac arrest and resuscitation and group C glycyrrhizin + cardiac arrest and resuscitation. The animals were anesthetized with fentanyl, intubated and mechanically ventilated and PaCO2 was maintained within normal range. The chest was opened. In group B and C cardiac arrest was produced by clamping of ascending aorta and coronary perfusion with hyperkalemic cardioplegic solution and maintained for 18 min and resuscitated by direct cardiac massage, adrenaline and defibrillation. The animals were observed for 8 h after spontaneous cardiac rhythm resumed. In group C glycyrrhizin injectio 40 ml?kg-1 was infused over 8 h as soon as spontaneous cardiac rhythm resumed. Brain function was evaluated according to Pittsburgh Brain stem score (PBSS). The animals were then killed and their brains removed for determination of (1) mitochondrial membrane fluidity and Na+-K+-ATPase and Mg2+ -ATPase activity and (2) brain MDA and water content.Results The mitochondrial membrane viscosity and cerebral MDA and water content were significantly higher and ATPase activity was significantly lower in group B (cardiac arrest) than in group A (control) . Brain function was also impaired by global cerebral ischemia-reperfusion (I/R) in group B. In group C glycyrrhizin infusion significantly attenuated the deleterious effects of cerebral I/R by reducing mitochondrial membrane viscosity and cerebral MDA and water content and increasing ATPase activity. Glycyrrhizin infusion also improved brain function.Conclusion Glycyrrhizin can ameliorate the deleterious effects of global cerebral I/R induced by cardiac arrest.