Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Language
Year range
1.
The Journal of Clinical Anesthesiology ; (12): 432-435, 2018.
Article in Chinese | WPRIM | ID: wpr-694953

ABSTRACT

Objective To investigate effects of postoperative analgesia with oxycodone on post-operative cognitive dysfunction in aged patients undergoing laparascopic cholecystectomy. Methods One hundred and twenty patients scheduled for laparascopic cholecystectomy with general anesthesia,57 males and 63 females,aged 70-80 years,ASA physical status Ⅰ or Ⅱ,were enrolled in the present study.The patients were divided randomly into fentanyl group,sufentanil group and oxycodone group (n=40)according to postoperative analgesia.Visual analog scale (VAS)scores, nausea or vomiting,itching and analgesics consumption of all patients were recorded in the postopera-tive 48 h.Neuropsychological testing was performed with mini-mental state examination (MMSE)on the 7th postoperative day.Results There was no statistical significance between the three groups in VAS scores at different time points in the postoperative 48 h.The incidence of itching,nausea or vomiting in oxycodone group was lower than that in fentanyl group and sufentanil group (P<0.05). Analgesics consumption in fentanyl group and sufentanil group exhibited a negative correlation with MMSE scores on the 7th postoperative day (P<0.01).There was no correlation between analgesics consumption and MMSE scores in oxycodone group.The incidence of POCD was 15 (37.5%)in fent-anyl group,13 (32.5%)in sufentanil group and 7 (17.5%)in oxycodone group.The incidence of POCD in oxycodone group was lower than those in fentanyl group and sufentanil group (P<0.05). Conclusion Oxycodone,replacing fentanyl or sufentanil,can be used for postoperative analgesia and reduce the incidence of POCD with less nausea,vomiting and itching in aged patients.

2.
Chinese Journal of Pharmacology and Toxicology ; (6): 419-424, 2011.
Article in Chinese | WPRIM | ID: wpr-423835

ABSTRACT

OBJECTIVETo investigate effects of exogenous hydrogen sulfide ( H2 S) on the spatial memory disorder induced by cerebral anoxia in mice and explore related mechanism.METHODS Sodium nitrite (NaNO2) 120 mg·kg-1 was sc given to mice for4 d in model group.Sodium hydrosulfide (NaHS) 1 mg·kg-1 was ip given and NaNO2 120 mg·kg-1 simultaneously was sc given to mice for4 d in NaHS group.All drugs were given to mice immediately after Morris water maze experiment every day and escape latency.The number of crossings over the target area (NCTA) and search time in target quadrant (STTQ) were recorded.The activity of superoxide dismutase (SOD) and malondialdehyde (MDA) level in the brain was determined with colorimetry.The morphological alterations in hippocampus slices were assessed by microscope.RESULTSOn the third and fourth days in Morris water maze experiment,compared with ( 16.1 ±9.6)s and ( 11.1 ±6.2)s in normal control group,the escape latency in model group was longer,(26.0 ±7.3)s(P<0.05) and (23.3 ±8.7)s(P<0.01).On the fifth day,compared with 7.2 ± 1.6 and (28 ± 8) s in normal control group NCTA and STTQ in model group were 4.1 ± 1.9and (20 ± 8 ) s ( P < 0.05 ),and they were obviously less.Compared with normal control group,SOD activity and M DA content of mice in model group were reduced by 12.6% (P < 0.01 ) and increased by 43.9% (P < 0.01 ),respectively.The neuron degenerative changes including karyopyknosis,dark cytoplasm and irregular pyramidal layer were observed in model group.On the third and fourth day,compared with model group,the escape latency in NaHS group was shorter,(17.9 ±7.0)s and (15.8 ±8.5)s (P<0.05).Compared with model group,NCTA and STTQ in NaHS group increased to 6.7 ± 2.5 and ( 30 ± 9) s ( P < 0.01 ).SOD activity and MDA content in NaHS group were increased by 8.9% ( P < 0.05 ) and reduced by 29.6% ( P < 0.01 ),respectively.Neuron degeneration was significantly attenuated in NaHS group (P < 0.01 ).CONCLUSIONNaHS can attenuate the spatial memory disorder induced by cerebral anoxia and the mechanism may be related to the antioxidation effect and alleviation of neuron damage of H2S.

SELECTION OF CITATIONS
SEARCH DETAIL