Background. Our previous studies indicated that the increased arginine vasopressin(AVP) in ischemic brain regions of gerbils could exacerbate the ischemic brain edema. This experiments is further clarify the relation between AVP and cerebral ischemia at the molecular level. Methods. The contents of AVP, AVP mRNA, AVP immunoreactive(ir) neurons in supraoptic nucleus(SON)and paraventricular nucleus(PVN) after cerebral ischemia and reperfusion were respectively determined by radioim-munoassay(RIA), immunocytochemistry( Ⅱ C), situ hybridization and computed image pattem analysis. Results. The contents of AVP in SON, PVN were increased, and the AVP ir positive neurons in SON and PVN were also significantly increased as compared with the controls after ischemia and reperfusion. And there were very light staining of AVP ir positive neurons in the other brain areas such as suprachiasmatic nucleus (SC) and periven-tricular hypothalamic nucleus (PE), but these have no significant changes as compared with the controls. During dif-ferent periods of cerebral ischemia (30～ 120 min) and reperfusion (30 min), AVP mRNA expression in SON and PVN were more markedly increased than the controls. Condusions. The transcription of AVP gene elevated, then promoting synthesis and release of AVP in SON,PVN. Under the specific condition of cerebral ischemia and repeffusion, the activity and contents of central AVP in-creased abnormally is one of the important factors which causes ischemia brain damage.

去氨加压素致低钠血症后引起的渗透性脱髓鞘综合征

渗透性脱髓鞘综合征(Osmotic demyelination syndrome,ODS)是一种罕见的中枢神经系统疾病,包括脑桥中央髓鞘容解症(eentral pontine myelinolysis,CPM)和脑桥外髓鞘溶解症(extrapontine myelinolysis,EPM),这种综合征与低钠血症的快速纠正、酒精中毒、肝功能衰竭、营养不良等有关[1].去氨加压素(Deamio arginine vasopressin,DDAVP)作为一种止血药物导致ODS则鲜有报道.我们报告1例应用去氨加压素后出现慢性低钠血症,在低钠血症纠正后,同时发生CPM和EPM的ODS,并有一系列磁共振成像(MRI)的典型表现分析,供读者参考.

Objective:　To study the changes and clinical significance of arginine vasopressin (AVP) and angiotensin II (AT-II) in patients with acute moderate and severe cerebral injury. 　　Methods:　The early plasma concentration was checked by radioimmunoassay in 47 cases of acute moderate and severe cerebral injury, 30 cases of non-cerebral injury and 30 healthy volunteers. 　　Results:　The early plasma concentrations of AVP (50.23 ng/L±15.31 ng/L) and AT-II (248.18 ng/L±82.47 ng/L) in cerebral injury group were higher than those in non-cerebral injury group (AVP for 30.91 ng/L±11.48 ng/L and AT-II for 120.67 ng/L±42.49 ng/L, P<0.01). The early plasma concentrations of AVP and AT-II in cerebral injury group were also obviously higher than those of the volunteers (AVP for 5.16 ng/L±4.23 ng/L and AT-II for 43.11 ng/L±16.39 ng/L, P<0.001). At the same time, the early plasma level of AVP (58.90 ng/L±18.12 ng/L) and AT-II (292.13 ng/L±101.17 ng/L) was higher in severe cerebral injured patients than moderate cerebral injured ones (AVP for 36.68 ng/L±12.16 ng/L and AT-II for 201.42 ng/L±66.10 ng/L, P<0.01). The early level of AVP and AT-II was negatively related to the GCS scales in acute cerebral injury. The early plasma concentrations of AVP (45.98 ng/L±13.48 ng/L) and AT-II (263.28 ng/L±80.23 ng/L) were lower in epidural hematoma group than those of subdural hematoma and cerebral injury group (AVP for 64.12 ng/L±15.56 ng/L and AT-II for 319.82 ng/L±108.11 ng/L, P<0.01). 　　Conclusions:　 AVP and AT-II may play an important role in pathophysiologic process in the secondary cerebral injury. The more severe the cerebral injury is, the higher the early level of AVP and AT-II will be. The early plasma level of AVP and AT-II may be one of the severity indexes of cerebral injury.