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博碩士論文 etd-0628105-130435 詳細資訊
Title page for etd-0628105-130435
論文名稱
Title
藉數位影像及立體重建模型分析P物質引發大鼠氣管水腫變化之研究
Change in substance P-induced edema in rat trachea : a digital photomicrography and 3-dimensional reconstruction study
系所名稱
Department
畢業學年期
Year, semester
語文別
Language
學位類別
Degree
頁數
Number of pages
53
研究生
Author
指導教授
Advisor
召集委員
Convenor
口試委員
Advisory Committee
口試日期
Date of Exam
2005-06-21
繳交日期
Date of Submission
2005-06-28
關鍵字
Keywords
P物質、氣管、水腫
substance P, trachea, edema
統計
Statistics
本論文已被瀏覽 5696 次,被下載 3
The thesis/dissertation has been browsed 5696 times, has been downloaded 3 times.
中文摘要
靜脈注射高劑量辣椒素會刺激大鼠呼吸道C型神經纖維釋放速激&#32957;並於氣管的黏膜組織產生急性發炎反應。大量外洩的血漿會堆積在氣管上皮的下方形成水腫。P物質是速激&#32957;類中誘發發炎最重要的神經胜&#32957;。本論文主要目的在於研究P物質 (3 &#181;g/ml/kg)誘發發炎後之水腫形成與消退,並藉數位型態分析法來分析氣管的切片影像拼圖。實驗中更進一步利用連續切片來建立氣管的立體影像,用來分析水腫區塊於呼吸上皮下方之相對分佈。本研究中設計了兩種水腫分析指標用來評估水腫的程度。水腫長度比率為氣管切片中水腫區域的總長度與氣管管腔內面周長之比率。水腫面積比率為氣管切片中水腫區域的總面積與氣管管腔上皮組織總面積之比率。藉由水腫區域之程度來表示黏膜層水腫之時程變化。實驗結果顯示,靜脈注射P物質後5分鐘氣管水腫長度比率與面積比率分別為35.80 ± 1.42 %及16.28±2.51%,為對照組的7.6倍與7.9倍,並於統計學上有顯著的差異(P<0.01)。靜脈注射完P物質,過了1小時之後,水腫長度比率與面積比率分別降為16.40 ± 2.46 % 與 8.00 ± 1.60 %, 為對照組的2.2倍與2.8倍,於統計學上仍有差異 (P < 0.05)。靜脈注射P物質後24小時與與72小時其水腫比率則與對照組之間於統計學上沒有差異(P > 0.05)。 氣管之立體影像顯示靜脈注射P物質後5分鐘呼吸上皮下方有許多水腫區塊的分佈,而且彼此會相互連接。水腫區塊的數量則在靜脈注射P物質後1小時快速的減少。在24小時與72小時後水腫區塊則很少見到。根據實驗結果發現水腫區塊緊鄰於氣管呼吸上皮之現象,推測黏膜表面也許是釋放水腫液之部位。
Abstract
Intravenous application of high dose of capsaicin to the rat stimulates C-fiber neurons that innervate the airways to release tachykinins that produce acute inflammation in the mucosal tissue. Large amount of extravasated plasma is retained underneath the tracheal epithelium to form edema. Substance P (SP) is the most important inflammation-producing peptide of tachykinin family. The present study was to investigate time-dependent formation and remission of edema induced by SP (3 &#181;g/ml/kg) by the use of digital morphometric analysis of montages of tracheal cross sections. Furthermore, 3-dimensional reconstruction of serial tracheal sections was carried out to analyze the relative distribution of subepithelial edematous loci. Two edema indexes were designated for evaluation of the status of edema. Edema length ratio was the ratio of the total length of edematous loci to the circumference of a tracheal section. Edema area ratio was the ratio of the total area of edematous loci to the area of tracheal epithelium and associated edema. The degree of edematous status in the mucosa exhibited a time-dependent change. Five min after application of SP, edema length ratio and edema area ratio in the trachea were 35.80±1.42% and 16.28±2.51%, that were 7.6 and 7.9 times, respectively, the values of vehicle control group. At 1 h after SP, edema length ratio and edema area ratio declined to 16.40±2.46% and 8.00±1.60%, 2.2 and 2.8 times the values of control, but still significantly different (P < 0.05). At 24 or 72 h after SP, the values of edema were not significantly different (P > 0.05) from the control values. Three- dimensional reconstruction study showed that, in the trachea of rats 5 min after receiving SP, there were many subepithelial edematous loci, evenly distributed along the inner circumference of trachea. They were interconnected. The number of edematous loci decreased drastically by 1 h after SP. Loci of edema were rarely found 24 or 72 h after SP. The close association of edema to the tracheal epithelium suggests that the mucosal surface may be the site for elimination of edema fluid.
目次 Table of Contents
致謝-------------------3
中文摘要---------------5
Abstract---------------7
前言-------------------9
研究目的--------------15
材料與方法------------16
實驗結果--------------23
討論------------------28
結論------------------33
參考文獻--------------35
圖表與圖解------------40
參考文獻 References
Barnes PJ 1986. Asthma as an axon reflex. Lancet. 40: 242-244.
