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Objective To investigate the effects of propofol and sevoflurane on adriamycin chemotherapy-induced myocardial damage in rats.Methods Twenty-four healthy male Wistar rats, aged 3 months, weighing 212-270 g, were randomly divided into 4 groups (n =6 each) using a random number table: control group (group C) , adriamycin group (group ADM) , adriamycin-propofol group (group ADM-Pro) , and adriamycin-sevoflurane group (group ADM-Sevo).The equal volume of normal saline was injected intraperitoneally in group C.In group ADM, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times (11 days in total).In group ADM-Pro, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times, and at 3 days after the last administration of adriamycin, propofol anesthesia was performed as follows : the total amount of propofol injected intraperitoneally was 200 mg/kg, the initial dose was 100 mg/kg, and 1 h later the remaining amount was added, and the duration of anesthesia was about 2 h.In group ADM-Sevo, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times, and at 3 days after the last administration of adriamycin, sevoflurane anesthesia was performed as follows: 1.5％-3.0％ sevoflurane was inhaled for 2 h.After the end of anesthesia, blood samples were collected for determination of serum cardiac troponin (cTnI) concentrations.Myocardial specimens were collected for detection of caspase-3 expression by immuno-histochemistry.Results Compared with group C, the serum cTnI concentration was significantly increased, and the caspase-3 expression was up-regulated in ADM, ADM-Pro and ADM-Sevo groups (P＜ 0.05).Compared with group ADM, the serum cTnI concentration was significantly decreased, and the caspase-3 expression was down-regulated in ADM-Pro and ADM-Sevo groups (P＜0.05).There was no significant difference in the parameters mentioned above between group ADM-Pro and group ADM-Sevo (P＞0.05).Conclusion Propofol and sevoflurane both can mitigate adriamycin chemotherapy-induced myocardial damage in rats, without significant difference in the efficacy.
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Objective To determine ff cognitive dysfunction induced by neonatal ketamine anesthesia can persist into adulthood.Methods Thirty 7-day-old SD rats of both sexes were randomly divided into 3 groups.Control group received normal saline 0.2 ml intraperitoneally (IP) (group C),while ketamine groups 1 and 2 received ketamine 25 and 50 mg/kg IP respectively (groups K1,K2 ).Morris water maze test was performed and hippocampal long-term potentiation (LTP) recorded when the rats were 2.5 months old.Results LTP was significantly lower in groups K1 and K2 than in group C.There was no significant difference in LTP between groups K1 and K2.The escape latency and swimming time were comparable among the 3 groups.Conclusion Neonatal ketamine anesthesia can decrease the cognitive function in adult rats.There is no significant difference between light and deep ketamine anesthesia.
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ObjectiveTo investigate the role of δ-opioid receptor in remifentanil-induced N-methyl-D-aspartate (NMDA) receptor miniature excitatory postsynaptic currents (mEPSCs) in rat spinal dorsal horn neurons.MethodsMale 14-18 d old Wistar rats weighing 50-60 g were used in this study.The animals were anesthetized with intraperitoneal choral hydrate 400 mg/kg and sacrificed.Their lumbar segments of spinal cord (L1-S1 ) were immediately removed and sliced.Twenty-four slices were randomly divided into 4 groups ( n =6 each): control group (group C) ; glycine group (group G) ; remifentanil group (group R) and remifentanil + naltrindole(a δ receptor antagon) (group RN).Slices were cultured in artificial cerebrospinal fluid (ACSF) (group C) or incubated in ACSF containing glycine 0.24 μmol/L (group G) or remifentanil 4 nmol/L (group R) or remifentanil 4 nmol/L+ naltrindole 1 nmol/L (group RN) for 60 min.Whole cell patch clamp technique was used to measure NMDA receptor mEPSCs.ResultsThe amplitude and frequency of mEPSCs were significantly higher in group R than in groups C and RN ( P ＜ 0.01).There were no significant differences in amplitude and frequency of mEPSCs among gorups C,G and RN ( P ＞ 0.05).ConclusionActivation of δ-receptor can enhance NMDA receptor function in spinal dorsal horn neurons in rats which may be the mechanism of remifentanil-induced hyperalgesia.
