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頁籤選單縮合
題 名 | Serum Complement Levels and Endothelial Markers in Patients with Exertional Heat Stroke=運動性熱中暑血清補體及內皮細胞傷害之研究 |
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作 者 | 林裕峰; 陳金順; 萬國良; 林石化; 謝善德; 王家儀; | 書刊名 | 醫學研究 |
卷 期 | 19:1 1998.07[民87.07] |
頁 次 | 頁39-46 |
分類號 | 415.124 |
關鍵詞 | 熱中暑; 補體活化; 內皮細胞標記; Heat stroke; Complement activation; Endothelial markers; |
語 文 | 英文(English) |
中文摘要 | 在嚴熱潮濕的環境下劇烈運動可以導致新兵熱中暑,同時可能誘發高燒、休克、瀰散性血液凝固出血,成人呼吸窘迫症候群、急性腎衰竭及多發性器官衰竭。許多學者發現內皮細胞傷害可能是導致系統性器官功能障礙之基本病因。補體活化、內皮細胞標記改變及細胞激素活化可能與熱中暑臨床表徵有密切之關係。然而,其中只有細胞激素一項曾被研究過,因此,我們進一步研究20位熱中暑病患及10位正常對照組,血清內皮細胞標記及補體系統之變化,以期對熱中暑的致病機轉有更進一步的了解。本結果顯示,中暑初期血管張力素轉化酵素較恢復期有顯著下降(10.2 ± 19.5 vs 21.21 ± 3.18 nmol hippuric acid min ml, p<0.05);而von Willebrand's因子抗原(1.34 ± 0.06 vs 0.63 ± 0.055%,p<0.001)以及血小板凝集素(79.12 ± 7.35 vs 63.47 ± 4.21 ng/ml,p<0.05)則在初期有明顯上升趨勢,而於恢復期下降至接近正常。補體C3(86.6 ± 1.5 vs 130.4 ± 3.3mg/dL;p<0.001),C4(17.9 ± 0.7 vs 23.5 ± 1.4 mg/dL,p<0.05)以及CH50(125.2 ± 11.9 vs 156.4 ± 9.3 mg/dL,p<0.01)在中暑初期亦有明顯下降,而C3a則有明顯上升(15.5 ± 1.6 vs 13.2 ± 1.7x104 mg/dL,p<0.05)。同時C3與血管張力素轉化酵素(r=0.64,p<0.05)及von Willebrand's因子抗原(r=0.68,p<0.05)有明顯相關性且C3a亦與血管張力素轉化酵素有明顯相關性。從以上資料顯示熱中暑病患補體活化在內皮細胞傷害及內皮細胞標記活化的致病機轉中扮演極重要角色。從另一個角度來看,熱中暑病患熱傷害、血液凝固系統活化、內毒素分泌以及氧化性傷害等亦可能導致補體活化。 |
英文摘要 | Exhaustive exercise or training in a humid and hot environment can cause exertional heat stoke in military recruits and lead to hyperthermia, shock, disseminated intravascular coagulation (DIC), adult respiratory distress syndrome (ARDS), acute renal failure and multiple organ failure. It has well been known that endothelial cell damage might be the original pathogenesis resulting in systemic organ dysfunction. Complement activation, endothelial cell marker changes as well as cytokine production might all be cascades contribute to the clinical manifestation of exertional heat stroke (ExHS). However, only cytokine production has been studied in patients with ExHS. We then investigated endothelial cell marker changes and complement components in 20 patients with ExHS and 10m normal controls for further understanding of the pathophysiology of severe heat injury. Our results showed that angiotensin converting enzyme levels were significantly lower in patients with ExHS on admission (10.12 ± 1.95 vs 21.21 ± 3.18 nmol hippuric acid min ml, (p<0.05) while von Willebrand's factor antigen (vWf: Ag) (1.34 ± 0.06 vs 0.63 ± 0.05%, p<0.001) and thrombomodulin (79.12 ± 7.34 vs 63.47 ± 4.21 ng/mL,p<0.05) were significantly higher on admission than those at recovery phase. Serum complement C3 (86.6 ± 1.5 vs 103.4 ± 3.3 mg/dL, (p<0.05) while von Willebrand's ractor antigen (vWf: Ag) (1.34 ± 0.06 vs 0.63 ± 0.05%, p<0.001) and thrombomodulin (79.12 ± 7.34 vs 63.47 ± 4.21 ng.ml, p<0.05) were significantly higher on admission than those at recovery phase. Serum complement C3 (86.6 ± 1.5 vs 103.4 ± 3.3mg/dL, p<0.001) C4 (17.9 ± 0.7 vs 23.5 ± 1.4 mg/dL, p<0.05) and CH50 (125.2 ± 11.9 vs 156.4 ± 9.3 mg/dL, p<0.01)were significantly lower on admission than those at recovery phase. C3a des Arg was significantly elevated on admission as compared to that at recovery phase (15.5 ± 1.6 vs 13.2 ± 1.7x10�� mg/dL, p<0.05). There were good correlation between C3 and angiotensin converting enzyme (ACE) (r=0.64, p<0.05), C3a and ACE (r=-0.58, p<0.05), and C3 and vWf;Ag (r=-0.68, p<0.05). From the above data, we might conclude that complement activation in ExHS could play important role in the pathogenesis of endothelial cell injury as well as endothelial marker changes. On the other hand, endothelial cell injury probably induced by heat itself, coagulation activation, endotoxin and oxidant injury might also contribute to complement activation. |
本系統中英文摘要資訊取自各篇刊載內容。