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Objective:To evaluate the role of hippocampal β-amyloid 42 (Aβ 42) deposition-induced accumulation of neutrophils in blood-brain barrier damage caused by sevoflurane anesthesia in aged rats. Methods:Seventy-two healthy male Wistar rats in which IT catheters were successfully planted, aged 18-20 months, weighing 600-650 g, were divided into 4 groups ( n=18 each) using a random number table method: control group (group C), γ-secretase inhibitor DAPT group (group D), sevoflurane anesthesia group (group S) and DAPT plus sevoflurane anesthesia group (group DS). Dimethyl sulfoxide 10 μl was intrathecally injected in group C and group S, and 30 min later group C inhaled 60% oxygen for 2 h, and group S inhaled 3.6% sevoflurane and 60% oxygen for 2 h and tibial fracture surgery was performed at the same time.DAPT 10 μl was intrathecally injected in group D and group DS, and 30 min later group D inhaled 60% oxygen for 2 h, and group DS inhaled 3.6% sevoflurane and 60% oxygen for 2 h and tibial fracture surgery was performed at the same time.The fear conditioning test was performed at 12 h after the end of treatment in each group, and the ratio of time spent freezing was calculated.The rats were sacrificed after the end of behavioral test, and hippocampal tissues were removed for determination of the expression of Aβ 42, occludin and matrix metalloproteinase-9 (MMP-9) (by Western blot), neutrophil count (by immuno-histochemistry), and content of Evans blue (EB) (by EB staining). Results:Compared with group C, the ratio of time spent freezing was significantly decreased, the expression of Aβ 42 and MMP-9 was up-regulated, the expression of occludin was down-regulated, the neutrophil count and content of EB were increased in group S and group DS ( P<0.05), and no significant change was found in the parameters mentioned above in group D ( P>0.05). Compared with group S, the ratio of time spent freezing was significantly increased, the expression of Aβ 42 and MMP-9 was down-regulated, the expression of occludin was up-regulated, the neutrophil count and content of EB were decreased in group DS ( P<0.05). Conclusion:The mechanism by which sevoflurane anesthesia leads to postoperative cognitive dysfunction is related to hippocampal Aβ 42 deposition-induced accumulation of neutrophils and causing damage to blood-brain barrier in aged rats.
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Objective To evaluate the efficacy of different doses of oxycodone for prevention of fen-tanyl-induced cough during induction of general anesthesia. Methods A total of 250 American Society of Anesthesiologists physical statusⅠor Ⅱ patients of both sexes, aged 22-62 yr, weighing 47-81 kg, un-dergoing elective surgery, were divided into 5 groups (n＝50 each) using a random number table method:different doses of oxycodone groups (O1-4groups) and control group (group C). Oxycodone 0. 025, 0. 050, 0. 075 and 0. 100 mg∕kg were intravenously injected in O1-4groups, respectively, while the equal volume of normal saline was given instead of oxycodone in group C. Five minutes later fentanyl 3 μg∕kg was intrave-nously injected within 5 s, and then 2 min later the other drugs were administered for induction. The occur-rence and severity of cough were observed within 2 min after fentanyl injection. The development of respira-tory depression and hypotension and severe bradycardia during induction of anesthesia were recorded within 5 min after oxycodone injection. Results The incidence of cough was significantly lower in O1-4groups than in group C (P＜0. 05). There was no significant difference in the incidence of cough among O1-4groups (P＞0. 05). No respiratory depression was found in C and O1-3groups. The incidence of respiratory depression was significantly higher in group O4than in C and O1-3groups (P＜0. 05). There were no significant differ-ences in the incidence of hypotension or severe bradycardia during induction of anesthesia among the five groups (P＞0. 05). Conclusion Oxycodone 0. 025 mg∕kg provides better efficacy in preventing fentanyl-induced cough during induction of general anesthesia.
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Objective To evaluate the changes in expression of cold-inducible RNA-binding protein (CIRP) in hippocampus during brain injury in a rat model of cardiac arrest-cardiopulmonary resuscitation.Methods Seventv-two clean-grade healthy male Sprague-Dawley rats,weighing 280-350 g,aged 8-10 weeks,were divided into 2 groups using a random number table:sham operation group (S group,n=18) and ischemia-reperfusion group (I/R group,n=54).Tracheal intubation was performed and artery and veins were punctured in group S.Ventricular fibrillation was induced by transoesophageal cardiac pacing to establish the model of cardiac arrest in group I/R.Rats were sacrificed at 12,24 and 48 h after resuscitation and the hippocampus was harvested for determination of CIRP,tumor necrosis factor-alpha (TNF-α) and interleukin-lbeta (IL-1β) protein and mRNA expression (by quantitative polymerase chain reaction or Western blot) and for determination of pathological changes of hippocampi (with a light microscope).Results Compared with group S,the expression of CIRP mRNA in hippocampus was up-regulated at 24 and 48 h after resuscitation,the expression of TNF-α mRNA was up-regulated at 12,24 and 48 h after resuscitation,the expression of IL-1β mRNA was up-regulated at 12 and 24 h after resuscitation,and the expression of CIRP,TNF-α and IL-1β was up-regulated at 12,24 and 48 h after resuscitation in group I/R (P＜0.05).Pathological changes in hippocampal CA1 region were found in group I/R.Conclusion The expression of CIRP in hippocampus is up-regulated,which promotes central inflammatory responses during brain injury in a rat model of cardiac arrest-cardiopulmonary resuscitation.
