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 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.

Objective To evaluate the effect of dexmedetomidine on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty pathogen-free male Sprague-Dawley rats,aged 12-16 months,weighing 300-360 g,were randomly divided into 3 groups (n =10 each) using a random number table:sham operation group (group Sham),focal cerebral I/R group (group I/R),and dexmedetomidine group (group D).Focal cerebral I/R was induced by occlusion of the right middle cerebral artery.In group D,dexmedetomidine was given as a loading dose of 1 μg/kg (over 10 min) starting from 1 h of ischemia,followed by an infusion of 0.05 μg · kg-1 · h-1 until 2 h of reperfusion.Neurological deficit was assessed and scored at 24 h of reperfusion,and then the rats were sacrificed.Brains were removed for determination of cerebral infarct size and expression of iNOS and COX-2 in the hippocampus (by Western blot).The percentage of cerebral infarct size was calculated.Results Compared with group Sham,the neurological deficit score,percentage of head swing to the left,percentage of cerebral infarct size,and expression of iNOS and COX-2 in the hippocampus were significantly increased in I/R and D groups (P＜0.05).Compared with group I/R,the neurological deficit score,percentage of head swing to the left,percentage of cerebral infarct size,and expression of iNOS and COX-2 in the hippocampus were significantly decreased in group D (P＜0.05).Conclusion The mechanism by which dexmedetomidine mitigates focal cerebral I/R injury may be related to inhibition of iNOS and COX-2 expression in rats.

Objective To evaluate the effect of controlled hypotension at the beginning of reperfusion on ischemia-reperfusion (I/R) injury of the liver in patients undergoing hepatectomy. Methods Forty ASA Ⅱ or Ⅲ patients aged 30-60 yr weighing 40-70 kg undergoing elective partial hepatectomy for liver cancer were randomly divided into 2 groups ( n = 20 each): group C normal BP and group H controlled hypotension. Hepatic portal was occluded during operation. In group C normal BP was maintained during reperfusion while in group H controlled hypotension (MAP was maintained at 60-70 mm Hg) was performed for 10 min since the beginning of reperfusion.Venous blood samples were taken before hepatic ischemia (T0 ,baseline) and at 15 min of ischemia (T1) and 25 min of reperfnsion (T2 ) for determination of plasma endothelin (ET), nitric oxide(NO), TNF-α and IL-1 concentrations. Results I/R of the liver led to significant increase in plasma ET, TNF-α and IL-1 concentrations and decrease in plasma NO concentration at T1,2 as compared with the baseline values at T0 in both groups. Plasma ET,TNF-α and IL- 1 concentrations were significantly lower while plasma NO concentration was significantly higher at T2 in group H than in group C. Conclusion Ten minutes controlled hypotension in the initial stage of reperfusion can attenuate I/R-induced injury to the liver in patients undergoing hepatectomy by balancing ET with NO and inhibiting inflammation response.

Objective To evaluate the effect of controlled hypotension at the beginning of reperfusion on ischemia-reperfusion (I/R) injury of the liver in patients undergoing hepatectomy.Methods Forty ASA Ⅱ or Ⅲ patients (aged 30-60 years and weighing 40-70 kg) undergoing elective partial hepatectomy for liver cancer were randomly divided into two groups (n =20 each):normal blood pressure group (control group,group C) and controlled hypotension group (group H).In group C,normal blood pressure was maintained during reperfusion,while in group H,controlled hypotension (the mean arterial blood pressure (MAP) was maintained at 60-70 mm Hg) was performed for 10 minutes since the beginning of reperfusion.Hepatic portal was occluded during operation.Venous blood samples were taken before hepatic ischemia (T0,baseline) and after 15 minutes of ischemia (T1) and after 25 minutes of reperfusion (T2) for determination of plasma levels of endothelin (ET),nitric oxide (NO),tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1).Results I/R of the liver led to significant increases in plasma levels of ET,TNF-α and IL-1 and a decrease in plasma level of NO at T1,2 as compared with the baseline values at T0 in both groups.Plasma levels of ET,TNF-α and IL-1 were significantly lower while plasma level of NO was significantly higher at T2 in group H than in group C.Conclusion Controlled hypotension for 10 minutes in the initial stage of reperfusion can attenuate I/R-induced injury to the liver in patients undergoing hepatectomy through balancing ET with NO and inhibiting inflammation responses.

