中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2008年
5期
440-443
,共4页
董振明%曹瑞旗%康荣田%任玉娥%黄立宁%李晓松
董振明%曹瑞旂%康榮田%任玉娥%黃立寧%李曉鬆
동진명%조서기%강영전%임옥아%황립저%리효송
麻醉%硬膜外%呼吸窘迫综合征%成人%炎症
痳醉%硬膜外%呼吸窘迫綜閤徵%成人%炎癥
마취%경막외%호흡군박종합정%성인%염증
Anesthesia,epidural%Respiratory distress syndrome,adult%Inflammation
目的 观察胸段硬膜外阻滞对油酸诱发猪急性肺损伤(ALI)时炎性反应的影响.方法 家猪14只,体重30~35kg,随机分为2组(n=7):对照组(C组)及硬膜外阻滞组(TEB组).于T3,4硬膜外置管后,采用静脉输注油酸的方法 制备ALI模型.ALI模型制备成功后,TEB组硬膜外注射0.25%罗哌卡因5ml,随后以2ml/h速率持续输注4 h,C组给予等容量生理盐水.分别于输注油酸前即刻、ALI模型制备成功后即刻、硬膜外给药1、2、3和4 h时测定PaO2.于硬膜外给药4 h时处死动物,行右侧支气管肺泡灌洗,计数支气管肺泡灌洗液(BALF)中细胞总数,计算中性粒细胞(PMN)百分比及PMN凋亡率;取左肺组织,测定总肺水量(TLW)及血管外肺水量(EVLW),并观察肺组织病理学结果 .结果 与C组比较,TEB组BALF中细胞总数、PMN百分比、TLW及EVLW均降低,PaO2和PMN凋亡率升高(P<0.05或0.01).TEB组肺组织病理学损伤程度较C组减轻.结论 胸段硬膜外阻滞可减轻猪ALI时肺组织的炎性反应.
目的 觀察胸段硬膜外阻滯對油痠誘髮豬急性肺損傷(ALI)時炎性反應的影響.方法 傢豬14隻,體重30~35kg,隨機分為2組(n=7):對照組(C組)及硬膜外阻滯組(TEB組).于T3,4硬膜外置管後,採用靜脈輸註油痠的方法 製備ALI模型.ALI模型製備成功後,TEB組硬膜外註射0.25%囉哌卡因5ml,隨後以2ml/h速率持續輸註4 h,C組給予等容量生理鹽水.分彆于輸註油痠前即刻、ALI模型製備成功後即刻、硬膜外給藥1、2、3和4 h時測定PaO2.于硬膜外給藥4 h時處死動物,行右側支氣管肺泡灌洗,計數支氣管肺泡灌洗液(BALF)中細胞總數,計算中性粒細胞(PMN)百分比及PMN凋亡率;取左肺組織,測定總肺水量(TLW)及血管外肺水量(EVLW),併觀察肺組織病理學結果 .結果 與C組比較,TEB組BALF中細胞總數、PMN百分比、TLW及EVLW均降低,PaO2和PMN凋亡率升高(P<0.05或0.01).TEB組肺組織病理學損傷程度較C組減輕.結論 胸段硬膜外阻滯可減輕豬ALI時肺組織的炎性反應.
목적 관찰흉단경막외조체대유산유발저급성폐손상(ALI)시염성반응적영향.방법 가저14지,체중30~35kg,수궤분위2조(n=7):대조조(C조)급경막외조체조(TEB조).우T3,4경막외치관후,채용정맥수주유산적방법 제비ALI모형.ALI모형제비성공후,TEB조경막외주사0.25%라고잡인5ml,수후이2ml/h속솔지속수주4 h,C조급여등용량생리염수.분별우수주유산전즉각、ALI모형제비성공후즉각、경막외급약1、2、3화4 h시측정PaO2.우경막외급약4 h시처사동물,행우측지기관폐포관세,계수지기관폐포관세액(BALF)중세포총수,계산중성립세포(PMN)백분비급PMN조망솔;취좌폐조직,측정총폐수량(TLW)급혈관외폐수량(EVLW),병관찰폐조직병이학결과 .결과 여C조비교,TEB조BALF중세포총수、PMN백분비、TLW급EVLW균강저,PaO2화PMN조망솔승고(P<0.05혹0.01).TEB조폐조직병이학손상정도교C조감경.결론 흉단경막외조체가감경저ALI시폐조직적염성반응.
Objective To investigate the influence of thoracic epidural blockade(TEB)on the pulmonary inflammatory response in a piglet model of oleie acid-induced acute lung injury(ALI).Methods Fourteen piglets of both sexes weighing 30-35 kg were randomly divided into 2 groups(n=7 each):I control group(C)and Ⅱ TEB group.The animals were anesthetized with 2.5% pentothal sodium,intubated and mechanically ventilated.Right internal carotid cartery wag cannulated for BP monitoring and blood sampling.Right internal jugular vein was cannulated for oleic acid administration.Epidural catheter was placed at T3.4 interspace and was advanced cephalad for 5 cm in the epidural space.Correct placement was confirmed by X-ray.ALI was induced by administration of oleic acid 0.1 ml/kg in 20 ml which was infused via internal jugular vein at 40 ml/h until Pa02/Fi02≤200.Abolus of 0.25% ropivacaine 5 ml was administered followed by continuous infusion at 2 ml/h for 4 h via epidural catheter after induction of ALI in TEB group.In control group equal volume of normal saline was administered instead of0.25% ropivacaine.Pa02 was measul'cd before ALI was induced (baseline),immediately after ALI induction and at 1,2,3 and 4 h after epidural rpivacaine.The animals were killed at 4 h after epidural ropivacaine and the lungs were immediately removed.The right main bronchus was lavaged and broncho-alveolar lavage fluid(BALF) was collected for determination of the total number of cells,the percentage of PMN and the rate of PMN apoptosis.The left lung was removed for determination of total lung water(TLW)and extravascular lung water(EVLW)and microscopic examination.Results The total number of cells and the percentage of PMN in BALF and TLW and EVLW were significantly decreased while the rate of apoptosis of PMN and PaO2,were significantly increasedin TEB group as compared with control group(P<O.05 orO.01).The histologicl damage was also significantly reduced in TEB group.Conclusion TEB can attenuate the pulmonary inflammatory response in a piglet model of oleic acid-induced ALI.