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Objective To study the median effective doses (ED50) of dexmedetomidine to induce adequate sedation in elderly patients undergoing epidural anaesthesia. Methods Seventy-five elderly patients undergoing lower extremity operation under epidural anesthesia were selected, and the patients were divided into 5 groups according to the random digits table method with 15 cases each: D1 group (dexmedetomidine 0.2 μg/kg), D2 group (dexmedetomidine 0.4 μg/kg), D3 group (dexmedetomidine 0.6 μg/kg), D4 group (dexmedetomidine 0.8μg/kg) and D5 group (dexmedetomidine 1.0μg/kg). After 20 min of dexmedetomidine injection, adequate sedation was defines as observer′s assessment of alertness/sedation score (OAA/S score) ≤ 3 scores. The ED50 and 95% effective dose (ED95) of dexmedetomidine and 95% CI in elderly patients undergoing epidural anaesthesia were calculated by probit regression method. The changes of mean arterial pressure (MAP), heart rate, pulse oxygen saturation (SpO2) and OAA/S score among 5 groups were compared. The incidences of adverse effects such as hypotension, bradycardia, hypoxemia and excessive sedation were compared. Results The ED50 in elderly patients was 0.36 μg/kg (95% CI 0.27 - 0.44 μg/kg); the ED95 was 0.94 μg/kg (95% CI 0.71 - 1.62 μg/kg). After dexmedetomidine injection, the MBP, heart rate, SpO2 and OAA/S scores in 5 groups were decreased, but in the D4 group and D5 group the decreases were more significant. The incidences of hypotension, bradycardia and excessive sedation in D1 group, D2 group and D3 group were significantly lower than those in D4 group and D5 group:2/15, 5/15 and 8/15 vs. 14/15 and 15/15;1/15, 6/15, 7/15 vs. 13/15 and 14/15;0, 0 and 1/15 vs. 5/15 and 7/15, the incidences of hypoxemia in D1 group, D2 group and D3 group were significantly lower than those in D5 group: 0, 0 and 0 vs. 3/15 and 4/15, and there were statistical differences (P0.05). Conclusions The ED50 of dexmedetomidine in elderly patients undergoing epidural anaesthesia is 0.36μg/kg, (CI 0.27-0.44μg/kg). The incidences of adverse effects are increased when single-dose dexmedetomidine is more than 0.8μg/kg.
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Objective To investigate the effects of butorphanol pretreatment on myocardial injury induced by limb ischemia/reperfusion.Methods Forty patients with distal lower extremity orthopedic surgery (ASA Ⅰ or Ⅱ) were divided into two groups by random digits table method with 20 cases each:butorphanol group and control group.Epidural anesthesia was selected in all patients.In butorphanol group,patients were given butorphanol 0.04 mg/kg intravenously 15 min before tourniquet.In control group,equal volume of normal saline was infused at the same time.Blood samples were taken from jugular vein before tourniquet (T0),then 5 min(T1),2 h (T2),6 h (T3),12 h (T4) and 24 h (T5) after the second reperfusion of tourniquet.The serum creatine kinase isoenzyme MB (CK-MB),cardiac troponin Ⅰ (cTnI),tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) levels were determined.Results Compared with those at T0,the serum C K-MB levels were increased at T2-T5,the serum cTnI,MDA,TNF-α levels were increased at T1-T5 in control group,and there were significant differences (P ＜ 0.05).Compared with those at T0,the serum CK-MB levels were increased at T3,T4,the serum TNF-α levels were increased at T1-T3,the serum cTnI levels were increased at T1-T5 in butorphanol group,and there were significant differences (P ＜ 0.05).Compared with those in control group,the serum CK-MB levels were decreased at T2-T5 [(20.2 ± 5.0) U/L vs.(35.3 ±6.8) U/L,(32.3 ±3.7) U/L vs.(48.6 ±8.5) U/L,(29.5 ±5.4) U/L vs.(51.5 ±8.0) U/L,(22.2 ±4.8) U/L vs.(33.7 ±6.7) U/L],the serum cTnI,TNF-α levels were decreased at T1-T5 [(0.158 ± 0.016) μg/L vs.(0.278 ±0.021) μg/L,(0.169 ±0.036) μg/L vs.(0.332 ± 0.062) μg/L,(0.357 ±0.049) μg/L vs.(0.623 ±0.083) μg/L,(0.178 ±0.045) μg/L vs.(0.383 ±0.059) μg/L,(0.138 ±0.016) μg/L vs.(0.263 ±0.023) μg/L; (1.63 ±0.13) μg/L vs.(2.12 ±0.08) μg/L,(1.69 ± 0.08) μ g/L vs.(2.28 ± 0.09) μ g/L,(1.63 ± 0.09) μ g/L vs.(2.25 ± 0.07) μ g/L,(1.23 ± 0.14) μμg/Lvs.(1.93±0.12) μg/L,(1.13±0.15) μμg/Lvs.(1.79±0.07) μμg/L],theserumMDAlevelswere decreased at T1-T4 [(4.82 ±0.53) nmol/L vs.(6.68 ±0.67) nmol/L,(4.99 ±0.61) nmol/L vs.(7.59 ±0.72) nmol/L,(5.02 ±0.43) nmol/L vs.(7.54 ±0.63) nmol/L,(4.52 ±0.55) nmol/L vs.(6.52 ±0.47) nmol/L] in butorphanol group,and there were significant differences (P ＜0.05).Conclusion Butorphanol pretreatment can improve the serum CK-MB,cTnI levels,and has a protective role for myocardial injury induced by limb ischemia/reperfusion.
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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.
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Objective To investigate the effect of curcumin on apoptosis in hippocampal neurons and the expression of c-Jun N-terminal kinase 3 (JNK3) and postsynaptic density protein 95 (PSD95) in hippocampus during cerebral ischemia-reperfusion (I/R) in rats with spontaneous hypertension (SH) .Methods One hundred and thirty-five male rats (homologous with WKY) with SH and 90 male normotensive WKY rats, weighing 275-325 g,were used in this study. The WKY rats were randomized into 2 groups ( n = 45 each) : sham operation group (WS group) and cerebral I/R group (W-I/R group) . The rats with SH were randomly divided into 3 groups ( n = 45each) : sham operation group (S-S group), cerebral I/R group (S-I/R group) and curcumin group (S-C group) .Global cerebral ischemia was produced by 4 vessel-occlusion method. The bilateral common carotid arteries were only exposed but not ligated in W-S and S-S groups. Intraperitoneal corn oil 10 ml/kg was injected at 30 min of reperfusion in W-I/R and S-I/R groups. Intraperitoneal curcumin 100 mg/kg was injected at 30 min of reperfusion in S-C group. Three animals in each group were sacrificed at 2 h, 6 h, 1 d, 3 d and 7 d of reperfusion and their brains were harvested for determination of apoptosis in hippocampal neurons and the expression of JNK3 and PSD95in hippocampus. Results The number of apoptotic neurons was significantly increased in S-S group compared with W-S group ( P < 0.05) . The number of apoptotic neurons was significantly increased and the expression of JNK3was up-regulated in S-I/R group compared with S-S group ( P < 0.05) . The number of apoptotic neurons was significantly decreased and the expression of JNK3 was down-regulated in S-C group compared with S-I/R group (P <0.05) . There was no significant difference in the expression of PSD95 among all the groups ( P > 0.05) . Conclusion Curcumin can inhibit apoptosis in hippocampal neurons and the mechanism is related to down-regulation of the expression of JNK3 in hippocampus. The mechanism by which curcumin down-regulates the expression of JNK3in hippocampus may not be related to PSD95 pathway.