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題名 | 休克時人類胰腺細胞微細構造之變化 |
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作者 | 李金德; 沈柏青; 黃宗人; | 書刊名 | 中華民國外科醫學會雜誌 |
卷期 | 21:5 1988.09[民77.09] |
頁次 | 頁525-532 |
分類號 | 416.123 |
關鍵詞 | 休克; 人類胰腺細胞; 微細構造; |
語文 | 中文(Chinese) |
中文摘要 | 病理解剖及動物實驗有許多資料証實休克缺血會造成肢職組織及血清澱粉酶的異常;而臨床上有些病例組織學上尚無變化時,胰腺細胞卻已因休克缺血而造成了某些程度的傷害。我們將報告十位可逆性休克的病例,他們的胰臟組學上沒有顯著變化,但微細構造上卻有異常變化;這些變化色括:粗面內質網擴張,它們有的形成大泡狀,有的斷裂成片,也有的形成小泡狀;粒腺體腫脹成圓形,內嵴排列紊亂;自噬小泡,殘餘體及脂肪小滴的增加;酶原顆粒周圍電子密度的下降,也有一些顆粒互相融合在一起。血清澱粉酶,有三例呈現輕度上升,其中以合併急性腎衰竭的病例為最高。我們也發現,所有病例的粒腺體雖然都呈現腫脹及內嵴排列紊亂,但卻未發現粒腺體內出現棉絮狀的緻密物質或鈣化現象,這表示著細胞雖因伙克而受到傷害,但這些傷害是屬於可逆性的;這種細胞可逆性傷害的徵細變化正可與臨床上休克為可逆性休克相吻合。 |
英文摘要 | Ischemia was considered to be one of the pathogenic factors of pancreatitis. Pancreas was vulnerable to shock like other vital organ such as kidney, heart and liver. Pancreatic injury after ischemia have been proved by laboratory test and histologic examination. In this study we will demonstrate the ultrastructural change of pancreatis acinar cells in shock patients. The patients with recorded hypotension are subjects for this study; they are 6 men and 4 women. Age range from 30 to 67 years old. The causes of shock are: splenic rupture 4 patients; liver laceration with complication of acute renal failure 1 patient; massive upper gastrointestinal bleeding 2 patients; mesentery laceration 2 patients and traumatic pancreatic transection 1 patient. The ultrastructural findings reveal that dilation of rough endoplasmic reticulum; swollen and round mitochondria; an increase of autophagic vacuoles and lipid droplets; alteration of zymogen granules with peripheral lucent of electron density. Three patients have concomitant elevation of serum amylase level. |
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