Effect of ulinastatin pretreatment on endoplasmic reticulum stress during myocardial injury in patients undergoing mitral valve replacement with cardiopulmonary bypass / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of ulinastatin pretreatment on endoplasmic reticulum stress during myocardial injury in the patients undergoing mitral valve replacement (MVR) with cardiopulmonary bypass (CPB).Methods One hundred patients of both sexes,aged 35-64 yr,weighing 40-80 kg,of American Society of Anesthesiologists physical status Ⅱ or Ⅲ (New York Heart Association Ⅱ or Ⅲ),scheduled for elective MVR with CPB,were divided into ulinastatin pretreatment group (UP group,n=50) and normal saline control group (NS group,n =50) using a random number table.Ulinastatin 0.5× 104 U/kg was intravenously infused over 1 h before skin incision,and administration was repeated every 4 h until the end of operation in group UP,while the equal volume of normal saline was given instead in group NS.Immediately after opening the right atrium (T0),at 30 min after aortic clamping (T1) and while suturing the right atrium (T2),blood samples were collected from the radial artery for measurement of the concentrations of plasma creatine kinase-MB and cardiac troponin T by enzyme-linked immunosorbent assay.Right auricle specimens were obtained after blood sampling at each time point for determination of the expression of glucose-regulated protein 78,CCAAT/enhancer-binding protein homologous protein and c-Jun N-terminal kinase protein and mRNA (by real-time polymerase chain reaction and Western blot,respectively) and apoptosis in cardiomyocytes (by TUNEL).The apoptosis rate was calculated.Results Compared with group NS,the plasma concentrations of creatine kinase-MB and cardiac troponin T at T1 and T2 and apoptosis rate at T2 were significantly decreased,and the expression of glucose-regulated protein 78,CCAAT/enhancer-binding protein homologous protein and c-Jun N-terminal kinase protein and mRNA was down-regulated at T1 and T2 in group UP (P＜0.05).Conclusion The mechanism by which ulinastatin pretreatment inhibits apoptosis in cardiomyocytes and attenuates myocardial injury is related to decrease in endoplasmic reticulum stress in the patients undergoing MVR with CPB.