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探讨了一种新的人红细胞源降压因子（erythrocyte-derived depressing factor,EDDF）对大鼠血管的保护作用.应用离体血管环生物灌流法、双光子激发荧光扫描显微镜及透射电子显微镜,观察了正常Wistar大鼠、钙超载大鼠和左旋硝基精氨酸（L-NNA）诱导的高血压大鼠的血管收缩功能以及EDDF的影响.结果显示,钙超载大鼠及L-NNA高血压大鼠离体主动脉环对苯肾上腺素的收缩反应明显增强,EDDF（10-3g/mL）灌流1h可以明显降低正常大鼠及钙超载大鼠血管的收缩反应,并通过减轻核损伤、改善线粒体肿胀以及其他细胞器异常,从而减轻钙超载大鼠主动脉血管平滑肌细胞（VSMC）的损伤.而EDDF对L-NNA高血压大鼠血管的收缩反应无明显影响.这提示EDDF通过影响胞内钙离子转运,减轻VSMC损伤,从而保护血管。进一步证实了EDDF是通过NO/EDRF-cGMP通路舒张血管和降低血压的。
To explore the protective effect of a novel human erythrocyte-derived depressing factor (EDDF) on the blood vessels in rats, the biologic perfusion method with two-photon excitation fluorescence scanning microscope and transmission electron microscopy The effects of EDDF on vasoconstriction and EDDF in normal Wistar rats, calcium-overload rats and L-NNA-induced hypertension rats were observed.The results showed that calcium overload rats and L-NNA hypertension The contractile response of phenylephrine to isolated aorta rings was significantly increased in rat aortic rings. EDDF (10-3g / mL) perfusion for 1h significantly reduced the vasoconstrictive response of normal and calcium-overload rats and relieved nuclear injury and improved Mitochondrial swelling and other organelle abnormalities, thereby reducing the injury of aortic vascular smooth muscle cells (VSMCs) in calcium-overload rats, while EDDF had no significant effect on the vasoconstrictive response of L-NNA hypertensive rats, suggesting that EDDF affects the intracellular calcium Ion transport, reduce VSMC damage, thereby protecting the blood vessels. It is further confirmed that EDDF relaxes blood vessels and reduces blood pressure through the NO / EDRF-cGMP pathway.