Archer D P, Pappius H M
Neurochem Pathol. 1986 Oct;5(2):117-30. doi: 10.1007/BF03160127.
The effect of two dihydropyridine calcium (Ca) channel blocking drugs on cerebral glucose metabolism (LCGU), blood flow (LCBF), and blood flow-metabolism coupling were studied in thermally injured rat brain using quantitative radioautographic techniques. No reversal of the previously noted LCGU depression caused by the freezing lesion (Pappius, 1981) was detected following treatment with either PY-108-068 (PY) or nimodipine (NIM). These results therefore provided no support for the role of Ca in the mechanism of functional disturbances induced by cold injury (Pappius and Wolfe, 1983b), though they do not rule out its involvement. Treatment with PY, but not NIM, reestablished the normal LCBF-LCGU relationship in cortical areas, which has been shown to be disturbed by the freezing lesion and in subcortical and brainstem structures, in which the alteration caused by the injury was not as pronounced. The results suggest that the mechanism that apparently uncouples LCBF from LCGU in injured brain is altered in the presence of PY. However, since NIM did not have the same effect on LCBF, it is not clear whether the effects of PY relate to blockade of Ca channels or some other effect of PY.
采用定量放射自显影技术，研究了两种二氢吡啶类钙（Ca）通道阻滞剂对热损伤大鼠脑葡萄糖代谢（LCGU）、血流量（LCBF）及血流-代谢偶联的影响。在用PY-108-068（PY）或尼莫地平（NIM）治疗后，未检测到先前由冷冻损伤引起的LCGU降低的逆转（帕皮厄斯，1981年）。因此，这些结果不支持Ca在冷损伤诱导的功能障碍机制中的作用（帕皮厄斯和沃尔夫，1983b），尽管它们并不排除Ca的参与。用PY治疗，但不用NIM，可恢复皮质区域正常的LCBF-LCGU关系，冷冻损伤已证明该关系受到干扰，在皮质下和脑干结构中也是如此，损伤引起的改变在这些结构中不那么明显。结果表明，在PY存在的情况下，损伤脑中明显使LCBF与LCGU解偶联的机制发生了改变。然而，由于NIM对LCBF没有相同的作用，尚不清楚PY的作用是否与Ca通道的阻断或PY的其他作用有关。
