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Objective To evaluate the role of the angiotensin Ⅱ type 2 receptor (AT2R) in repeated propofol anesthesia-induced neuroapoptosis in the basal ganglia of newborn rats.Methods Fiftyfour pathogen-free Sprague-Dawley rats,aged 7 days,weighing 10-15 g,were divided into 3 groups (n=18 each) using a random number table:control group (group C),repeated propofol anesthesia group (group P) and AT2R agonist CGP42112A group (group G).In group C,0.9％ sodium chloride injection 3 ml/kg was intraperitoneally injected,and half of the initial dose 1.5 ml/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group P,propofol 30 mg/kg was intraperitoneally injected,and half of the initial dose 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group G,CGP42112A 1 mg/kg was intraperitoneally injected,propofol 30 mg/kg was intraperitoneally injected 5 min later,and half of the initial dose of propofol 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.Six rats were sacrificed at 2 h after emergence from anesthesia,and brains were removed for detection of neuroapoptosis in the basal ganglia by TUNEL assay.The apoptosis index was calculated.Another 6 rats were sacrificed,and the basal ganglia were isolated from brains to detect the expression of activated caspase-3,AT2R and peroxisome proliferator-activated receptor gamma (PPARγ) (by Western blot) and the expression of AT2R and PPARγ mRNA (by real-time polymerase chain reaction).The other 6 rats were fed until 28 days old,and the cognitive function was then assessed using Morris water maze test.Results Compared with group C,the escape latency was significantly prolonged,the time of staying at the target quadrant was shortened,the frequency of crossing the platform was decreased,the apoptosis index of the basal ganglia was increased,the expression of activated caspase-3 was up-regulated,and the expression of AT2R and PPARγprotein and mRNA was down-regulated in group P (P＜0.05),and no significant change was found in the parameters mentioned above in group G (P＞0.05).Compared with group P,the escape latency was significantly shortened,the time of staying at the target quadrant was prolonged,the frequency of crossing the platform was increased,the apoptosis index of the basal ganglia was decreased,the expression of activated caspase-3 was down-regulated,and the expression of AT2R and PPARγ protein and mRNA was up-regulated in group G (P＜0.05).Conclusion Inhibited activation of AT2R is involved in repeated propofol anesthesia-induced neuroapoptosis in the basal ganglia of newborn rats.
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Objective To evaluate the role of δ-opioid receptors in hydromorphone postcondition-ing-induced maintenance of electrophysiological stability during ischemia-reperfusion(I∕R)in isolated rat hearts. Methods Healthy male Sprague-Dawley rats, aged 2-3 months, weighing 280-360 g, were used in this study. The animals were anesthetized with intraperitoneal pentobarbital 60 mg∕kg. Their hearts were immediately removed and perfused in a Langendorff apparatus. Thirty-two isolated hearts were divided into 4 groups after successful preparation of Langendorff perfusion model(n=8 each)using a random number ta-ble: control group(group C), group I∕R, hydromorphone postconditioning group(group HP)and hydro-morphone plus δ-opioid receptor antagonist naltridole postconditioning group(group HNP). In HP and HNP groups, the hearts were perfused for 10 min with K-H solution containing 41 ng∕ml hydromorphone and 41 ng∕ml hydromorphone plus 5 μmol∕L naltridole, respectively, and then with K-H solution for 50 min. At 20 min of stabilization(T0)and 10, 25 and 60 min of reperfusion(T1-2), heart rate(HR), monophasic action potential(MAP)duration at 90% repolarization(MAPD90)of the two layers(endocar-dium, epicardium)of the anterior left ventricular wall were recorded. Transmural dispersion of repolariza-tion(TDR)was calculated. The development of arrhythmia, time for restoration of spontaneous heart beat and duration of arrhythmia were recorded during the period of reperfusion. Results Compared with group C, MAPD90of endocardium at T1-2and MAPD90of epicardium at T1were significantly prolonged in I∕R and HP groups, HR was significantly decreased at T2-3, MAPD90of endocardium and epicardium was prolonged at T1-3in group HNP, TDR was significantly enlarged at T1in group I∕R and at T2in group HNP, and TDR was decreased at T3in group HP(P<005). Compared with group I∕R, no significant change was found in arrhythmia score(P>005), the time for restoration of spontaneous heart beat was significantly shortened, and TDR was decreased at T1in HP and HNP groups, duration of arrhythmia was significantly shortened, and MAPD90of endocardium was shortened at T1in group HP, and HR was significantly decreased at T2-3, MAPD90of endocardium and epicardium was prolonged at T1-3, and TDR was decreased at T2-3in group HNP(P<005). Compared with group HP, no significant change was found in time for restoration of spon-taneous heart beat, duration of arrhythmia or arrhythmia score(P>005), HR was significantly decreased at T2-3, MAPD90of endocardium and epicardium was prolonged at T1-3, and TDR was increased at T3in group HNP(P<005). Conclusion The mechanism underlying hydromorphone postconditioning-induced maintenance of electrophysiological stability during I∕R is related to activating δ-opioid receptors in isolated rat hearts.
