呼吸道發炎反應是氣喘形成的原因之一，對於許多患者而言，這種疾病在嬰兒時期便可發病，其遺傳因素與環境因素對此疾病的開始與演變有著相當重要的影響。經由學者的研究指出，食道與呼吸道之間有著相當複雜的神經分佈及反射機制，他們經由食道灌注1當量濃度鹽酸後，透過食道與呼吸道間的神經反射路徑而產生類速激肽物質，進而引起呼吸道血漿滲漏情形。在本研究中，我們先給予大鼠內含有200微克卵白蛋白-氫氧化鋁之懸浮液1毫升，在第1、2、3及第11天經由腹膜腔內注射，使之產生致敏作用，然後再改以食道灌注卵白蛋白，在經過不同時間點後予以灌流固定犧牲大鼠，並觀察下呼吸道及食道的血漿滲漏和白血球聚集情形。血漿滲漏計量方法是利用印地安染劑標定滲漏血管面積密度百分比。實驗結果顯示在食道灌注75 mg/kg卵白蛋白可造成下呼吸道血漿滲漏增加情形，並在給予卵白蛋白刺激後的30分鐘為最明顯。血管滲漏面積密度分別如下：氣管為22.43 ± 3.34％，右主支氣管為20.57 ± 4.91％，左主支氣管為18.47 ± 5.03％，會厭為27.85 ± 2.71％。灌注3小時後幾乎看不到血漿滲漏，然而在4小時後又可見下呼吸道出現明顯的血漿滲漏。由組織切片染色可清楚地看到實驗組有多個肥胖細胞出現且有去顆粒作用產生。於是在實驗過程中可得知此發炎反應有早期和晚期反應作用。為了研究迷走神經是否參與此發炎反應，本實驗還藉由雙側迷走神經切除術進一步探討了神經反射機制。結果顯示不論是經由雙側迷走神經切除或注射組織胺H1接受器的拮抗劑-mepyramine前處理，均可以有效地抑制經食道灌注卵白蛋白所引發的下呼吸道發炎反應。結果証明，大鼠經卵白蛋白致敏化後再由食道灌注卵白蛋白給予刺激，會引發早期及晚期的發炎反應，且這些反應可能與迷走神經C型纖維和組織胺H1接受器有關。

Inflammatory response in the airway may lead to asthma. Asthma may develop during the childhood in some asthmatic patients. Both environmental and genetic factors may influence the onset and progress of asthma. It is well-known that there may be complex neural innervation and reflex mechanisms between trachea and esophagus. Intraesophgeal infusion of 1N HCl could lead to tracheal inflammation by activating neural reflex pathway and cause tachykinin-like substance to release. In this study, we first sensitized rats with 1ml of OVA-Al［OH］3 mixture containing 200μg OVA via intraperitoneal injection on days 1, 2, 3 and 11, then perform intraesophageal infusion of ovalbumin to see whether stimulation of esophagus in sensitized rat model could involve inflammatory response in the lower airways. Animals were perfused with saline and fixative at various time points and the esophagus and airway tissues were processed for the subsequent analysis. We observed the extent of plasma leakage and migration of leukocytes in the lower airway. India ink was used to label the leaky blood vessels.The magnitude of plasma leakage was expressed by the area density of India ink-labeled blood vessels. The results showed that the intraesophageal infusion of ovalbumin 75 mg/kg caused an increase in plasma leakage in the lower airways. The plasma leakage peaked at 30 min, the area density of plasma leakage in trachea was 22.43 ± 3.34％; and 20.57 ± 4.91％ in right bronchus; 18.47 ± 5.03％ in left bronchus and 27.85 ± 2.71％ in epiglottis. The extent of leakage gradually diminished 3 hours after ovalbumin infusion. However, a second increased plasma leakage peaked at about 4 hours of ovalbumin infusion. Tissue sections clearly showed degranulation of mast cells in OVA infusion group. Experimental data showed that pretreatment with either bilateral vagotomy, or mepyramine, the histamine H1 receptor antagonist, significantly inhibited the inflammatory response in the lower airways induced by intraesophageal infusion of OVA. In conclusion, there were clearly two phases, early and late phase responses, in inflammatory response in OVA-sensitized rats receiving intra-esophageal OVA challenge. The underlying mechanisms may involve vagal C-fibers and histamine H1 receptors.

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