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題名 | Prophylactic Octreotide Reduces the Severity of Histopathologic Changes and Hemodynamic Shock in Early Taurodeoxycholate-induced Experimental Pancreatitis=預防性Octreotide對早期去氧牛膽酸鹽誘發實驗性胰臟炎可降低其組織病理變化及休克的嚴重度 |
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作者 | 陳俊嘉; 王聖賢; 李發耀; 蔡世豪; 吳淑玲; 盧瑞華; 張扶陽; 李壽東; | 書刊名 | Proceedings of the National Science Council : Part B, Life Science |
卷期 | 23:1 1999.01[民88.01] |
頁次 | 頁1-6 |
分類號 | 415.145 |
關鍵詞 | 去氧牛膽酸鹽; 組織病理變化; 急性胰臟炎; 血流動力學; Acute pancreatitis; Hemodynamics; Histopathology; Octreotide; Rat; |
語文 | 英文(English) |
中文摘要 | 體抑素(somatostatin)或 octreotide 對急性胰臟炎的療效尚無定論。本研究 乃探討預防性 octreotide 在急性實驗性胰臟炎的早期療效。大白鼠以逆行性灌注去氧甘膽 酸( glycodeoxycholic acid )或去氧牛膽酸鹽( sodium taurodeo-xycholate )到胰膽 管來誘發急性胰臟炎並給予皮下注射預防性 octreotide 10 μ g/Kg 或生理鹽水當作對照 組。 在誘發胰臟炎 5 小時後測定血清澱粉�t及脂肪�t的濃度,胰臟組織病理變化,系統性 血流動力學包括平均動脈壓、心臟指數、系統性血管阻力及心跳。去氧甘膽酸及去氧牛膽酸 鹽分別誘發輕度及重度胰臟炎。Octreotide 明顯降低在誘發胰臟炎 5 小時後血清澱粉�t及 脂肪�t的濃度。 Octreotide 明顯減少以去氧牛膽酸鹽誘發胰臟炎的胰臟水腫、壞死及出血 的嚴重度。 此外與對照組相比,octreotide 明顯改善去氧牛膽酸鹽誘發胰臟炎的血流動力 學上的休克(平均動脈壓 70.3 ± 7.7 vs. 95.0 ± 3.5 mmHg; 心臟指數 16.7 ± 2.5 vs.24.0 ± 5.1 ml. min �笐薄D 100g �笐薄Ap<0.05 )。然而 octreotide 對以去氧甘膽 酸誘發輕度胰臟炎的胰臟組織病理及系統性血流動力學的變化並無明顯助益。本研究的結論 是:預防性 octreotide 可改善去氧牛膽酸鹽誘發胰臟炎的胰臟組織病理變化及休克。 |
英文摘要 | The findings related to the effects of somatostatin and octreotide in experimental and clinical acute pancreatitis are so far inconclusive. In this study, we examined the early effects of prophylactic octreotide in acute experimental pancreatitis. Serum levels of amylase and lipase, pancreatic histopathology and systemic hemodynamic profiles, including mean arterial pressure, cardiac index, systemic vascular resistance and heart rate, were evaluated 5 hours after glycodeoxycholic acid (GDOC) or sodium taurodeoxycholate (TDC)-induced pancreatitis with or without prophylactic octreotide (10 mg/Kg) in rats. GDOC and TDC induced mild and severe pancreatitis, respectively. Octreotide significantly reduced serum levels of amylase and lipase at 5 hours in GDOC and TDC-induced pancreatitis. Octreotide significantly reduced the severity of pancreatic edema, necrosis and hemorrhage in TDC-induced pancreatitis. In addition, hemodynamic shock in TDC-induced pancreatitis was improved significantly by the administration of octreotide (mean arterial pressure 70.3 ± 7.7 vs. 95.0 ±3.5 mmHg, p < 0.05; cardiac index 16.7 ±2.5 vs. 24.0 ±5.1 ml . min-1 .100 g-1, p < 0.05). However, octreotide did not show significant beneficial effect in pancreatic histopathology and hemodynamics in GDOC-induced pancreatitis. Thus we conclude that prophylactic octreotide improves pancreatic histopathology and hemodynamic shock in TDC-induced pancreatitis. |
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