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Myeloid-derived suppressor cells (MDSCs),a heterogeneous population of immature myeloid cells,play an important role in immune tolerance and immune suppression.In recent years,more and more research results show that the prostaglandin E2 (PGE2) has an inseparable relationship with MDSCs,and PGE2 through its relevant receptors,regulating signal transducer and activator of transcription 3 (STAT3) and protein kinase A cell signaling pathways and secretion cytokines in tumor microenvironment,affects the development,differentiation and function of MDSCs.
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Objective To evaluate protective effects of dexmedetomidine combined with lung-protective ventilation on lungs in patients undergoing thoracic surgery.Methods Eighty patients with normal pulmonary function,aged 40-64 yr,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,with body mass index of 20-25 kg/m2,scheduled for elective right lobectomy for lung cancer performed via a thoracoscope,were divided into 4 groups (n =20 each) using a random number table:conventional ventilation group (group C),dexmedetomidine combined with conventional ventilation group (group DC),lung-protective ventilation group (group P) and dexmedetomidine combined with lung-protective ventilation group (group DP).In DC and DP groups,dexmedetomidine was intravenously infused as a loading dose of 0.5 μg/kg (over 10 min) starting from 10 min before anesthesia induction,followed by an infusion of 0.6 μg · kg 1 · h-1 until the end of surgery.In C and DC groups,the tidal volume was set at 9 ml/kg,positive end-expiratory pressure 0 cmH2O,fraction of inspired oxygen 100％,respiratory rate 10-12 breaths/min,inspiratory/expiratory ratio 1 ∶ 2,and end-tidal pressure of carbon dioxide was maintained at 35-45 mmHg during both two-lung ventilation (TLV) and one-lung ventilation (OLV).In P and DP groups,the tidal volume was set at 6 ml/kg,positive end-expiratory pressure 5 cmH2O,fraction of inspired oxygen 70％,respiratory rate 14-16 breaths/min,i nspiratory/expiratory ratio 1 ∶ 2,and end-tidal pressure of carbon dioxide was maintained at 35-45 mmHg during TLV and OLV.Airway peak pressure (Ppe~),airway plateau pressure (Pp~t),dynamic lung compliance and airway resistance (Raw) were monitored and recorded immediately before OLV (T1),at 30 min,1 h and 2 h of OLV (T2-4) and at 15 min after restoration of TLV (T5).Arterial blood samples were collected at 10 min before induction of anesthesia (T0) and T1-5 for blood gas analysis,and oxygenation index was calculated.At T0,T1,T3,T4 and 2 and 24 h after surgery (T6,7),blood samples were taken from the right internal jugular vein for determination of the concentrations of serum tumor necrosis factor-alpha (TNF-α),interleukin-6 (IL-6) and high-mobility group box 1 protein (HMGB1) by enzyme-linked immunosorbent assay.Results Compared with group C,Raw was significantly decreased at T2-4 in group DC,Ppeak,Pplat and Raw were significantly decreased at T2-4 in P and DP groups,oxygenation index was significantly increased at T5 in DC and P groups,oxygenation index was significantly inereased at T2-5 in group DP,the concentrations of serum TNF-α and IL-6 were significantly decreased at T3,4 and T6,7 in P,DC and DP groups,and the concentrations of serum HMGB1 were significantly decreased at T6,7 in DC and DP groups (P＜0.05).Compared with group DC,Ppeak,Pplat and Raw were significantly decreased at T2-4,oxygenation index was increased at T3-5,and the concentrations of serum TNF-α and IL-6 were decreased at T3,4 and T6,7 in group DP (P＜0.05).Compared with group P,Raw was signifieantly decreased at T2-4,oxygenation index was increased at T2-5,and the concentrations of serum TNF-α and IL-6 were decreased at T3,4 and T6,7,and the concentrations of serum HMGB1 were decreased at T6,7 in group DP (P＜0.05).There was no significant difference in dynamic lung compliance at each time point among the four groups (P＞0.05).Conclusion The combination of dexmedetomidine and lung-proteetive ventilation provides protective effects on lungs and exterts better efficacy than either alone,and the mechanism may be related to inhibiting systemic inflammatory responses of patients undergoing thoracic surgery.
