ABSTRACT
Objective To investigate the effect of sepsis on vecuronium-induced inhibition of acetylcholine release in neuromuscular junction in rats.Methods Thirty-six adult male SPF SpragueDawley rats,aged 2-3 months,weighing 200-220 g,were randomly divided into 3 groups (n=12 each) using a random number table:control group (group C),sham operation group (group S) and sepsis group (group Sep).Sepsis was induced by cecum ligation and puncture (CLP) in rats anesthetized with intraperitoneal chloral hydrate 350 mg/kg.At 12 h after CLP,the sciatic nerve-pretibial muscle was prepared.Vecuronium was added to the culture medium with the final concentration of 0.08 μg/ml,and the sciatic nerve-pretibial muscle was incubated for 15 min.Before and after administration,evoked endplate potentials (EPPs) and miniature endplate potentiais (MEPPs) were recorded by using intracellular microelectrode.EPP/MEPP ratio was calculated.Results Compared to C and S groups,EPPs,MEPPs and EPP/MEPP ratio were significantly increased before and after administration in group Sep.EPPs,MEPPs and EPP/MEPP ratio were significantly lower after administration than before administration in the three groups.Conclusion Sepsis can promote acetylcholine release in neuromuscular junction,thus weakening vecuronium-induced inhibition of acetylcholine release in neuromuscular junction in rats.
ABSTRACT
Objective To evaluate the effects of unilastatin on brain injury in children undergoing aortic arch surgery under cardiopulmonary bypass (CPB).Methods Twenty ASA physical status Ⅲ or Ⅳ children of both sexes,aged 1-24 months,weighing 3-12 kg,undergoing repair of coarctation of aorta or interrupted aortic arch complicated with intracardiac malformations under CPB,were randomly divided into 2 groups (n =10 each):control group (group C) and ulinastatin group (group U).Ulinastatin 20 000 U/kg was diluted into 10 000 U/ml with normal saline and it was then injected intravenously in 3 parts (1/3 was injected via the internal jugular vein after induction of anesthesia; 1/3 at the beginning of CPB and 1/3 at 5 min before aortic unclamping).In group C the equal volume of normal saline was given instead of ulinastatin.Blood samples were taken from the radial artery after induction of anesthesia (T1),at 10 min after aortic clamping (T2),at 10 min after aortic unclamping (T3),at the end of CPB (T4),and at 6 and 24 h after termination of CPB (T5,T6) for determination of plasma S100B protein and neuron-specific enolase (NSE) concentrations.Results There was no significant difference in plasma levels of S100B protein and NSE at T1 between the two groups (P ＞ 0.05).Plasma S100B protein and NSE levels were significantly increased at T2-5 as compared to the baseline values at T1 in both groups (P ＜ 0.05).Plasma S100B protein and NSE levels were significantly lower at T2-5 in group U than in group C (P ＜ 0.05).Conclusion Ulinastatin can attenuate brain injury in children undergoing aortic arch surgery under CPB.