De Riu P L, Demontis M P, Anania V, Caria M A, Mameli O, Becciu A, Tolu E
Department of Traumatology, Chair of Neurological Rehabilitation, Turin University, Italy.
Pharmacol Res. 1995 Mar-Apr;31(3-4):169-73. doi: 10.1016/1043-6618(95)80014-x.
The protective effect of nimodipine, a calcium entry blocker, and MK-801, an excitatory amino acid antagonist, on the cortical electrobiogenesis of hypertensive SHR-Charles-River adult rats during a 90-s session of acute hypoxia, was tested either with a single treatment or with a therapeutic association. Pretreatment with nimodipine alone (0.1 mg kg-1, i.v.) was particularly effective in increasing the rat brain resistence to hypoxia when compared to the controls. MK-801 pretreatment alone (3 mg kg-1, subcutaneous), improved significantly the recovery of brain electrical activity from hypoxia, as it not only shortened the recovery time but also abolished the post-hypoxic burst activity. The combined pretreatment with both drugs, using the same doses, displayed a more powerful brain protective effect on the cortical electrobiogenesis than the single drug pretreatment, suggesting the existence of a synergy between nimodipine and MK-801.
在90秒的急性缺氧期间,测试了钙通道阻滞剂尼莫地平以及兴奋性氨基酸拮抗剂MK-801对成年高血压SHR-Charles-River大鼠皮层电发生的保护作用,分别采用单一治疗或联合治疗。与对照组相比,单独静脉注射尼莫地平(0.1毫克/千克)预处理在增强大鼠脑对缺氧的抵抗力方面特别有效。单独皮下注射MK-801预处理(3毫克/千克)可显著改善缺氧后脑电活动的恢复,因为它不仅缩短了恢复时间,还消除了缺氧后爆发活动。使用相同剂量的两种药物联合预处理对皮层电发生的脑保护作用比单一药物预处理更强,表明尼莫地平和MK-801之间存在协同作用。