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Objective To observe the effects of aerosolized prostaglandin E1 (PGE1 )via right lung before one-lung ventilation (OLV ) on shunt rate (Qs/Qt ) and oxygenation in patients undergoing surgery for oesophageal cancer.Methods Sixty patients scheduled for elective trans-left-thoracic esophagectomy for esophageal cancer were randomly and single-blindly located into two groups.Patients in each group received different therapy before OLV,namely inhaling PGE1 0.2μg/kg via right lung in group P and inhaling normal saline in group C.The PaO 2 and hemodynamic indicators of two groups were recorded at these points:before OLV(T1 ),OLV 10 min (T2 ),OLV 1 5 min (T3 ),OLV 30 min (T4 ),OLV 60 min (T5 ),OLV 120 min (T6 ),.Results PaO 2 in both groups were declined straightly since OLV and fell to the lowest point at T4 in group C.PaO 2 in group P at T2-T4 were significantly higher than that in group C (P <0.05),and the lowest point of which was recorded at T5 .Qs/Qt in group P was significantly lower than that in group C at T2-T4 (P <0.05).There were no significant differences in hemodynamics indicators between the two groups. Conclusion Inhalation of 0.2 μg/kg PGE1 before OLV via one lung can reduce pulmonary shunt and improve PaO 2 in thoracic surgery patients.
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Objective To compare the cellular immune function during postoperative analgesia with dezocine and fentanyl in the patients with gynecologic malignant tumors.Methods Fifty patients scheduled for elective surgery for gynecologic malignant tumors, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ , were equally and randomly divided into either dezocine group (group D) or fentanyl group (group F) using a random number table.Total intravenous anesthesia was used for all the patients, and the intraoperatively administered anesthetics was the same.The patient-controlled intravenous analgesia (PCIA) was used for postoperative analgesia.PCIA solution contained dezocine 0.8 mg/kg and tropisetron 6 mg in 100 ml of normal saline in group D.PCIA solution contained fentanyl 0.01 mg/kg and tropisetron 6 mg in 100 ml of normal saline in group F.The PCA pump was set up to deliver a 1 ml bolus dose with a 15-min lockout interval and background infusion at 2 ml/h after a loading dose of 2 ml in the two groups.Tramadol 100 mg was given intravenously as rescue analgesic to maintain visual analogue scale score ≤ 4.Before surgery (T0), at the end of surgery, and at 24 and 48 h after surgery (T2,3) , venous blood samples were collected for detection of T lymphocyte subsets CD3+, CD4+ , CD8+ and natural killer (NK) cell levels (by flow cytometry).CD4+/CD8+ ratio was calculated.The requirement for rescue analgesics and occurrence of adverse reactions such as nausea, vomiting, hypotension and respiratory expression were recorded after surgery.Results No patients required tramadol as rescue analgesic in either group.Compared with the value at T0, the levels of CD3+ , CD4+ and NK cells and CD4+/CD8+ ratio were significantly decreased at T1,2, and the CD8+level was increased at T1 in group D, and the levels of CD3+ cells at T1,2, CD4+ cells at T1 and NK cells at T1-3 were decreased (P＜0.05) , and no significant change was found in CD8+ cell level and CD4+/CD8+ ratio in group F (P＞0.05).Compared with group F, the levels of CD3+ and NK cell were significantly increased at T3 (P＜0.05) , and no significant change was found in the incidence of adverse reactions after surgery in group D (P＞0.05).Conclusion The inhibitory degree of the cellular immune function is reduced when postoperative analgesia is performed with dezocine as compared with that when fentanyl is used in the patients with gynecologic malignant tumors.
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Objective To investigate the effects of desflurane on cardiac troponin I (cTnI) and myocardial enzyme. Methods Thirty ASA Ⅰ~Ⅱpatients scheduled for selective operation were randomly divided into three groups of tenin each: Desflurane group(D group), Isoflurane group(I group) and Enflurane group(E group). Anesthesia was maintained with inhalation of 1.0MAC of desflurane, isoflurane, and enflurane in each group respectively. Blood samples were taken before anesthesia, 1 h after inhalation and at the end of inhalation for the determination of plasma cTnI, CK, CK-MB, AST and LDH activities. Results cTnI, AST, LDH, CK and CK-MB levels were normal before anesthesia. At the end of inhalation, CK increased significantly in three groups, CK-MB increased markedly in Enflurane group and Isoflurane group, but CK-MB level was normal in desflurane group. However, the CK-MB level was normal in all patients. cTnI, AST, LDH showed little changes during inhalation. Conclusions Inhalation of 1.0 MAC of desflurane, isoflurane and enflurane doesn't result in myocardial injury.