Objective To evaluate the role of 2B subunit-containing NMDA receptors ( NR2B) in the rostal anterior cingulate cortex ( rACC) in development of pain-related aversion in a rat model of bone cancer pain using siRNA technique. Methods Forty-five healthy male Wistar rats, weighing 220-250 g, were divided into 3 groups ( n=15 each) using a random number table method: normal saline blank control group ( group NS) , NR2B-siRNA lentivirus group ( group LV-NR2B) and pGC-FU-siRNA lentivirus group (group LV-NC). A total volume of MADB-106 cells 3μl (4. 8×109 cells∕ml) was inoculated into the bone marrow cavity of the right tibia of rats. At day 2 after inoculation, NR2B∕siRNA recombinant lentivirus 0. 2μl was injected into rACC in group LV-NR2B, and pGC-FU-siRNA negative recombinant lentivirus 0. 2μl was injected into rACC in group LV-NC. The mechanical paw withdrawal threshold ( MWT) was measured at 1 day before inoculation and 3, 7, 14 and 21 days after inoculation. Conditioned place avoidance test was performed at 1 day before inoculation and 14 days after inoculation, and the percentage of residence time in room A was calculated. The rats were sacrificed at 21 days after inoculation and the rACC was re-moved for detecting NR2B protein and mRNA expression by Western blot or real-time polymerase chain re-action. Results Compared with the baseline at 1 day before inoculation, the MWT was significantly de-creased at 7, 14 and 21 days after inoculation, and the percentage of residence time in room A was de-creased at 14 days after inoculation in NS and LV-NC groups (P<0. 05), and no significant change was found in the parameters mentioned above in LV-NR2B group (P>0. 05). Compared with group NS, the MWT was significantly increased at 14 and 21 days after inoculation, the percentage of residence time in room A was increased at 14 days after inoculation, and the expression of NR2B protein and mRNA was down-regulated in group LV-NR2B ( P<0. 05) , and no significant change was found in the parameters men-tioned above in group LV-NC (P>0. 05). Conclusion Up-regulated expression of NR2B in rACC is in-volved in development of pain-related aversion in a rat model of bone cancer pain.

Objective To build a Monte Carlo dose verification tool for IMRT Plan by implanting an irradiation source model into DPM code and to extend the ability of DPM to calculate any incident angles and irregular-inhomogeneous fields.Methods The virtual source and the energy spectrum unfolded from the accelerator measurement data were used,in combination with optimized intensity maps,to calculate the dose distribution of the irradiation irregular-inhomogeneous field.The irradiation source model of accelerator was substituted by a grid-based surface source.The contour and the intensity distribution of the surface source were optimized by IMRT.The dose calculation was realized by combining the position of the emitter with the fluence map from the IMRT plan.The weight of the emitter was decided by the grid intensity.The direction of the emitter was decided by the combination of the virtual source and the emitting position.The weighted fraction of the emitter was also combined with the flux grid intensity based on the particle transport model of DPM code.Results The accuracy of calculation was verified by comparing with the measured data.It was illustrated that the differences were acceptable (＜ 2％ inside the field,2-3 mm in the penumbra).The dose calculation of irregular field by DPM simulation was also compared with that of FSPB (Finite Size Pencil Beam).The passing rate of gamma analysis was 95.1％ for peripheral lung cancer.The regular field and the irregular rotational field were all within permissible range of error.The calculation time of regular fields were less than 2 h,and that of the test of peripheral lung cancer was 160 min.Conclusions The adapted DPM code with its simple irradiation source model is faster than that with classical Monte Carlo procedure.Its computational accuracy and speed satisfy the clinical requiremcnt,and it can be useful as a Monte Carlo dose verification tool for IMRT Plan.

Objective To investigate the change in NF-κB activity in astrocytes in spinal dorsal horn in a rat model of neuropathic pain and the underlying mechanism. Methods Sixteen male SD rats aged 2-3 months weighing 220-280 g were randomly divided into 2 groups ( n = 8 each) : sham operation group (group S) and CCI group. Neuropathic pain was induced by chronic constrictive injury (CCI) . Right sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 chromic catgut. In group S the right sciatic nerve was exposed but not ligated. The paw withdrawal threshold (PWT) to von Frey filament stimulation and paw withdrawal latency (PWL) to radiant heat stimulation were measured at 1 d before (baseline) and 7 d after operation. The animals were then killed and the lumbar segment of the spinal cord (L_(4-6)) was removed. The expression of NF-κB in the astrocytes in spinal dorsal horn was determined by immuno-histochemistry. Results PWT and PWL to mechanical and thermal stimuli were significantly decreased after operation as compared with the baseline before operation in group CCI. The number of NF-κBp65 immunoreaction positive cells in the spinal dorsal horn on the operated side was significantly larger in group CCI than in group S. Conclusion NF-κB signal transduction pathway in the astrocytes in the spinal dorsal hom may be involved in neuropathic pain.

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