• Title/Summary/Keyword: 점막 손상

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Effect of Aspirin on the Fine Structure of Rat Gastric Mucosal Cells (Aspirine투여(投與)가 Rat의 위점막(胃粘膜) 세포(細胞)에 미치는 미세형태학적연구(微細形態學的硏究))

  • Jang, In Ho
    • Current Research on Agriculture and Life Sciences
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    • v.1
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    • pp.201-214
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    • 1983
  • A study was undertaken on rats in order to clarify the gastric mucosal, morphologic response to oral and subcutaneous administration of acetylsalicylic acid(aspirin). Aspirin was administered orally (oral group) and subcutaneously (subcutaneous group) at does rate of 60 mg per kg of body weight per day to 40 normal rats. On the 1st, 3rd, 7th, and 15th day of administration, in addition to clinical observation, 5 rats each from the both groups were sacrificed and examined macroscopically, histologically and electron-microscopically for the morphological changes of gastric mucosal cells with the following results. Although the clinical, macroscopic and histological changes were not significant, marked ultrastructural changes were observed. Parietal and chief cells were affected most severely by the administration of aspirin ; parietal cells showed increase in the number of SER and intracellular canaliculi, where-as in chief cells fragmentation, luminal dilatation, decrease in the number and structural abnormalities of RER were seen. Relatively mild changes were observed in mucous, mucous neck and basal-granulated cells. Although the degree of changes was milder than those of oral group, the similar changes were also observed in the subcutaneous group. From these results, it would be concluded that aspirin injury of gastric mucosa is effected not only by the direct injury to the mucosa but also indirectly by the blood concentration of aspirin.

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Radioprotective Effects of Granulocyte-Colony Stimulating Factor in the Jejunal Mucosa of Mouse (생쥐에서 과립구 집락형성인자(Granulocyte-Colony Stimulating Factor)의 공장점막에 대한 방사선 보호효과)

  • Ryu, Mi-Ryeong;Chung, Su-Mi;Kay, Chul-Seung;Kim, Yeon-Shil;Yoon, Sei-Chul
    • Radiation Oncology Journal
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    • v.19 no.1
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    • pp.45-52
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    • 2001
  • Purpose : Granulocyle-colony stimulating factor (G-CSF) has been widely used to treat neutropenia caused by chemotherapy or radiotherapy. The efficacy of recombinant human hematopoietic growth factors in improving oral mucositis after chemotherapy or radiotherapy has been recently demonstrated in some clinical studies. This study was designed to determine whether G-CSF can modify the radiation injury of the intestinal mucosa in mice. Materials and Methods : One hundred and five BALB/c mice weighing 20 grams were divided into nine subgroups including G-CSF alone group $(I:10\;{\mu}g/kg\;or\;II:100\;{\mu}g/kg)$, radiation alone group (7.5 or 12 Gy on the whole body), combination group with G-CSF and radiation (G-CSF I or II plus 7.5 Gy, G-CSF I or II plus 12 Gy), and control group. Radiation was administered with a 6 MV linear accelerator (Mevatron Siemens) with a dose rate of 3 Gy/min on day 0. G-CSF was injected subcutaneously for 3 days, once a day, from day -2 to day 0. Each group was sacrificed on the day 1, day 3, and day 7. The mucosal changes of jejunum were evaluated microscopically by crypt count per circumference, villi length, and histologic damage grading. Results : In both G-CSF I and II groups, crypt counts, villi length, and histologic damage scores were not significantly different from those of the control one (p>0.05). The 7.5 Gy and 12 Gy radiation alone groups showed significantly lower crypt counts and higher histologic damage scores compared with those of control one (p<0.05). The groups exposed to 7.5 Gy radiation plus G-CSF I or II showed significantly higher crypt counts and lower histologic damage scores on the day 3, and lower histologic damage scores on the day 7 compared with those of the 7.5 Gy radiation alone one (p<0.05). The 12 Gy radiation plus G-CSF I or II group did not show significant difference in crypt counts and histologic damage scores compared with those of the 12 Gy radiation alone one (p>0,05). Most of the mice in 12 Gy radiation with or without G-CSF group showed intestinal death within 5 days. Conclusion : These results suggest that G-CSF may protect the jejunal mucosa from the acute radiation damage following within the tolerable ranges of whole body irradiation in mice.