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Objective To evaluate the effect of hydromorphone postconditioning on the electrophysiological stability during ischemia-reperfusion (I/R) in isolated rat hearts.Methods Healthy adult male Sprague-Dawley rats,aged 2-3 months,weighing 280-360 g,were heparinized and anesthetized with pentobarbital sodium.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.Twenty-four Langendorff-perfused hearts were divided into 3 groups (n =8 each) using a random number table:control group (group C),I/R group and hydromorphone postconditioning group (group HM).The isolated hearts were subjected to 60 min ischemia followed by 60 min reperfusion to establish the model of isolated heart I/R injury.The isolated hearts were perfused with K-H solution containing 4.1 ng/ml hydromorphone for 10 min starting from onset of reperfusion in group HM.Heart rate,electrocardiogram,coronary flow,and monophasic action potential amplitude,in the left ventricular endocardium,mid-myocardium and epicardium the maximal increase rate (Vmax) at the 0 phase,and monophasic action potential duration at 50％ and 90％ repolarization (MAPD50 and MAPD90,respectively) were recorded at 20 min of stabilization (T0) and 10,25,40 and 60 min of reperfusion (T1-4).The transmural dispersion of repolarization (TDR) was calculated,and the time for restoratiou of spontaneous heart beat was recorded.Results There was no significant difference in the heart rate,coronary flow or monophasic action potential amplitude between the three groups (P＞0.05).Compared with group C,V in the epieardium was significantly decreased,MAPD50 and MAPD90 in the three transmural layers were prolonged,and TDR was prolonged in group I/R (P＜0.05).Compared with group I/R,the time for restoration of spontaneous heart beat,MAPD50 in the endoeardium and mid-myocardium,and MAPD90 and TDR in the endocardium were significantly shortened (P＜0.05),and no significant change was found in V in group HM (P＞0.05).Conclusion Hydromorphone postconditioning is helpful in maintaining the electrophysiological stability during I/R in isolated rat hearts.
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Objective To evaluate the role of the angiotensin Ⅱ type 2 receptor (AT2R) in repeated propofol anesthesia-induced neuroapoptosis in the hippocampus of newborn rats.Methods Fiftyfour pathogen-free Sprague-Dawley rats,aged 7 days,weighing 10-15 g,were divided into 3 groups (n=18 each) using a random number table:control group (group C),repeated propofol anesthesia group (group P) and AT2R agouist CGP42112A group (group G).In group C,0.9％ sodium chloride injection 3 ml/kg was intraperitoneally injected,and half of the initial dose 1.5 ml/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group P,propofol 30 mg/kg was intraperitoneally injected,and half of the initial dose 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group G,a single bolus of CGP42112A 1 mg/kg was intraperitoneally injected,propofol 30 mg/kg was intraperitoneally injected 5 min later,and half of the initial dose of propofol 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.At 2 h after emergence from anesthesia,6 rats were sacrificed and brains were removed for detection of neuroapoptosis in the hippocampus by TUNEL assay.The apoptosis index was calculated.Another 6 rats were sacrificed,brains were removed and hippocampi were isolated for determination of the expression of activated caspase-3,AT2R and peroxisome proliferator-activated receptor gamma (PPARγ) in hippocampal tissues by Western blot.The other 6 rats were fed until 28 days old,and the cognitive function was then assessed using Morris water maze test.Results Compared with group C,the escape latency was significantly prolonged,the time of staying at the target quadrant was shortened,the frequency of crossing the platform was decreased,the apoptosis index was increased,the expression of activated caspase-3 was up-regulated,and the expression of AT2R and PPARγ was down-regulated in group P (P＜0.05),and no significant change was found in the parameters mentioned above in group G (P＞0.05).Compared with group P,the escape latency was significantly shortened.the time of staying at the target quadrant was prolonged,the frequency of crossing the platform was increased,the apoptosis index was decreased,the expression of activated caspase-3 was down-regulated,and the expression of AT2R and PPARγ was up-regulated in group G (P＜0.05).Conclusion Inhibited activity of AT2R is involved in repeated propofol anesthesia-induced neuroapoptosis in the hippocampus of newborn rats.
