目的　研究登革病毒感染对人血管内皮细胞分泌重要的血管活性物质ＥＴ１ 及ＰＧＩ２ 的影响，以了解登革出血热及登革休克综合征（ＤＨＦＤＳＳ）的发病机制。方法　用登革病毒Ⅱ型，感染人脐静脉内皮细胞（ＨＵＶＥＣ） ，于感染后４ 、２４ 、４８ 、７２ 及９６ 小时，分别收集病毒感染上清液，用放射免疫检测法测定ＥＴ１ 及ＰＧＩ２ 的含量。结果　登革病毒感染可使ＨＵＶＥＣ分泌ＥＴ１ 及ＰＧＩ２ 的能力受到明显抑制。在病毒感染早期（４ 小时），ＨＵＶＥＣ分泌ＥＴ１ 及ＰＧＩ２ 的能力即受到明显抑制。登革病毒对ＨＵＶＥＣ分泌ＥＴ１ 抑制作用强烈而持久，至感染后９６ 小时，ＨＵＶＥＣ分泌ＥＴ１ 的能力与未受感染的阴性对照组比较，差异仍有显著性。然而，登革病毒对ＨＵＶＥＣ 分泌ＰＧＩ２ 的抑制作用，可随时间的推移而减弱，至感染后９６ 小时，ＨＵＶＥＣ分泌ＰＧＩ２ 的能力已达正常水平。结论　登革病毒感染可影响血管内皮细胞分泌血管活性物质ＥＴ１ 及ＰＧＩ２ 的功能，导致血管通透性增加和凝血、止血功能障碍。因此，登革病毒所致的血管内皮细胞功能障碍，可能是ＤＨＦＤＳＳ重要的发病机制 Objective To study the effect of dengue virus infection on the secretion of important vascular endothelial progenitor cells ET1 and PGI2 in human vascular endothelial cells to understand the pathogenesis of dengue hemorrhagic fever and dengue shock syndrome (DHFDSS). Methods Human umbilical vein endothelial cells (HUVECs) were infected with dengue virus type Ⅱ and supernatant was collected at 4, 24, 48, 72 and 96 hours after infection. The levels of ET1 and PGI2 content. Results Dengue virus infection can HUVEC secretion of ET 1 and PGI2 was significantly inhibited. Early in the virus infection (4 hours), HUVEC secretion of ET 1 and PGI2 ability to be significantly inhibited. Dengue virus on HUVEC secretion of ET 1 inhibition strong and lasting, to 96 hours after infection, HUVEC secretion of ET 1 compared with the uninfected negative control group, the difference was still significant. However, the inhibitory effect of dengue virus on PGI2 secretion by HUVECs may be weakened over time, and the ability of HUVEC to secrete PGI2 reached its normal level 96 hours after infection. Conclusion Dengue virus infection can affect endothelial cell secretion of vascular endothelial ET 1 and PGI2 function, leading to increased vascular permeability and coagulation, hemostatic dysfunction. Therefore, dengue virus-induced endothelial dysfunction may be an important pathogenesis of DHFDSS