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Trophic Factors of Gastrointestinal Tract (위장관의 영양인자)

  • Kim, Yong Joo
    • Clinical and Experimental Pediatrics
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    • v.46 no.1
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    • pp.6-10
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    • 2003
  • 동물과 사람의 연구에서 위장관 영양 인자는 위장관 점막이 점막손상으로부터의 회복에 중요하고 출생 후 경구 영양에 적응할 수 있게 하는 데에 중요하다. 경구적으로든 전신적으로 투여된 성장 인자들은 위장관의 성장과 발달을 촉진시킨다. 신생아 혈중의 영양인자들이 장관 세포의 수용체를 통해 작용하여 위장관의 성장을 조율한다. 위장관 영양인자들은 체내에서 합성될 수도 있고 모유를 통해 공급된다. 사람에서 출생 후 위장관이 장관영양에 신속히 적응할 수 있도록 위장관 영양 인자들이 중요한 작용을 한다. 모유 내의 성장 인자들이 신생아 생존에 필수적인 것들은 않아도 모유를 먹은 영아들이 조제분유를 먹은 영아들에 비하여 급성 설사, 괴사성 장염, 크론씨 병과 같은 위장관 질환의 위험율이 낮다. 위장관 영양 인자들의 대부분이 시판 조제분유에는 존재하지 않고 주로 모유에 존재함을 앎으로써 모유의 장점을 설명하는 데에 적용할 수 있을 것이다. 그리고 위장관 영양인자는 위장관 점막 손상된 경우 치료 목적으로 사용될 수 있는 여지가 높다. 이러한 임상적 이용은 특히 미숙아, 수술 후의 영아 등에서 적용될 수 있다. 그러나 향후 더욱 연구되어야 할 항목들로는 작용기전, 경구 및 정맥 투여 방법에 의한 효과의 차이, 체내 성장 인자들과의 상호 작용, 외부적 투여가 체내 인자에 대한 영향, 위장관 이외의 타 기관에 대한 영향, 그리고 안전성과 약물 역동학적인 특성 등이다.

Clinical Characteristics of Intracordal Cysts (성대낭종에 대한 임상적 고찰)

  • 홍기환;박병암;정우철
    • Proceedings of the KSLP Conference
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    • 1996.11a
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    • pp.81-81
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    • 1996
  • 성대낭종은 후두미세수술의 발달로 보다 정확한 진단 및 치료가 가능하므로서 관심도가 증가하고 있다. 성대 낭종은 낭종의 내용물 및 점막상태에 따라 저류성 낭종과 유표피성 낭종으로 분류하고 있는데, 저류성 낭종은 점액 분비선의 폐쇄로 점액이 저류되어 발생하며 유표피 낭종은 선천성으로 상피하층에 파묻힌 상피세포의 잔여물이거나 혹은 파묻힌 상피세포 위에 외상(음성남용)으로 손상된 점막이 재생하는 과정에서 발생한다는 설이 있다. (중략)

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Radiation-Induced Proctitis in Rat and Role of Nitric Oxide (백서모델에서 방사선 직장염 유발인자로서의 Nitric oxide의 역할)

