中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
12期
2775-2776
,共2页
呼吸机相关肺损伤%氯胺酮%核因子-κB
呼吸機相關肺損傷%氯胺酮%覈因子-κB
호흡궤상관폐손상%록알동%핵인자-κB
Ventilator-induced lung injury%Ketamine%Nuclear factor-κB
目的 探讨氯胺酮预先给药对大鼠呼吸机所致肺损伤(VILI)的影响及机制.方法 将60只雄性SD大鼠随机分为3组:对照组(C组),不行机械通气;大潮气量组(H组)和氯胺酮组(K组),每组15只.H组和K组接受机械通气,参数均设为:潮气量40 ml/kg,呼吸频率40次/分.K组在机械通气前给予腹腔内注射氯胺酮(10 mg/kg).4h后放血处死大鼠,测定肺湿/干重比(W/D);检测支气管肺泡灌洗液(BALF)中的蛋白含量、白细胞总数以及血清和BALF中肿瘤坏死因子-α(TNF-d)水平,Western blot测定肺组织中核因子κB (NF-κB)的表达.结果 与C组比较,在大潮气量机械通气4h后,H组BALF中总蛋白含量、肺W/D值、WBC计数和TNF-α水平[(2.18±0.41) g/ml、5.51 ±0.30、(7.10±1.30)×106/L、(451.69±112.35) ng/L]均显著升高(P＜0.05);肺组织中NF-κB表达水平(0.47 ±0.09)也显著升高;与H组比较,在大潮气量机械通气4h后,H组BALF中总蛋白含量、肺W/D值、WBC计数和TNF-α水平[(0.29 ±0.12) g/ml、4.48±0.24、(2.56 ±0.41)× 106/L、(198.57±59.76)ng/L]均显著降低(P＜0.05);肺组织中NF-κB表达水平(0.33 ±0.08)也显著降低.结论 氯胺酮预先给药能减轻大鼠VILI,其机制可能与降低了肺内炎性细胞因子的释放和抑制了NF-κB通路有关.
目的 探討氯胺酮預先給藥對大鼠呼吸機所緻肺損傷(VILI)的影響及機製.方法 將60隻雄性SD大鼠隨機分為3組:對照組(C組),不行機械通氣;大潮氣量組(H組)和氯胺酮組(K組),每組15隻.H組和K組接受機械通氣,參數均設為:潮氣量40 ml/kg,呼吸頻率40次/分.K組在機械通氣前給予腹腔內註射氯胺酮(10 mg/kg).4h後放血處死大鼠,測定肺濕/榦重比(W/D);檢測支氣管肺泡灌洗液(BALF)中的蛋白含量、白細胞總數以及血清和BALF中腫瘤壞死因子-α(TNF-d)水平,Western blot測定肺組織中覈因子κB (NF-κB)的錶達.結果 與C組比較,在大潮氣量機械通氣4h後,H組BALF中總蛋白含量、肺W/D值、WBC計數和TNF-α水平[(2.18±0.41) g/ml、5.51 ±0.30、(7.10±1.30)×106/L、(451.69±112.35) ng/L]均顯著升高(P＜0.05);肺組織中NF-κB錶達水平(0.47 ±0.09)也顯著升高;與H組比較,在大潮氣量機械通氣4h後,H組BALF中總蛋白含量、肺W/D值、WBC計數和TNF-α水平[(0.29 ±0.12) g/ml、4.48±0.24、(2.56 ±0.41)× 106/L、(198.57±59.76)ng/L]均顯著降低(P＜0.05);肺組織中NF-κB錶達水平(0.33 ±0.08)也顯著降低.結論 氯胺酮預先給藥能減輕大鼠VILI,其機製可能與降低瞭肺內炎性細胞因子的釋放和抑製瞭NF-κB通路有關.
목적 탐토록알동예선급약대대서호흡궤소치폐손상(VILI)적영향급궤제.방법 장60지웅성SD대서수궤분위3조:대조조(C조),불행궤계통기;대조기량조(H조)화록알동조(K조),매조15지.H조화K조접수궤계통기,삼수균설위:조기량40 ml/kg,호흡빈솔40차/분.K조재궤계통기전급여복강내주사록알동(10 mg/kg).4h후방혈처사대서,측정폐습/간중비(W/D);검측지기관폐포관세액(BALF)중적단백함량、백세포총수이급혈청화BALF중종류배사인자-α(TNF-d)수평,Western blot측정폐조직중핵인자κB (NF-κB)적표체.결과 여C조비교,재대조기량궤계통기4h후,H조BALF중총단백함량、폐W/D치、WBC계수화TNF-α수평[(2.18±0.41) g/ml、5.51 ±0.30、(7.10±1.30)×106/L、(451.69±112.35) ng/L]균현저승고(P＜0.05);폐조직중NF-κB표체수평(0.47 ±0.09)야현저승고;여H조비교,재대조기량궤계통기4h후,H조BALF중총단백함량、폐W/D치、WBC계수화TNF-α수평[(0.29 ±0.12) g/ml、4.48±0.24、(2.56 ±0.41)× 106/L、(198.57±59.76)ng/L]균현저강저(P＜0.05);폐조직중NF-κB표체수평(0.33 ±0.08)야현저강저.결론 록알동예선급약능감경대서VILI,기궤제가능여강저료폐내염성세포인자적석방화억제료NF-κB통로유관.
Objective To investigate the effect of Ketamine pretreatment in a rat model of ventilator-induced lung injury (VILI) and the possible mechanisms.Methods Sixty male SD rats were randomly divided into 3 groups (n =20 each):control group (group C),no mechanical ventilation; high tidal ventilation group (group H),and Ketamine group (group K).The set parameters of mechanical ventilation were VT =40 ml/kg,and RR =40 breathes/min.The animals were sacrificed by exsanguinations after 4 h mechanical ventilation.The wet-to-dry weight ratios (W/D),and total protein (TP) contents,WBC counts and the levels of tumor necrosis factor (TNF)-α in broncho-alveolar lavage fluid (BALF) were mesured.Nuclear factor-κB (NF-κB) protein was detected by Western blotting in each group.Results W/D,WBC counts,TP contents and the levels of TNF-α in groups H and K were [(2.18 ± 0.41),(0.29±0.12) g/ml],(5.51±0.30,4.48±0.24),[(7.10±1.30),(2.56±0.41)× 106/L],and [(451.69 ± 112.35),(198.57 ±59.76) ng/L],respectively.The average values of NF-κB protein in groups H and K were (0.47 ± 0.09) and (0.33 ± 0.08) respectively.Conclusion Pretreatment with Ketamine can significantly attenuate VILI in rats through suppressing the release of inflammatory cytokines and inhibiting the NF-κB pathway.
