Wendling W W, Daniels F B, Chen D, Harakal C, Carlsson C
Department of Anesthesiology, Temple University Hospital, Philadelphia, PA 19140.
J Neurosurg Anesthesiol. 1994 Jul;6(3):186-92. doi: 10.1097/00008506-199407000-00007.
This in vitro study was performed to determine the role of calcium in ketamine-induced cerebral vasodilation. Isolated bovine middle cerebral arteries were cut into rings to measure isometric tension development or into strips to measure radioactive 45Calcium (45Ca) uptake. Ketamine produced direct relaxation of arterial rings; the relaxation was attenuated in Ca(2+)-deficient media. Ketamine produced dose-related relaxation of arteries preconstricted with potassium, a stable thromboxane A2 analogue, or endothelin. Endothelial stripping with Triton X-100 had no effect on subsequent ketamine-induced relaxation. In Ca(2+)-deficient media containing potassium or the stable thromboxane A2 analogue, ketamine produced competitive inhibition of subsequent Ca(2+)-induced constriction. Ketamine blocked potassium- and thromboxane A2-stimulated 45Ca uptake in a dose-dependent manner, but had no effect on basal 45Ca uptake, the externally bound 45Ca content, or the volume of the 3H-sorbitol space. These results indicate that ketamine can directly dilate cerebral arteries by acting as a calcium channel antagonist; ketamine inhibits 45Ca uptake through both potential-operated (potassium) and receptor-operated (thromboxane A2) channels in cerebrovascular smooth muscle.
本体外研究旨在确定钙在氯胺酮诱导的脑血管舒张中的作用。将分离的牛大脑中动脉切成环状以测量等长张力的发展，或切成条带以测量放射性45钙（45Ca）摄取。氯胺酮使动脉环直接舒张；在缺钙培养基中，这种舒张作用减弱。氯胺酮使预先用钾、一种稳定的血栓素A2类似物或内皮素预收缩的动脉产生剂量相关的舒张。用Triton X-100进行内皮剥脱对随后氯胺酮诱导的舒张没有影响。在含有钾或稳定的血栓素A2类似物的缺钙培养基中，氯胺酮对随后的钙诱导收缩产生竞争性抑制。氯胺酮以剂量依赖的方式阻断钾和血栓素A2刺激的45Ca摄取，但对基础45Ca摄取、细胞外结合的45Ca含量或3H-山梨醇空间体积没有影响。这些结果表明，氯胺酮可作为钙通道拮抗剂直接舒张脑动脉；氯胺酮通过脑血管平滑肌中的电压门控（钾）通道和受体门控（血栓素A2）通道抑制45Ca摄取。
