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題 名 | Chronic Thalidomide Administration Enhances Vascular Responsiveness to Vasopressin in Portal-systemic Collaterals of Bile Duct-ligated Rats=慢性Thalidomide治療可增強肝硬化大鼠側枝血管對血管升壓素的反應性 |
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作 者 | 張景智; 王聖賢; 黃惠君; 李發耀; 林漢傑; 李靜宜; 陳億周; 李壽東; | 書刊名 | Journal of the Chinese Medical Association |
卷 期 | 72:5 2009.05[民98.05] |
頁 次 | 頁234-242+CA45 |
分類號 | 415.534 |
關鍵詞 | 門脈側枝循環血管; 腫瘤壞死因子; 血管內皮成長因子; 血管升壓素; Thalidomide; Portal-systemic collaterals; Tumor necrosis factor (TNF)-α; Vascular endothelial growth factor; VEGF; Vasopressin; |
語 文 | 英文(English) |
英文摘要 | Background: Arginine vasopressin (AVP) controls gastroesophageal variceal bleeding, partly due to its vasoconstrictive effect on portal-systemic collaterals. It has been shown that chronic thalidomide treatment decreases portal pressure, attenuates hyperdynamic circulation and inhibits vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF)-α in partially portal vein-ligated rats. This study investigated the effects of chronic thalidomide treatment on portal-systemic collateral vascular responsiveness to AVP in common bile duct-ligated (CBDL) cirrhotic rats. Methods: In the first series, CBDL-induced cirrhotic rats received thalidomide (50 mg/kg/day orally) or distilled water (control) from the 35th to 42th day after ligation. On the 43th day after ligation, the body weight, mean arterial pressure, portal pressure, and heart rate were measured. An in situ collateral vascular perfusion model was used to obtain the cumulative concentration–response curves of collateral vessels to AVP (10–10 to 3 × 10–7 M). Plasma levels of VEGF and TNF-α were measured, and expressions of VEGF and TNF-α mRNA in the left adrenal veins were also determined. In the second series, the cumulative concentration–response curves of collateral vessels to AVP in CBDL rats with or without thalidomide (10–5 M) preincubation in the perfusate were obtained. Results: The thalidomide and control groups were not significantly different in terms of heart rate, mean arterial pressure and portal pressure (p > 0.05). The collateral vascular perfusion pressure change to AVP was significantly enhanced at 10–8 M after thalidomide treatment (p = 0.041). Compared with the control group, thalidomide-treated rats had significantly lower plasma VEGF levels (p < 0.001), accompanied by an insignificant reduction in plasma TNF-α levels (p > 0.05). The expressions of VEGF and TNF-α mRNA in the left adrenal veins of thalidomide-treated CBDL rats were not significantly changed compared with those of the control group. In addition, thalidomide did not significantly elicit changes in vascular responsiveness to AVP in collateral vessels of CBDL rats when it was added into the perfusate. Conclusion: In cirrhotic rats, chronic thalidomide treatment improves the portal-systemic collateral vascular responsiveness to AVP, which was partly related to VEGF inhibition. |
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