Zivin J A, Kochhar A, Saitoh T
Department of Neurology, Veterans Administration Medical Center, San Diego, CA.
Brain Res. 1989 Mar 13;482(1):189-93. doi: 10.1016/0006-8993(89)90560-x.
We found substantial alterations in reactions catalyzed by calcium/phospholipid-dependent and calcium/calmodulin-dependent protein kinases during CNS ischemia which suggested that phenothiazines, drugs capable of inhibiting these reactions, might reduce neurologic damage. To test this hypothesis, we used chlorpromazine and trifluoperazine. Both drugs reduced neurologic function deficits relative to controls in a rabbit multiple cerebral embolism model and a rabbit spinal cord ischemia model. Chlorpromazine was effective despite reduction of blood pressure, and trifluoperazine did not alter blood pressure. These findings suggest that phenothiazines may be useful for preserving neurologic function when administered shortly after the onset of CNS ischemia.
我们发现在中枢神经系统缺血期间,钙/磷脂依赖性蛋白激酶和钙/钙调蛋白依赖性蛋白激酶催化的反应发生了显著变化,这表明能够抑制这些反应的药物吩噻嗪可能会减轻神经损伤。为了验证这一假设,我们使用了氯丙嗪和三氟拉嗪。在兔多发性脑栓塞模型和兔脊髓缺血模型中,与对照组相比,这两种药物均减轻了神经功能缺损。尽管氯丙嗪会导致血压降低,但其仍有效果,而三氟拉嗪不会改变血压。这些发现表明,在中枢神经系统缺血发作后不久给药,吩噻嗪可能有助于保护神经功能。