Li J, Wang L, Zhu X, Wu Z
Department of Emergency, Second affiliated Hospital, Hunan Medical University, Changsha.
Hunan Yi Ke Da Xue Xue Bao. 1998;23(2):184-6.
To investigate the mechanism that monocytes participate in ischemic brain injury, endothelin (ET) levels in plasma, supernatants of cultured monocytes in vitro and those pretreated by dexamethason (DXM) were assayed by radioimmunoassay in 31 patients with acute cerebral infarction and 16 patients with hypertension (served as control). Compared with the control group, the ET levels in supernatants of cultured monocytes increased and positively related with those in plasma and degree of neurological damage in the acute cerebral infarction group, while the ET levels in supernatants of cultured monocytes pretreated by DXM decreased. This suggests that intensifying the synthesis and release ET may be one of the mechanisms for the involvement of monocytes in the pathologic process of ischemic brain injury during acute cerebral infarction. DXM can improve this process by inhibition of producing monocyte-derived ET.
为探讨单核细胞参与缺血性脑损伤的机制，采用放射免疫法检测了31例急性脑梗死患者及16例高血压患者（作为对照）血浆、体外培养单核细胞上清液及地塞米松（DXM）预处理后单核细胞上清液中的内皮素（ET）水平。与对照组相比，急性脑梗死组培养单核细胞上清液中ET水平升高，且与血浆中ET水平及神经损伤程度呈正相关，而DXM预处理的培养单核细胞上清液中ET水平降低。这表明增强ET的合成与释放可能是急性脑梗死期间单核细胞参与缺血性脑损伤病理过程的机制之一。DXM可通过抑制单核细胞源性ET的产生来改善这一过程。
