Objective To evaluate the effect of morphine on synaptic long-term potentiation (LTP) in the spinal dorsal horn evoked by electric stimulation of sciatic nerve in rats. Methods Twenty-seven healthy male SD rats aged 60-90 d weighing 180-200 g were randomly divided into 4 groups: group Ⅰ control (group C, n=7), group Ⅱ morphine (group M, n=7), group Ⅲ naloxone (group N, n=6), and group Ⅳ morphine + naloxone (group MN, n=7). The animals were anesthetized with intraperitoneal 10% urethane 1 g/kg, intubated and then mechanically ventilated. The bipolar insulated stainless steel recording electrode (impedance 0.5-1 MΩ, diameter 0.1 mm) was inserted into the left side of the spinal dorsal horn at T13-L1 to stimulate the left side of the sciatic nerve. Single square pulses (15 V, 0.5 ms, 1/60 Hz for 30 min) was applied to evoke spinal field potentials. Normal saline 10 μl, morphine 10 μl (15 μg/μl), naloxone 10 μl (2.5 μg/μl), and the mixture 10 μl of naloxone 5 μl (2.5 μg/μl) and morphine 5 μl (15 μg/μl) was gradually instilled over 2 rain in the 4 groups respectively. Five minutes later, high-frequency and intensity tetanic stimulation (30-40 V, 0.5 ms, 100 Hz, given in 4 trains of 1-s duration at 10-s intervals) was used to induce LTP. Then single square stimuli (15 V, 5 ms, 1/60 Hz) were applied to the sciatic nerve for 210 min. The amplitude and latency period of the field potential were recorded 30 min before tetanic stimulation, and 0-30, 35-60, 65-120 and 125-210 min after titanic stimulation. Results Compared with group C, the amplitude of the field potential was significantly decreased and the latency period prolonged in group M and MN, but there was no significant difference in the above indices between group N and C. Compared with group M, the amplitude of the field potential was significantly increased and the latency period shortened in group MN. Compared with those 30 min before the tetanic stimulation, the amplitude of the field potential was significantly increased and latency period shorted at the time points after the tetanie stimulation in group C and N, the amplitude of the field potential was significantly decreased and latency period prolonged at the time points after the tetanie stimulation in group M, and the amplitude of the field potential was significantly increased 0-30 and 35-60 min after the tetanic stimulation and latency period shortened 0-30 min after the tetanie stimulation, the amplitude of the field potential was significantly decreased and latency period prolonged 65-120 and 125-210 min after the tetanic stimulation in group MN. Conclusion Morphine can inhibit synaptic LTP in the spinal dorsal horn evoked by electric stimulation of sciatic nerve in rats, and it may be one of the mechanisms of the central sensitization inhibition.

Objective To investigate the effect of 20‐HETE on the isolated myocardial ischemia reperfusion injury and to ex‐plore its underlying mechanisms .Methods Experiments were performed in isolated rat hearts subjected to 35 min of ischemia fol‐lowed by 40 min of reperfusion in Langendorff preparations .HET0016 (1 μmol/L) and various concentrations (10 ,30 or 50 nmol/L) of 20‐HETE were infused 10 min before the onset of ischemia and throughout the reperfusion period .Cardiac hemodynamic changes and myocardial contractility were continuously recorded with the Powerlab /8P system .Myocardial infarct size was meas‐ured by TTC staining .The level of ROS and the protein carbonyl content were determined by DHE fuorescence and DNPH method , respectively .Results Perfusion with HET0016 significantly improved myocardial ischemia reperfusion injury reduction in cardiac contractility ,after inhibited the production of 20‐HETE significantly reduced the occurrence of myocardial infarction area (P<0 .05) ,but exogenous join 20‐HETE aggravated I/R‐induced myocardial injury (P<0 .05) .Myocardial ischemia reperfusion injury significantly increased production of ROS and oxidative stress ,both of which were significantly inhibited by HET 0016 and enhanced by 20‐HETE administration(P< 0 .05) .Conclusion 20‐HETE stimulates ROS production and enhance protein carbonylation , which aggravates myocardial ischemia reperfusion injury .

