內毒素（lipopolysaccharide，簡稱LPS）為革蘭式陰性菌細胞壁外膜的成份，可活化巨噬細胞釋放細胞激素而引起局部性或全身性發炎反應，其發炎反應的特徵為血漿滲漏和多形性白血球浸潤至組織間隙。本實驗研究LPS誘導皮下發炎損傷的效應，包括在不同時間點上的血漿外洩之程度和白血球滲出的情形，將LPS(500 μg/site)以皮下注射的方式，在大鼠後肢足背皮膚誘發血漿滲漏，利用靜脈注射印地安墨汁(1 ml/kg)作為追蹤染料以計量被ink標示滲漏血管的面積密度百分比，實驗結果發現在注射LPS後5分鐘，即刻引起微血管後小靜脈中的血漿滲漏產生，被標定的滲漏血管面積密度為33.9 %±5.6 % (n=5)，為注射生理食鹽水之對照組(16.6 %±1.8 %, n=5)的2倍；尤其在間隔30分鐘血漿滲漏值達到最高(42.5 %±2.5 %, n=11)。硝酸銀染色法展現微小血管中的靜脈內皮細胞之間出現的內皮隙，與血漿滲漏呈正相關。後肢足背皮膚做過氧化酶組織化學染色，白血球（嗜中性球和嗜伊紅性白血球）的細胞質顆粒呈正反應，白血球予以計數，結果顯示LPS引誘白血球黏附及浸潤情形相當嚴重，為對照組注射生理食鹽水組別的5倍之多。由實驗結果推論，局部皮下注射LPS引起內皮隙的形成和白血球浸潤而導致局部血管通透性增加。

Endotoxin (lipopolysaccharide, LPS), is a constituent of the outer membrane of Gram-negative bacteria, activates macrophages to release cytokines that can cause local or systemic inflammatory responses. Plasma leakage and polymorphonuclear leukocyte infiltration are characteristic features of inflammation. This study examined the effect of LPS to induce subcutaneous inflammatory lesions, including time course of changes in plasma extravasation and level of leukocyte influx into the tissue interstitium. To investigate LPS-induced plasma leakage in the skin, LPS (500 μg/site) was administered by subcutaneous injection in the hindpaw skin. India ink (1 ml/kg) was used as tracer dye to measure the area density of ink-labeled leaky blood vessels. Our results showed that the postcapillary venules were leaking immediately at five minutes after LPS. The area density of India ink-labeled leaky vessels was 33.9 %±5.6 % (n=5) after the administration of LPS. The magnitude of plasma leakage was 2 times as the value of saline control (16.6 %±1.8 %, n=5). Plasma leakage peaked at 30 min (42.5 %±2.5 %, n=11) after LPS. Staining of the microvasculature by silver nitrate showed endothelial gap formation in venules and indicated the positive relevance to plasma leakage. Leukocytes (neutrophils and eosinophils) in hindpaw skin whole mounts were stained by a histochemical reaction for myeloperoxidase and the numbers of leukocytes quantified. LPS caused a severe response in leukocyte adhesion and accumulation. The number of leukocytes after LPS was 5 times as the number after saline. It is concluded that local injection of LPS in the skin caused formation of endothelial gaps and leukocyte infiltration that resulted in an increase in local vascular permeability.

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賴宗鼎,黃鎮國 編譯 Cotran, Kumar, Robbins原著1998. Robbins Pathologic Basis of Disease（羅賓氏病理學）藝軒圖書出版社