• Title/Summary/Keyword: 자극과 반응

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An Anatomical Study of the Posterior Tympanum (한국인 중이강후벽에 관한 형태해부학적 고찰)

  • 양오규;윤강묵;심상열;김영명
    • Proceedings of the KOR-BRONCHOESO Conference
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    • 1982.05a
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    • pp.17.2-19
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    • 1982
  • The sinus tympani is subject to great variability in the size, shape and posterior extent. A heavy compact bony zone, especially in the posterior portion and the narrow space between the facial nerve and posterior semicircular canal are the limitation of surgical approach. The facial recess should be opened, creating a wide connection between the mesotympanum and mastoid in the Intact canal wall tympanoplasty with mastoidectomy. The surgically created limits of the facial recess are the facial nerve medially, the chorda tympani laterally and the bone adjacent to the incus superiorly. Using adult Korean's thirty-five temporal bones, the authors measured the osteologic reslationship in the posterior tympanum, especially sinus tympani and facial recess. The result was as followed. 1. The average distance from the anterior end of the pyramidal eminence. 1) to the edge of the sinus tympani directly posterior was 2.54(1.05-5.40)mm. 2) to the maximum posterior extent was 3.22(1.25-7.45)mm. 3) to the maximum cephaled extent was 0.67 (0.40-1.75)mm. 2. The boundary of the sinus tympani was 82.9% from the lower margin oval window to the upper margin round window niche. 3. The deepest part of the sinus tympani was 62.9% in the mid portion, between the ponticulus and subiculum. 4. The oblique dimension from the fossa incudis above to the hypotympanum below was 8.13(7.90-9.55)mm. 5. The transverse dimensions midway between the oval window above and round window below was 3.00(2.85-3.45)mm. 6. The transverse dimension at the level of the fossa incudis was 1.81(1.40-2.15)mm. 7. The facial nerve dehiscence was 14.3%. 8. Anterior-posterior diameter of the footplate was 2.98(2.85-3.05) mm. 9. The average distance from the footplate. 1) to the cochleariform process was 1.42(1.35-1.55) mm. 2) to the round window niche was 1.85(1.45-2.10) mm.

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Time Course Change of Phagocytes and Proinflammatory Activities in BALF in Endotoxin-induced Acute Lung Injury (시간별 내독소 정맥주입으로 유발된 급성폐손상의 변화양상에 대한 고찰)

  • Moon, Seung-Hyug;Oh, Je-Ho;Park, Sung-Woo;NamGung, Eun-Kyung;Ki, Shin-Young;Im, Gun-Il;Jung, Sung-Whan;Kim, Hyeon-Tae;Uh, Soo-Tack;Kim, Yong-Hoon;Park, Choon-Sik;Jin, Byeng-Weon
    • Tuberculosis and Respiratory Diseases
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    • v.44 no.2
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    • pp.360-378
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    • 1997
  • Background : Severe acute lung injury(ALI), also known as the adult respiratory distress syndrome(ARDS), is a heterogenous nature of dynamic and explosive clinical synrome that exacts a mortality of approximately 50%. Endotoxin(ETX) is an abundant component of the outer membrane of gram-negative bacteria capable of inducing severe lung injury in gram-negative sepsis and gram-negative bacterial pneumonia, which are among the most common predisposing causes of ARDS. The influx of PMNs into airway tissue is a pathological hallmark of LPS-induced lung injury. And there is a substantial evidence suggesting that cytokines are important mediators of lung injury in gram-negative sepsis. However, the kinetics of phagocytes and cytokines by an exact time sequence and their respective pathogenic importance remain to be elucidated. This study was performed to investigate the role of phagocytes and proinflammatory cytokines in ETX-induced ALI through a time course of changes in the concentration of protein, $TNF{\alpha}$ and IL-6, and counts of total and its differential cells in BALF. The consecutive histologic findings were also evaluated. Method : The experimental animals, healthy male Sprague-Dawley, weighted $200{\pm}50g$, were divided into control- and ALI- group. ALI was induced by an intravenous administration of ETX, 5mg/kg. Above mentioned all parameters were examined at 0(control), 3, 6, 24, 72 h after administration of ETX. $TNF{\alpha}$ and IL-6 cone. in BALF were measured by a bioassay. Results : The protein concentration and total leukocyte count(TC) in BALF was significantly increased at 3h compared to controls(p < 0.05). The protein conc. was significantly elavated during observation period, but TC was significantly decreased at 72h(p < 0.05 vs. 24h). There was a close relationship between TC and protein cone. in BALF(r = 0.65, p < 0.001). The PMN and monocyte count was well correlated with TC in BALF, and the correlation of PMN(r = 0.97, p < 0.001) appeared to be more meaningful than that of monocyte(r = 0.61, p < 0.001). There was also a significant correlation between protein cone. and PMN or monocyte count in BALF(PMN vs. monocyte : r = 0.55, p < 0.005 vs. r = 0.64, p < 0.001). The count of monocyte was significantly elavated during observation period though a meaningful reduction of PMN count in BALF at 72h, this observation suggested that monocyte may, at least, partipate in the process of lung injury steadly. In this study, there was no relationship between IL-6 and $TNF{\alpha}$ cone., and $TNF{\alpha}$ but not IL-6 was correlated with TC(r = 0.61, p < 0.05) and monocyte(r = 0.67, p < 0.05) in BALF only at 3, 6h after ETX introduced. In particular, the IL-6 cone. increased earlier and rapidly peaked than $TNF{\alpha}$ cone. in BALF. In histologic findings, the cell counts of lung slices were increased from 3 to 72h(p < 0.001 vs. NC). Alveolar wall-thickness was increased from 6 to 24h(p < 0.001 vs. NC). There was a significant correlation between the cell counts of lung slices and alveolar wall-thickness(r= 0.61, p < 0.001). This result suggested that the cellular infiltrations might be followed by the alterations of interstitium, and the edematous change of alveolar wall might be most rapidly recovered to its normal condition in the process of repair. Conclusion : We concluded that although the role of PMN is partly certain in ETX-induced ALI, it is somewhat inadequate to its known major impact on ALL Alveolar macrophage and/or non-immune cells such as pulmonary endothelial or epithelial cells, may be more importantly contributed to the initiation and perpetual progression of ETX-induced ALI. The IL-6 in ETX-induced ALI was independent to $TNF{\alpha}$, measured by a bioassay in BALF. The early rise in IL-6 in BALF implies multiple origins of the IL-6.

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