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Objective To compare the effects of sevoflurane and propofol anesthesia on inflammatory response and pulmonary function during perioperative period in patients undergoing lung cancer resection．MethodsThirty ASA Ⅰ or Ⅱ patients(23 male，7 female) aged 41-64 yr having a body weisht index of 22-30 kg/m2 undegoing elective left lower lobe resection were randomlydivided into 2 groups(n=15 each)：sevoflurane group (group S) and propofol group(group P)．Anesthesia was induced with 6％-8％ sevoflurane or propofol 2 mg/kg and fentanyl 4-6 μg/kg．Intubation with double lumen catheter was facilitated with vecuroniunl 0．1 mg/kg． Anesthesia was maintained with 1％-3％ sevoflurane/propofol infusion(6-10 mg·kg-1·h-1)and intermittent iv boluses of fentanyl and vecuronium．Radial artery was cannulated．Swan-Ganz catheter was placed via right internal jugular vein．The patients were mechanically ventilated．During one lung ventilation(OLV)I：E and VT were adjusted to maintain airway pressure <30 cm H2O．Arlerial and mixed venous blood samples were collected for blood gas analysis before induction of anesthesia(T0)，before OLV(T1)，at the end of OLV(T2)，when the chest was closed(T3) and at 24 h after operation (T4)．PA-aO2，Qs/Qt and respiratory index(RI，PA-aO2/PaO2) were calculated. Serum matrix metallo-proteinase-9 (MMP-9) and MDA were measured at T0, T3 and T4. Dynamic lung compliance (Cd) was calculated at T1-3 .Results PA-aO2, RI and Qs/Qt at T1-3 and serum MMP-9 and MDA concentrations at T3 were significantly increased as compared with the baseline values at T0 in both groups. In group S, Cd was significantly lower at T3 than at T1.PA-AO2, and serum MMP-9 and MDA concentrations at T3, RI at T2,3 and Qs/Qt at T1-3 were significantly higher in group S than in group P. Conclusion The inflammatory response is lower and the injury to pulmonary function is lighter during propofol anesthesia than sevoflurane anesthesia in patients undergoing lung cancer resection.
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Objective To observe the expression of neuron apoptotic protein caused by whole body gyperthermis (WBH) in rats anesthetized using propofol and chloral hydrate,and to explore the pathway of any hippocampal neuron apoptosis induced by WBH. Methods Sixty-three male Wistar rats were randomly divided into 3groups,21 in each group.One guoup received neither anesthesia nor WBH treatment sa a control (group A);group B were anesthetized with an intraperitoneal injection of 100 mg/kg of propofol;group C receivde a similar injection of chloral hydrate. This was followed by WBH (keeping the rats' core temperature at 42°for 30 min) for all three groups. The rats'brains were then removed 24 h after WBH to separate the ghpplcampal CA1,CA2 zones and the dentate gyrus regions.Any neuron apoptosis was detected using the TUNEL methol;Bax/Bcl-2/caspase-3 protein expression was measured with a SABC immmunogistochemical technique;and the changes in ultrastructure were observed tith an electron microscope. Results Compared with group A,the changes in the ultrastructure of neurons in the hippocampus changed after WBh were the most severe in group C.The changes included edema of the organelles,vacuolization of mitochondria,rarefaction of the endocytoplasmic reticulum,incopleasmic reticulum,incomplete synaptic membranes and autophagy.Both the number of apoptotic neurons and the expression of Bax and capase-3 protein in the hippocampus increased in the following order: group A＜group B＜group C.Expression of Bcl-2 protein in the hippocampus increased in the following order: group A＜group C＜group B. Conclusion Hippocampal apoptosis induced by WBh involves upregulating the expression of Bax and caspase-3 and downregulating the expression of Bcl-2.