  • Chun Mison;Kang Seunghee;Jin Yoon-Mi;Oh Young-Taek;Kil Hoon-Jong;Oh Tae-Young;Ahn Byoung-Ok
    • Radiation Oncology Journal
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    • v.19 no.3
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    • pp.265-274
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    • 2001
  • Purpose : Proctitis is one of acute complications encountered when radiotherapy was appled to the pelvis. Radiation-induced proctitis represents similar microscopic findings that are observed in inflammatory bowel disease (IBD). Nitric oxide (NO) plays an important role in the inflammatory process and many data suggest a close relationship between NO production and gastrointestinal inflammation. This study was aimed to establish the optimal radiation dose for radiation-induced proctitis in rat and to find a relationship between radiation proctitis and NO production. Materials and methods : Female Wistar rats, weighing from 150 to 220 g, received various doses(10-30 Gy) of radiation to the rectum. On the 5th and 10th day after irradiation, rectal specimens were evaluated grossly and microscopically. In addition, the degree of NO production by irradiation dose was evaluated by study with NOS expression and nitrite production in the irradiated rectal tissue. To evaluate relationship between radiation proctitis and NO, we administered aminoguanidine, iNOS inhibitor and L-arginine, substrate of NOS to rats from 2 days before to 7 days after the irradiation. Results : There were obvious gross and hostological changes after 17.5 Gy or higher radiation dose but not with 15 Gy or less radiation dose. Twenty Gy or higher dose of radiation caused Grade 4 damage in most of rectal specimens which were more likely to be related to the late complications such as fibrosis, rectal bleeding and rectal obstruction. A single fraction of 17.5 Gy to the rat rectum is considered to be an optimal dose to produce commonly experienced proctitis in the clinic. The result demonstrated that severity of microscopic damage of rectal mucosa from irradiation significantly correlated with iNOS over-expression. However, administration of iNOS inhibitor or substrate of iNOS did not influence the degree of rectal damage. Conclusion : A single fraction of 17.5 Gy irradiation to the rat rectum considered to be an optimal dose for radiation induced proctitis model. These results indicated that an excess production of NO contributes to pathogenesis of radiation-induced proctitis in part but was not the direct cause of rectal damage.

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노출평가를 위한 BEI 근거 - SODIUM HYDROXIDE(1)

  • Kim, Chi-Nyeon
    • 월간산업보건
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    • s.353
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    • pp.29-33
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    • 2017
  • 수산화나트륨(Sodium hydroxide)의 직업적 노출에 대한 TLV-Ceiling은 $2mg/m^3$으로 권고하였다. 권고수준은 수산화나트륨 에어로졸이 눈, 점막, 피부에 심한 자극을 유발하고 수산화나트륨 분진이 상기도 기관에 자극을 유발하는 농도에 근거하였다. 노출기준은 눈과 상기도 기관에 자극을 최소화하기 위하여 권고하였다. 고농도의 수산화나트륨에 장기간 노출되면 비강 궤양과 눈과 피부에 심한 손상을 유발할 수 있다. "피부", "감작제(SEN)", "발암성"의 경고주석을 권고하기에는 유용한 자료가 충분하지 않다.

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Pathogenesis of Inflammation in H. pylori Infection

  • 정현채
    • Journal of Gastric Cancer
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    • v.2 no.2
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    • pp.63-68
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    • 2002
  • 위의 parietal cell 혹은 대식세포와 유사한 세포 내부에서 H. pylori가 발견된다는 보고가 있기는 하나 일반적으로 H. pylori는 Shigella와 같은 침습성 세균은 아닌 것으로 알려져 있다. 그럼에도 불구하고 H. pylori에 감염된 위점막에는 많은 수의 호중구를 위시한 염증세포의 침윤이 관찰되는데 H. pylori가 위상피세포에 부착할 경우 위상피세포를 자극하여 interleukin-8을 위시한 cytokine을 발현케하고 이에 의하여 호중구 등의 염증세포가 몰려들게 된다. 한편 고유층에 몰려든 호중구에서는 다시 interleukin-8을 위시한 일련의 호중구 활성화 chemokine을 분비하여 염증반응을 증폭해 나갈 것이다. 호중구에서 발현되는 myeloperxidase나 활성산소 등도 위점막의 조직 손상에 기여할 것이다. 위상피세포를 덮고 있는 점액층은 위상피세포를 보호한다고 알려져 있으나 H. pylori 감염의 경우 점액층에 의하여 H. pylori의 운동성이 증가하고 이것이 위상피세포로부터의 cytokine 발현을 자극하여 염증반응을 증폭하는 데 관여할 가능성도 있다. H. pylori는 위상피세포에 대하여 apoptosis를 유도함과 동시에 고유층에 몰려든 호중구에 대하여는 apoptosis를 억제케하여 궁극적으로 염증반응을 증폭 및 지속시켜 나가는 쪽으로 작용한다. 한편 H. pylori는 위상피세로로부터 COX-2의 발현을 증가시키는데 이는 위상피세포의 APOPTOSIS를 억제하는 방향으로 작용한다. 이외에 H. pylori의 urease에 의하여 발생한 암모니아나 H. pylori 자신이 분비하는 세포독소가 세포 손상을 유발할 가능성도 있다. 상술한 여러 독성 인자들 중 어느 하나가 단독으로 작용하기보다는 여러 인자가 같이 동시에 또는 시차를 두고 작용할 가능성이 많다고 생각된다.

