Wahl M, Schilling L, Parsons A A, Kaumann A
Dept. Physiology, University of Munich, Germany.
Brain Res. 1994 Feb 21;637(1-2):204-10. doi: 10.1016/0006-8993(94)91234-3.
The aim of the present study was to examine whether the initial transient arterial dilatation during cortical spreading depression (CSD) was mediated by the release of calcitonin gene-related peptide (CGRP) and/or nitric oxide (NO). This question is of interest as the initial phase of CSD appears to be a model of events occurring during functional hyperemia and during the first period of classic migraine. Using an open cranial window technique, pial arterial diameter in the parietal cortex of cats was recorded with an image splitting method. Employing micropuncture technique, perivascularly applied CGRP8-37 did not alter the resting diameter of pial arteries but antagonized concentration dependently (5 x 10(-9)-10(-6) M) the dilatation (35%) due to 5 x 10(-8) M CGRP. NG-Nitro-L-Arginine (NOLAG, 10(-4) M) also had no effect on resting diameter of pial arteries, indicating that their resting tone is neither mediated by a continuous release of CGRP nor of NO. CSD was triggered by a remote intracortical injection of KCl (150 mM) and recorded by a microelectrode placed adjacent to the artery under investigation. CSD elicited a transient negative DC shift which was accompanied by a peak dilatation of 44 +/- 5.2% (S.E.M.). This dilatation was reduced by approximately 50% during topical application of 10(-7) M CGRP8-37 and 10(-4) M NOLAG each. A 75% inhibition of the CSD-induced dilatation was found during simultaneous application of both compounds. These data indicate that the initial dilatation during CSD is mediated, at least in part, by a release of CGRP and NO.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是检测皮质扩散性抑制（CSD）期间最初的短暂性动脉扩张是否由降钙素基因相关肽（CGRP）和/或一氧化氮（NO）的释放介导。这个问题备受关注，因为CSD的初始阶段似乎是功能性充血和典型偏头痛第一阶段所发生事件的一个模型。采用开放颅骨窗技术，用图像分割法记录猫顶叶皮质软脑膜动脉直径。运用微穿刺技术，血管周围应用CGRP8 - 37不会改变软脑膜动脉的静息直径，但能浓度依赖性地（5×10⁻⁹ - 10⁻⁶ M）拮抗由5×10⁻⁸ M CGRP引起的35%的扩张。NG - 硝基 - L - 精氨酸（NOLAG，10⁻⁴ M）对软脑膜动脉的静息直径也没有影响，这表明它们 的静息张力既不是由CGRP的持续释放介导，也不是由NO介导。通过远距离皮质内注射氯化钾（150 mM）引发CSD，并通过置于所研究动脉附近的微电极进行记录。CSD引发短暂的负向直流偏移，同时伴有44±5.2%（标准误）的峰值扩张。在局部应用10⁻⁷ M CGRP8 - 37和10⁻⁴ M NOLAG时，这种扩张分别减少了约50%。在同时应用这两种化合物时，发现CSD诱导的扩张受到75%的抑制。这些数据表明，CSD期间的初始扩张至少部分是由CGRP和NO的释放介导的。（摘要截短于250词）
