Nagao S, Kagawa M, Bemana I, Kuniyoshi T, Ogawa T, Honma Y, Kuyama H
Department of Neurological Surgery, Kagawa Medical School, Japan.
Acta Neurochir Suppl (Wien). 1994;60:502-4. doi: 10.1007/978-3-7091-9334-1_137.
We determined the effect of a centrally administered V1 receptor antagonist of arginine vasopressin on the brain water content in an animal model of vasogenic brain edema. Using adult rats, a cold injury was induced in the left hemisphere of the brain by applying a frozen copper rod. 50 ng of V1 receptor antagonist was administered into the left lateral ventricle 10 minutes prior to and/or 1 hour after injury. Twenty four hours after the cold injury, the brain water and sodium contents and plasma osmolality were measured. The V1 receptor antagonist significantly suppressed the increase of the brain water and sodium contents in the cortical structure adjacent to the lesion without any changes in plasma osmolality. Our results demonstrate the effectiveness of a V1 receptor antagonist of vasopressin on vasogenic brain edema.
我们在血管源性脑水肿动物模型中,确定了精氨酸加压素的中枢给予V1受体拮抗剂对脑含水量的影响。使用成年大鼠,通过应用冷冻铜棒在大脑左半球诱导冷损伤。在损伤前10分钟和/或损伤后1小时,将50 ng的V1受体拮抗剂注入左侧脑室。冷损伤后24小时,测量脑含水量、钠含量和血浆渗透压。V1受体拮抗剂显著抑制了病变相邻皮质结构中脑含水量和钠含量的增加,而血浆渗透压没有任何变化。我们的结果证明了加压素V1受体拮抗剂对血管源性脑水肿的有效性。