Belvisi MG 2003. Sensory nerves and airway inflammation: role of Aδ and C-fibers. Pulmonary Pharmacology & Therapeutics 16: 1-7.
Brokaw JJ, Hillenbrand CM, White GW, McDonald DM 1990. Mechanism of tachyphylaxis associated with neurogenic plasma
extravasation in the rat trachea. Am. Rev. Respir. Dis. 141: 1434-1440.
Couture R, and Regoli D 1981. Inactivation of substance P and its C-terminal fragments in rat plasma and its inhibition by Captopril. Can. J. Physiol. Pharmacol. 59: 621-625.
Euler USV, and Gaddum JH 1931. An unidentified depressor substance in certain tissue extracts. J. Physiol. (Lond) 72: 74-87.
Fiala JC, Allwardt B, Harris KM 2002. Dendritic spines do not split during hippocampal LTP or maturation. Nat Neurosci. 5: 297-298.
Fiala JC, Harris KM 2002. Computer-based alignment and reconstruction of serial sections. Microscopy and Analysis. USA Edition. 52: 5-7.
Gamse R, Molnar A, and Lembeck F 1979. Substance P release from spinal cord slices by capsaicin. Life Sci. 25: 629-636.
Guo JJ, Wang DS, Huang HT 2003. Spontaneous remission of edema and regranulation of goblet cells in rat trachea after capsaicin-induced acute inflammation. Anat. Embryol. 206: 301-309.
Holzer P 1988., Local effector functions of capsaicin-sensitive sensory nerve endings: involvement of tachykinins, calcitonin gene-related peptide and other neuropeptides. Neuroscience 24: 739-68.
Huang HT 1993. Unlateral cervical vagotomy decrease the magnitude of neurogenic inflammation induced by capsaicins in the ispilateral bronchial tree of rats, Anat. Embryol. 180: 325-341.
James AL, Hogg JC, Dunn LA, Par&#233; PD 1988. The use of the internal perimeter to compare airway size and to calculate smooth muscle shorteing. Am. Rev. Respir. Dis. 138: 136-139.
Jancso N, Jancso-Gabor A, and Szolcsanyi J 1967. Direct evidence for neurogenic inflammation and its prevention by denervation and by pretreatment with capsaicin. Br. J. Pharmac. Chemother. 31: 138-151.
Jancso G, Kiraly E, Jancso-Gabor A 1977., Pharmacologically induced selective degeneration of chemosensitive primary sensory neurons. Nature (Lond) 270: 741-743.
Lembeck F, and Gamse R 1982. Substance P in peripherial sensory process. In substance P in the nervous system, ed. By Proter, R & O’connor, M., pp35-54, Pitman, London.
Lindemann B 2001. Receptors and transduction in taste. Nature 413: 219-225.
Lundberg JM, Saria A 1983. Capsaicin-induced desensitization of airway mucosa to cigarette smoke, mechanical and chemical irritants. Nature (Lond) 302: 251–253
McDonald DM 1987. Neurogenic inflammation in the respiratory tract: actions of sensory nerve mediators on blood vessels and epithelium of the airway mucosa. Am. Rew. Respir. Dis. 136: S65-S72.
McDonald DM 1988 Neurogenic inflammation in the rat trachea. I. Changes in venules, leukocytes, and epithelial cells. J. Neurocytol. 17: 583-603.
McDonald DM 1994. Endothelial gaps and permeability of venules in rat tracheas exposed to inflammatiory stimuli. Am . J. Physiol. 266: L61-L83.
Moncada S, Radomski MW, and Palmer RM 1988. Endothelium-derived relaxing factor. Biochem. Pharmacol. 37: 2495-2501.
Nadel JA 1992. Regulation of neurogenic inflammation by neutral endopeptidase. Am. Rev. Respir. Dis. 145: S48-S52.
Nicholl JG, Martin AR, Wallace BG 1992., From neuron to brain. Sinauer press 3rd ed. pp. 272-274.
Olgart L, Gazelius B, Brodin E, and Nilsson G 1977. Release of substance P-like immunoreactiviyt from the dental pulp. Acta. Physiol. Scand. 101: 510-512.
Persson C. G. A. 1986. Role of plasma exudation in asmatic airways. Lancet 42: 1126-1128.
Persson C. G. A. 1988. Plasma exudation and asthma. Lung 166: 1-23.
Saria A, Lundberg JM 1983. Evans blue fluorescence: quantitative and morphological evaluation of vascular permeability in animal tissues. J. Neurosci. Methods. 8: 41–49
Solway J, Leff AR 1991., Sensory neuropeptides and airway function. J. Appl. Physiol. 71: 2077-2087.
Steinhoff M, Vergnolle N, Young SH, Tognetto M, Amadesi S, Ennes HS 2000. Agonists of proteinase-actived receptor 2 induce inflammation by a neurogenic mechanism. Nature Med. 6: 151-158.
Ventura R, Harris KM 1999. Three-dimensional relationships between hippocampal synapses and astrocytes. J. Neurosci. 19: 6897-6906.
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