Vascular responses to compound 48/80 in rat mesenteric vascular beds
Vascular responses to compound 48/80 in rat mesenteric vascular beds
复制标题
大鼠肠系膜血管床对化合物 48/80 的血管反应
DOI：
10.1139/cjpp-2015-0442
复制
发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Sun P
中科院分区：
文献类型：
--
作者：
Jin H;Li Z;Takatori S;Koyama T;Jin X;Zamami Y;Kawasaki H;Sun P
用组胺释放剂化合物48/80在活性紧张的大鼠肠系膜血管床中进一步研究内源性组胺的血管效应。在具有完整内皮的制剂中，低浓度的化合物48/80（1.53 × 10−5- 3 × 1.53 × 10− 5 mg/mL）灌注1分钟仅诱导小的血管舒张。高浓度的化合物48/80（1.53 × 10−4- 3 × 1.53 × 10− 2 mg/mL）诱导了双相血管反应，最初的血管收缩随后是长期的血管舒张。奥洛他定可抑制低浓度化合物48/80引起的血管舒张和高浓度化合物48/80引起的血管收缩。然而，西咪替丁不影响化合物48/80诱导的反应。内皮素去除扩大了化合物48/80诱导的2相血管收缩，而它减弱了3相血管舒张。此外，吲哚美辛和塞曲司特显著抑制血管收缩，但不影响高浓度化合物48/80诱导的持久血管舒张。钌红抑制低浓度和高浓度化合物48/80引起的血管舒张。这些结果表明，高浓度化合物48/80引起的血管收缩是由肥大细胞释放的内源性组胺介导的。提示肥大细胞释放的血栓素A2与血管收缩有关。
A further investigation was performed on the vascular effect of endogenous histamine using the histamine releaser, compound 48/80, in rat mesenteric vascular beds with active tone. In preparations with intact endothelium, low concentrations of compound 48/80 (1.53 × 10−5– 3 × 1.53 × 10−5mg/mL) perfusion for 1 min only induced a small vasodilation. High concentrations of compound 48/80 (1.53 × 10−4– 3 × 1.53 × 10−2mg/mL) induced a biphasic vascular responses, an initial vasoconstriction followed a subsequent long-lasting vasodilation. The vasodilation induced by low concentrations of compound 48/80 and the vasoconstriction induced by high concentration of compound 48/80 was inhibited by olopatadine. However, cimetidine did not affect the responses induced by compound 48/80. Endothelium removal enlarged the compound 48/80-induced phase-2 vasoconstriction, while it attenuated the phase-3 vasodilation. Additionally, indomethacin and seratrodast significantly inhibited vasoconstriction but it did not affect the long-lasting vasodilation induced by high concentrations of compound 48/80. Ruthenium red inhibited the vasodilation induced by low concentrations and high concentrations of compound 48/80. These results suggest that the vasoconstriction induce by high concentrations of compound 48/80 is mediated by endogenous histamine released from mast cells. It is also suggested that thromboxane A2released from mast cells is related to the vasoconstriction.