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Objective:To evaluate the effect of age factors on the pharmacodynamics of intranasal dexmedetomidine for sedation in the pediatric patients undergoing transthoracic echocardiography(TTE).Methods:American Society of Anesthesiologists Physical Status classification Ⅰ-Ⅲ pediatric patients, aged 1-24 months, undergoing TTE from August 2019 to May 2022, were selected. This trial was performed in two parts. Part Ⅰ Pediatric patients were divided into 4 age groups: 1-6 month group, 7-12 month group, 13-18 month group and 19-24 month group. The initial dose of dexmedetomidine was 2.0 μg/kg in 0.1 μg/kg increment/decrement. The dose of dexmedetomidine was determined by using modified Dixon′s up-and-down method. The ED 50 and 95% confidence interval of intranasally administered dexmedetomidine for sedation were calculated by the Dexon-Massey method. Part Ⅱ One hundred patients were divided into 4 age groups ( n= 25 each): 1-6 month group, 7-12 month group, 13-18 month group and 19-24 month group. The 4 groups were further divided into 5 subgroups ( n=5 each) according to the dose of dexmedetomidine: 2.1 μg/kg subgroup, 2.2 μg/kg subgroup, 2.3 μg/kg subgroup, 2.4 μg/kg subgroup, and 2.5 μg/kg subgroup. Part Ⅰ and part Ⅱ trials were combined, and the ED 95 and 95% confidence interval of intranasally administered dexmedetomidine for sedation were calculated using the probit method. Results:A total of 220 pediatric patients were enrolled. There was no significant difference in ED 50 and ED 95 of dexmedetomidine intranasally administered for sedation among groups ( P>0.05). Conclusions:The pharmacodynamics of intranasal dexmedetomidine for sedation shows no significant difference in age in the pediatric patients aged 1-24 months undergoing TTE.
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Objective To analyse clinical features of dead children in pediatric intensive care unit(PICU) of Children's Hospital of Chongqing Medical University from 2005 to 2014.Methods Clinical data of 917 dead cases in PICU from January 2005 to December 2014 in this hospital were collected,then distribution characteristics of age,length of hospital stay,time of dead and transfer department were analysed.The death cause analysis was conducted as well.Results According to systematic classification of disease,the top 10 leading causes of death for 917 dead cases in PICU from 2005 to 2014 in this hospital were congenital deformity,infectious disease,respiratory disease,injury and poisoning,digestive system disease,tumor,symptoms,signs and abnormal clinical and laboratory findings not elsewhere classified,circulation system disease,nervous system disease,blood system disease.Compared with 2005-2014,the ratio of dead cases due to infectious diseases to the total cases was declined,while that due to non-infectious diseases was increased,there was statistically significant difference (x2 =26.29,P =0.00).Whereas,the ranks of septicopyemia and hand-foot-mouth disease in the rank order of death causes both were increased.Condusion Congenital deformity is the first cause of death in PICU of this hospital.The key to cutting children's mortality is to reduce newborn with congenital deformity.
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Objective To evaluate the effect of propofol on docetaxel-induced toxicity to cervical cancer Hela cells transfected with Cx32 plasmid.Methods Cervical cancer Hela cells transfected with Cx32 plasmid were seeded at two different densities and induced to express Cx32 by incubation with doxycycline for 48 h.The cells at high density were seeded at 1 × 105 cells/ml such that the cells would be confluent at the time of docetaxel exposure.The cells at low density were seeded at 500 cells/ml and the cells did not attach at the density.Each type of cells obtained was randomly divided into 5 groups (n =8 each):control group (group C),docetaxel group (group D),docetaxel + intralipid group (group D + I),docetaxel + 18-α-GA group (D + 18-α-GA),and docetaxel +propofol group (group D + P).Groups D,D + I,D + 18-α-GA and D + P were exposed to 5 nmol/L docetaxel,5 nmol/L docetaxel + 10μg/ml intralipid,5 nmol/L docetaxel + 10 μmol/L 18-α-GA,and 5 nmol/L docetaxel +2.8 μg/ml propofol,respectively.18-α-GA,intralipid and propofol were added prior to docetaxel,and the action time for 18-α-GA alone was 1 h and for intralipid or propofol alone 2 h.The time for coaction between the three drugs and docetaxel was 2 h.Cell survival was determined by a standard colony-forming assay.Results The colony formation rate of the cells seeded at high density in group D was significantly lower than that of the cells seeded at low density in group D (P ＜ 0.05).For the cells seeded at high density,the colony formation rate was significantly decreased in the other groups when compared with group C (P ＜ 0.05).The colony formation rate was significantly higher in groups D + 18-α-GA and D + P than in groups D and D + I (P ＜ 0.05).There was no significant difference in the colony formation rate between groups D and D + I (P ＞ 0.05).For the cells seeded at low density,the colony formation rate was significantly decreased in the other groups when compared with group C (P ＜ 0.05) and there was no significant difference in the colony formation rate between D,D + I,D + 18-α-GA and D + P groups (P ＞ 0.05).Conclusion Propofol can attenuate docetaxel-induced toxicity to Hela cells transfected with Cx32 plasmid and inhibition of gap junction function is involved in the mechanism.
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Objective To investigate the effect of different doses of propofol on cisplatin-induced hepatotoxicity in rats.Methods Eighty male SD rats weighing 200-250 g,aged 3 months,were randomly divided into 8 groups (n =10 each) ∶ control group (group C),cisplatin 7.5 mg/kg group (group Cis),propofol 180 mg/kg group (group P),intralipid 15 ml/kg group (group Ⅰ),cisplatin 7.5 mg/kg + intralipid 15 ml/kg group (group CisI),cisplatin 7.5 mg/kg + propofol 60 mg/kg group (group CisP1),cisplatin 7.5 mg/kg + propofol 120 mg/kg group (group CisP2),and cisplatin 7.5 mg/kg + propofol 180 mg/kg group (group CisP3).The rats in groups C,Cis,P and I received single intraperitoneal injection of normal saline,cisplatin,propofol and intralipid respectively.While in the groups CisI,CisP1,CisP2 and CisP3,rats received a single intraperitoneal injection of propofol or intralipid at 1 min before a single intraperitoneal injection of cisplatin.At 24 h after cisplatin injection,venous blood samples were taken from inferior vena cava for measurement of plasma ALT and AST activities.The liver tissues were taken for microscopic examination.Results Compared with group C,plasma ALT and AST activities were significantly increased and pathological injury was aggravated in groups Cis,CisI and CisP1-3 (P ＜ 0.05).The activities of ALT and AST were gradually decreased and the pathologic injury was attenuated in groups Cis and CisP1-3 (P ＜ 0.05).Conclusion Propofol can reduce cisplatin-induced hepatotoxicity in a dose-dependent manner in rats.