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Objective To describe the importance of anesthesia management in performing interventional procedures. Methods A total of 24 382 patients, who were admitted to authors’ hospital during the period from April 2011 to April 2015 to receive level Ⅲ or level Ⅳ interventional procedures, were enrolled in this study. According to the anesthesia method, the patients were divided into (1) mechanical ventilation group (group A), i.e. intravenous general anesthesia combined with laryngeal mask or endotracheal intubation, (2) intravenous general anesthesia and autonomous respiratory group (group B), (3) conscious sedation group (group C) and (4) local anesthesia group (group D). The heart rate (HR), mean arterial pressure (ABP), blood oxygen saturation (SpO2) and anesthesia-related complications of the patients of all four groups were kept under close observation before, during and after the interventional procedures, the results were statistically analyzed. Results The anesthesia was successfully implemented according to the operation plan in all 24 382 patients. Interventional procedure of level Ⅲ was performed in 16 702 patients(68.5%) and interventional procedure of levelⅣwas adopted in 7 680 patients (31.5%). The patients receiving interventional procedure of level Ⅲof group A, B, C and D were 6 797 (40.7%), 3 608 (21.6%), 5 095(30.5%) and 1 202(7.2%) respectively;while the patients receiving interventional procedure of level Ⅳ of group A, B, C and D were 4 193 (54.6%), 2 527 (32.9%), 699 (9.1%) and 261 (3.4%)respectively. No statistically significant differences in preoperative HR, ABP and SpO2 existed between each other among the four groups (P>0.05). In group A, B and C the HR and ABP values determined in operation were not statistically different from the preoperative ones(P>0.05), and the differences in HR and ABP values among the three groups were also not statistically different (P>0.05);SpO2 levels showed no obvious changes (P>0.05). In group D, the HR and ABP values determined in operation were significantly higher than the preoperative ones (P0.05). In 22 patients of group D the operation had to be stopped as they were unable to tolerate the procedure. Conclusion In performing different levels of interventional procedures, level Ⅲ and level Ⅳ intervention surgeries in particular, careful selection of individualized anesthesia plan on the base of patient’s condition and operation requirement is an important guarantee for ensuring a safe operation with no interference, and it is also a good way to reduce the pain severity of patient. Therefore, individualized anesthesia plan is worth to be widely used in interventional procedures.
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Objective To investigate the effect of ketamine injected via the radicular arteries on spinal cord. Methods Twenty healthy mongrel dogs of both sexes weighing 12-18 kg were randomly divided into 2 groups ( n = 10 each): control group (group C) and ketamine group (group K). The animals were anesthetized with intravenous pentobarbital 30-35 mg/kg, fentanyl 50-100 μg and vecuronium 0.2 mg/kg and maintained with propofol ically ventilated after tracheal intubation. A catheter was inserted into T8 poster intercostal artery and advanced toward the opening of radicular artery which supplies the spinal cord. Ketamine 100 mg (in 2 ml of normal saline)was injected via the catheter in group K. Three hours after ketamine administration, the animals were sacrificed. A 1.5 cm long segment of spinal cord at the level of T8 was removed for microscopic examination and determination of the expression of NSE, S100β and Tau protein by immuno-histochemistry. Results There was no significant difference in the number of Nissl' s staining-negative neuronal cells and the expression of NSE, S100β and Tau protein in the spinal cord between the 2 groups ( P ＞ 0.05 ). Conclusion Ketamine injected via the radicular arteries does not induce spinal cord injury.