Objective To determine whether re-expansion of the collapsed lung with room air can attenuate oxidative stress injury following one-lung ventilation during esophageal cancer resection. Methods Twenty-four ASA Ⅰ or Ⅱ patients aged 40-60 yr weighing 44-65 kg undergoing esophageal cancer resection were randomly divided into 2 groups (n=12 each) : room air group and pure oxygen group. Anesthesia was induced with midazolam, fentanyl, etomidate and atracurium and maintained with propofol and atracurium infusion and intermittent iv boluses of fentanyl. Right or left side double-lumen catheter (Fr 35, 37, 39) was inserted in each patient. Correct placement was verified by fiber-optic bronchoscopy. The patients were mechanically ventilated ( V_T 7-10 ml/kg, RR 12-16 bpm, FiO_2 1.0 during one-lung ventilation). P_(ET)CO_2 was maintained at 35-45 mm Hg. SpO_2 was maintained at 95%-100% during one-lung ventilation. Blood samples were collected at the beginning of one-lung ventilation (T_1 ), immediately before re-expansion of the collapsed lung (T_2) and 30 rain after re-expansion of the collapsed lung (T_3) for determination of serum levels of MDA, SOD and plasma level of protein carbonyl. Arterial blood samples were obtained at 2 h after operation for blood gas analysis. Results The plasma protein carbonyl level and serum MDA level were significantly increased while the serum SOD level was significantly decreased at T_3 as compared with thost at T_1 and T_2 in pure oxygen group. No significant change in serum levels of MDA, SOD and plasma level of protein carbonyl occurred during operation in room air group. The oxygenation index was significantly higher at 2 h after operation in room air group than in pure oxygen group. Conclusion Re-expansion of the collapsed lung with room air can attenuate the oxidative stress injury following one-lung ventilation during esophageal cancer resection.

Objective To investigate the effect of ketamine on the expression of HSP 70 in myocardium in severely burned rats for its possible mechanism of myocardial protection. Methods Seventy-two male Wistar rats were randomly divided into 3 groups: normal control group (group C, n=8), burn injury group (group BI, n= 32) and ketamine group (group K,n=32). 30% Wtal body surface area of Ⅲ degree burn model was developed in group BI and group K. Ketamine 20 mg/kg was injected IM in group K 15 min after the burn model was made. Equal volume of normal saline was given instead of ketamine in group BI. Group C received no treatment. The rats were sacrificed at 3, 6, 12 and 24 h after administration in group BI and group K respectively(8 rats at each time point). Myocardial samples were obtained for determination of the expression of HSP 70 by Western blot analysis. The myocardial ultrastructure was observed at 3 h after administration with electron microscope. Results The myocardial damage was milder in group K than in group BI. The expression of HSP 70 was significantly higher at 3, 6, 12 and 24 h after administration in group K and group BI than in group C(P<0.05).The HSP 70 expression was significantly higher at 3 and 6 h after administration in group K than in group BI ( P<0.05). Conclusion Ketamine can reduce the myocardial injury induced by severe burn through up-regulating the expression of HSP 70 in cardiocytes.

Objective To investigate the effect of dexmedetomidine on postoperative patient-controlled intravenous analgesia (PCIA) with sufentanil in patients with essential hypertension. Methods Sixty ASA Ⅱ or Ⅲ patients with essential hypertension aged 42-63 yr weighing 48-72 kg undergoing hysterectomy were randomly divided into 3 groups ( n = 20 each): control group ( group C) and different doses of dexrmedetomidine groups ( group D1.2 ). PCIA was performed with sufentanil 1 μg/ml + tropisetron 5 μg/ml in 100 ml of normal saline within 24 h after operation (background infusion at 2 ml/h with a bolus dose of 0.5 ml and a 15 min lockout interval). Dexmein group C. Ramsay score was recorded. The number of attempts, consumption of sufentanil, the number of patients who needed nifedipine or ephedrine and side effects such as vomiting and respiratory depression were recoded within 24 h after operation. The level of sedation was evaluated with Ramsay sedation score at 24 h after operation.Results Compared with group C, the number of attempts, consumption of sufentanil, the number of patients who needed nifedipine and incidences of vomiting and respiratory depression were significantly decreased, while Ramsay score was significantly increased in D1 and D2 groups, and the number of patients who needed ephedrine was significanlly increased in group D2 ( P ＜ 0.05). The number of attempts and consumption of sufentanil were significantly decreased, and Ramsay score and the number of patients who needed ephedrine were significantly increased in group D2 compared with group D1 ( P ＜ 0.05). Conclusion Dexmedetomidine can not only reduce the consumption of sufentanil for postoperative PCIA, but also prevent postoperative hypertension from deteriorating in patients with essential hypertension.

Dexmedetomidine is an α2-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of 1 μg/kg load dose, followed by 0.05 μg/kg/min infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-1β, interleukin-6 and tumor nevrosis factor-α as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κBp65, inhibitor of κBα and phosphorylated of κBα in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-κB pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.
Animals ; Brain Edema ; CA1 Region, Hippocampal ; Cyclooxygenase 2 ; Cytokines ; Dexmedetomidine* ; Heart ; Hippocampus ; Infarction, Middle Cerebral Artery ; Inflammation* ; Interleukin-6 ; Kidney ; Neuroprotection* ; Nitric Oxide Synthase Type II ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Reperfusion Injury* ; RNA, Messenger

Dexmedetomidine is an α2-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of 1 μg/kg load dose, followed by 0.05 μg/kg/min infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-1β, interleukin-6 and tumor nevrosis factor-α as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κBp65, inhibitor of κBα and phosphorylated of κBα in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-κB pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.
Animals ; Brain Edema ; CA1 Region, Hippocampal ; Cyclooxygenase 2 ; Cytokines ; Dexmedetomidine* ; Heart ; Hippocampus ; Infarction, Middle Cerebral Artery ; Inflammation* ; Interleukin-6 ; Kidney ; Neuroprotection* ; Nitric Oxide Synthase Type II ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Reperfusion Injury* ; RNA, Messenger