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Quantitative Analysis of Small Intestinal Mucosa Using Morphometry in Cow's Milk-Sensitive Enteropathy (우유 과민성 장병증(cow's milk-sensitive enteropathy)에서 소장 생검조직의 형태학적 계측을 이용한 정량적 분석)

  • Hwang, Jin-Bok;Kim, Yong-Jin
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.1 no.1
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    • pp.45-55
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    • 1998
  • Purpose: To make objective standards of small intestinal mucosal changes in cow's milk-sensitive enteropathy (CMSE) we analyzed histological changes of endoscopic duodenal mucosa biopsy specimens from normal children and patients of CMSE. Methods: We review the medical records of patients who had been admitted and diagnosed as CMSE by means of gastrofiberscopic duodenal mucosal biopsy following cow's milk challenge and withdrawal. Thirteen babies with CMSE, ranging from 14 days to 56 days of age, were studied. Five non-CMSE patients were used as control, ranging from 22 days to 72 days of age. The morphometric parameters under study were villous height, crypt zone depth, ratio of villous height to crypt zone depth, total mucosal thickness and length of surface epithelium by using H & E stained specimens under the drawing apparatus attached microscope. In addition, the numbers of lymphocytes in the epithelium and eosinophil cells in the lamina propria and epithelium were measured. Results: In the duodenal mucosal biopsy specimens in CMSE we found partial and subtotal villous atrophy with an increased number of interepithelial lymphocytes. The mean villous height($135{\pm}59\;{\mu}m$), ratio of villous height to crypt zone depth ($0.46{\pm}0.28$), total mucosal thickness ($499{\pm}56\;{\mu}m$), length of surface epithelium of small intestinal mucosa ($889{\pm}231\;{\mu}m$) in CMSE was significantly decreased compared with the control (p<0.05). The mean crypt zone depth ($311{\pm}65\;{\mu}m$) was significantly greater than the control ($188{\pm}24\;{\mu}m$)(p<0.05). Infiltration of interepithelial lymphocytes ($34.1{\pm}10.5$) were significantly greater than the control ($13.6{\pm}3.6$)(p<0.05). The number of eosinophil cells in both lamina propria and epithelium was no significant differences between groups (p>0.05). The small intestinal mucosa in treated CMSE showed much improved enteropathy of villous height, crypt zone depth, interepithelial lymphocytes compared with the control as well as untreated CMSE. Conclusion: Quantitation of mucosal dimensions confirmed the presence of CMSE. It seems to be a limitation in the capacity of crypt cells to compensate for the loss of villous epithelium in CMSE. Specimens obtained by gastrofiberscopic duodenal mucosal biopsy were suitable for morphometric diagnosis of CMSE. Improvement of CMSE also can be confirmed histologically after the therapy of protein hydrolysate.

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Intramural Dissection and Mucosal Laceration of the Esophagus in a Patient Who Was on Antiplatelets Medication - A case report - (항혈소판 제재 복용 중 발생한 식도 벽 박리 및 점막 열상 - 1예 보고 -)

  • Kim, Kyung-Hwa;Kuh, Ja-Hong;Lee, Jung-Moon
    • Journal of Chest Surgery
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    • v.42 no.5
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    • pp.657-661
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    • 2009
  • Intramural esophageal dissection is a rare disorder that's characterized by a lengthy laceration between the mucosal and submucosal layers of the esophageal wall, and the esophageal wall is without perforation. The three different types of acute esophageal injury are a mucosal tear (Mallory-Weiss syndrome), full-thickness rupture (Boerhaave's syndrome) and intramural esophageal dissection. Most intramural esophageal dissections respond to conservative management with a very good prognosis. This rare condition should be considered in patients who present with acute chest pain, dysphagia or odynophagia, and particularly in the presence of a bleeding disorder or where there has been recent administration of antiplatelet medication, anticoagulantsorthrombolyticsto avoid inappropriate treatment with surgery. We present here a rare case of intramural dissection of the esophagus that occurred when the patient was taking anti platelet medication.