ABSTRACT
Objective To evaluate the effects of butorphanol pretreatment on myocardial damage induced by limb ischemia/reperfusion (I/R) in rats.Methods One hundred and eight male Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 3 groups (n =36 each) using a random number table:sham operation group (group S),I/R group and butorphanol pretreatment group (group B).Limb ischemia was induced by occlusion of bilateral hind limbs for 2 h followed by reperfusion in I/R and B groups.At 10 min before ischemia,butorphanol 0.2 mg/kg was injected via the right jugular vein in group B,while the equal volume of normal saline was injected in group I/R.Six rats were chosen randomly before ischemia (baseline,T0) and at 2,6,12,24 and 48 h after reperfusion (T1-5) and blood samples were taken from the abdominal aorta for determination of the serum creatine kinase isoenzyme-MB (CK-MB) activity and cardiac troponin Ⅰ (cTnI) concentration.The animals were then sacrificed and myocardial specimens were obtained for determination of myocardial apoptosis (using TUNEL) and the expression of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated protein kinase (ERK) (using Western blot analysis).Apoptosis index was calculated.Results Compared with group S,the serum CK-MB and cTnI levels were significantly increased at T1-5,and the apoptosis index and expression of JNK and ERK were increased at T2-5 in group I/R (P ＜ 0.05).Compared with group I/R,the pathological changes of myocardium were significantly reduced at T4,the serum CK-MB and cTnI levels were decreased at T2-5,the apoptosis index was decreased at T4,5,the expression of ERK was up-regulated at T2-5,and the expression of JNK was down-regulated at T2-4 (P ＜ 0.05).Conclusion Butorphanol pretreatment can reduce apoptosis in myocardial cells through activating MAPK signal transduction pathway,up-regulating ERK expression and down-regulating JNK expression,thus attenuating myocardial damage induced by limb I/R in rats.
ABSTRACT
Objective To evaluated the acccuracy of the two quantitative electroencephalographic parameters-bispectral index (BIS) and 95% specrral edge frequency (95% SEF) for measuring the depth of sedation induced by propofol, midazolam and ketamine. Methods Forty-five ASA Ⅰ - Ⅱ patients aged 30-59 yr weighing 46-80 kg scheduled for elective general thoracic or abdominal surgery were randomized to receive an infusion of propofol at a rate of 8 mg?kg-1?h-1 (group P , n = 15) or midazolam at 0.5 mg?kg-1?h-1 (group M, n = 15) or ketamine at 4 mg?kg-1? h-1 (group K, n = 15) . The patients were unpremedicated. The depth of sedation was assessed using OAAS scale (5 = wide awake , 1 = no response to prodding or shaking ) at 3 min intervals. BIS and 95 % SEF were continuously monitored. The BIS and 95% SEF values at each OAAS score (5-1) were recorded. The relations between BIS, 95 % SEF and sedation scores were determined in each group. The ED50 values of BIS and 95% SEF50 for loss of consciousness and their 95% confidence internals were calculated. Prediction probability(Pk) values for BIS and 95% SEF were compared among the drugs. Results There were no significant differences among the 3 groups with respect to age, body weight, sex and duration of drug infusion. With increasing sedation there was a progressive decrease in BIS and 95 % SEF values in group P and M but no significant changes in BIS and 95 % SEF values were seen in group K. The BIS and 95 % SEF positively correlated with OAAS score in group P and M but not in group K. The BIS50 was 65.9 in group P and 70.7 in group M,but inestimable in group K.The 95% SEF50 was 20.4 in group P and inestimable in group M and K. The Pk values for BIS and 95 % SEF were higher in P group than in M group and were not significantly different from 0.5 indicating a very poor predictive performance . Conclusion The accuracy of BIS and 95 % SEF for assessing the depth of sedation is greater with propofol. BIS is more sensitive than 95% SEF for the same anesthesia.