ObjectiveTo investigate the role of heme oxygenase-1 (HO-1 ) in process of sevoflurane preconditioning attenuating hypoxia-reoxygenation (H/R) injury in cultured neonatal rat cardiomyocytes.Methods Primary cultured neonatal rat cardiomyocytes were randomly divided into four groups ( n ＝ 25 each):control group (group C),group H/R,sevoflurane preconditioning group(group S + H/R),and HO-1 inhibitor zinc protoporphyria (ZnPP) and sevoflurane preconditioning group(group ZnPP + S + H/R).In group H/R,the cardiomyocytes were exposed to 2 hours of hypoxia,followed by 1 hour of reoxygenation.Group S+ H/R received 2.5％ sevoflurane preconditioning for 20 minutes followed by 10 minutes of wash-out before H/R.ZnPP was added to the culture medium with final concentrations of 3 μMol/L 1 hour before sevoflurane preconditioning and H/R in group ZnPP +S + H/R.HO- 1 expression,apoptosis rate,concentration of free calcium ( [ Ca2 + ] i),mitochondrial membrane permeability transition pore (PTP),cytoohrome C ( Cyto C) expression and activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in culture supernatant were detected after reoxygenation.ResultsCompared with group C,the expression of HO-1 and cytoplasmic Cyto C of cardiomyocytes were up-regulated,mitochondrial Cyto C was down-regulated,while the [Ca2+ ]i,opening degree of PIP,apoptosis rate and activities of LDH and CK in culture supernatant were increased in group H/R.Compared with group H/R,the expression of HO-1 and mitochondrial Cyto C of cardiomyocytes were up-regulated,cytoplasmic Cyto C was down-regulated,while the [Ca2+ ] i,opening degree of PTP,apoptosis rate and activities of LDH and CK in culture supernatant were decreased in group S + H/R.Compared with group S + H/R,the expression of HO-1 and mitochondrial Cyto C of cardiomyocytes were down-regulated,cytoplasmic Cyto C was up-regulated,while the [Ca2+ ]i,opening degree of PTP,apoptosis rate and activities of LDH and CK in culture supematant were increased in group ZnPP + S + H/R.ConclusionThe up-regulation of HO-1 is involved in the process of sevoflurane preconditioning attenuating hypoxia-reoxygenation injury in cultured neonatal rat cardiomyocytes.

Objective To compare the effects of different doses of propofol on cardiac pump function in morbidly obese patients. Methods Forty morbidly obese patients undergoing laparoscopic Roux-en-Y gastric by-pass were randomly divided into lean body weight(LBW)group and total body weight(TBW)group,with 20 cases in each group.In LBW group,patients were induced by propofol with a dose according to LBW(kg)×2.0 mg/kg but in TBW group,patients were induced by propofol depending on TBW of the patients.We monitored the changes of left ventricular ejection fraction(LVEF)and stroke volume(SV)in patients before anesthetic induction(T1)and at 1 min(T2)after propofol administration.At the same time,we monitored invasive arterial pressure,noninvasive arterial pressure,BIS,and SpO2.Results Compared with those measured at T1,LVEF and SV were decreased af-ter the induction of anesthesia in the 2 groups(P < 0.05);compared with LBW,TBW had greater influence on LVEF and SV after the induction of anesthesia(P<0.05);compared with those at T1,non invasive arterial blood pressure,invasive arterial blood pressure and mean arterial pressure decreased after theinduction of anesthesia (P<0.05);compared with LBW,TBW had no significant effect on noninvasive arterial blood pressure,invasive arterial blood pressure and mean arterial pressure after the induction of anesthesia(P < 0.05);BIS was less than 50 after the induction of anesthesia in 2 groups. Conclusion Propofol induction with a LBW-dependent dose has less influence on cardiac pump function in morbidly obese patients while ensuring the depth of anesthesia.