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研究生:李才宇
論文名稱:一氧化氮對於空氣栓塞引發急性肺損傷的影響
論文名稱(外文):The Effects of Nitric Oxide on Air Embolism-Induced Acute Lung Injury
指導教授:李敏輝李敏輝引用關係
學位類別:碩士
校院名稱:國防醫學院
系所名稱:航太醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:1999
畢業學年度:87
語文別:中文
論文頁數:58
中文關鍵詞:一氧化氮空氣栓塞
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  肺空氣栓塞(air embolism)是飛行時發生減壓症或是爆炸減壓時常見的問題。而空氣栓塞造成肺部傷害的機轉,除了氣泡栓子的機械性阻塞作用以外,氣泡表面活性作用所造成的持續性血液變化,也是其原因之一。此外,一氧化氮近年來在不同原因所造成的肺損傷研究中發現:它可以改善肺高血壓的現象,並可能參與肺水腫形成的機轉。所以一氧化氮在空氣栓塞所造成的肺部傷害中,可能也扮演著若干的影響。因此我們利用大鼠原位離體肺(isolated rat lung in situ )的實驗模型,混合10 ml 的鼠血及等體積之Hank's balanced salt solution(HBSS)做為灌流液,以灌注空氣(0.25 ml/min,1 min)模擬空氣栓塞引發肺損傷,同時並利用一氧化氮(nitric oxide,NO)生成之前驅物(L-arginine,15 mg/kg),以及一氧化氮合成□抑制劑(N*-nitro-L-arginine methyl ester,L-NAME,15 mg/kg),來探討一氧化氮對於肺部空氣栓塞引發之肺高血壓及肺水腫等急性肺損傷現象的影響。
  實驗結果發現:肺空氣栓塞造成肺高血壓及肺水腫的現象,空氣栓塞組之肺動脈壓增加值(the increase of pulmonary arterial pressure ,△PAP)於灌注空氣後為31.9□0.8mmHg,之後肺動脈壓漸漸下降,肺動脈壓由最大值下降至5分鐘時的差與肺動脈壓增加值的比值(即肺動脈壓下降速率,P5)為0.39□0.02,而60分鐘時的肺重增加值(lung weight gain,LWG)為1.39□0.08 g,肺微血管通透係數(pulmonary filtration coefficient,Kfc)由0.3492□0.0212增至0.8549□0.1135 g/min/cmH2O/100g (P<0.05),肺沖洗液蛋白質濃度(lung lavage protein concentration,LPC)則為135.6□47.3 mg/dl(與對照組LPC=26.5□3.0 mg/dl比較,P<0.05),肺組織切片並發現肺泡中隔增厚,以及發炎細胞的浸潤。而前置給予L-arginine,則減輕肺損傷的程度。其△PAP值為31.0□0.5 mmHg,但肺動脈壓下降較快(P5=0.49□0.01,P<0.05),Kfc值則降為0.3425□0.0058 g/min/cmH2O/100g(P<0.05),肺沖洗液蛋白質濃度也降低(LPC=41.2□7.7 mg/dl,P<0.01),且60分鐘時的肺重則沒有增加,肺組織切片並與對照組接近。而前置給予L-NAME,△PAP值為33.5□0.3 mmHg,之後肺高血壓現象仍持續,肺動脈壓下降較慢(P5=0.22□0.01,P<0.01),且在5分鐘時肺重即增加為3.17□0.15 g(P<0.01),其Kfc值則因在灌注空氣後5分鐘即因肺水腫情形嚴重而終止實驗,因而無法測量,肺沖洗液蛋白質濃度則為431.0□128.9 mg/dl(P<0.01),肺組織切片發現更嚴重之肺泡中隔增厚及發炎細胞浸潤,反而更加重肺損傷的程度。
  所以,綜合以上的結果,一氧化氮對於因空氣栓塞所引發之肺高血壓及肺水腫等急性肺損傷的現象,可能具有保護的作用,而其機轉可能是藉由減輕肺高血壓的程度,以及減少肺微血管通透性的增加而達成。


  Air embolism, occurring in pilots during high-altitude tests, in divers undergoing decompression after hyperbaric exposure, and in a number of clinical situations, can lead to pulmonary hypertension, lung edema, and lung injury. Accumulating evidences suggest that nitric oxide (NO) plays a key role in the development of lung edema in various models of acute lung injury. Therefore, we conducted the present study to evaluate the role of endogenous NO in air emboli-induced acute lung injury. The in situ isolated rat lungs perfused with blood-HBSS buffer solution, a mixture of 10 ml rat blood and 10 ml Hank's balanced salt solution (HBSS), were applied to quantify the effects of NO precursor (L-arginine) and NO synthase inhibitor (L-NAME) on acute lung injury induced by air emboli which was produced by infusion of air into pulmonary artery. Lung weight gain (LGW) and pulmonary artery pressure (PAP) were continuously monitored, and pulmonary filtration coefficient (Kfc) as an index of microvascular injury was measured by elevation of venous pressure and time zero extrapolation of the slope of the weight gain curve. In the end of experiment, lung lavage was also collected to analyze the protein concentration (LPC).
  Infusion of air with the rate of 0.25 ml/min for 1 minute into the pulmonary artery resulted in pulmonary hypertension and lung injury. PAP increased steeply and reached its maximum when air infusion stop and then fell progressively with P5 (the reducing ratio of pulmonary artery pressure at time 5 minute) as 0.39□0.02. The maximal increase of pulmonary artery pressure (△PAP) was 31.9□0.8 mmHg. Air embolism caused the increase of LWG, LPC, and Kfc with the values of 1.39□0.08 g, 135.6□47.3 mg/dl, 0.8549□0.1135 g/min/cmH2O/100g, respectively (P<0.05). Histological findings of the lung tissue demonstrated pulmonary congestion, alveolar septum edema, and inflammatory cell infiltration. Pretreatment with L-arginine (15 mg/kg) completely abolished the development of lung injury with LWG=0□0.1 g, LPC=41.2□7.7 mg/dl, and Kfc=0.3425□0.0058 g/min/cmH2O/100g (P<0.05). The pathology showed no sign of lung edema and inflammatory cell infiltration. Although L-arginine could not attenuate the pulmonary hypertension with △PAP=31.0□0.5 mmHg (P>0.05). However, it speeded up the reduction of pulmonary hypertension with P5=0.49□0.01 (P<0.05). In contrast to the effects of L-arginine, pretreatment with L-NAME (15 mg/kg) worsened the LWG, LPC and P5 with the values of 3.17□0.15 g, 431.0□128.9 mg/dl, and 0.22□0.01, respectively (P<0.05). More sever lung edema was also observed in pathological examination.
  In conclusion, our findings suggest that endogenous NO plays a key role in the development of lung edema and pulmonary hypertension induced by air-emboli. NO precursor, L-arginine, can prevent the lung from air emboli-induced lung injury.

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