Hirashima Y, Endo S, Ohmori T, Kato R, Takaku A
Department of Neurosurgery, Toyama Medical and Pharmaceutical University, Japan.
J Neurosurg. 1994 Jan;80(1):31-6. doi: 10.3171/jns.1994.80.1.0031.
The authors studied the sequential changes in platelet-activating factor (PAF) and PAF acetylhydrolase in the cerebrospinal fluid (CSF) of patients with subarachnoid hemorrhage (SAH). Levels of PAF in CSF showed a gradual increase after the onset of SAH, with a subsequent decrease. The PAF concentration between 5 and 9 days after SAH was greater in patients with cerebral infarction due to vasospasm than in patients without infarction. Conversely, PAF acetylhydrolase activity decreased gradually after SAH, then increased. The enzyme activity for the same period was smaller in patients with cerebral infarction than in patients without infarction. The distribution of the days of maximum PAF concentration and minimum PAF acetylhydrolase activity did not differ significantly between the two groups. The CSF as a source of PAF acetylhydrolase activity gave an apparent Michaelis constant value of 90.8 microM and a maximum velocity of 0.2 nmol/min/mg. The optimum pH level for the PAF acetylhydrolase activity obtained from CSF was 6.5. The enzyme activity of CSF increased, depending on the incubation temperature, ranging from 25 degrees to 45 degrees C. Ethylene-glycol tetra-acetic acid (1 mM) was found to inhibit PAF acetylhydrolase activity in CSF obtained from patients with SAH. Unaltered PAF acetylhydrolase activity was inhibited by adding an aliquot of CSF and minimum PAF acetylhydrolase activity decreased following SAH. Two peaks of inhibitory activity were detected on Sephacryl S-200 HR gel filtration: one was eluted in void volume and the other with an apparent molecular mass of 13 kD. The inhibitory activity was very labile and was lost completely within 3 days of incubation at 4 degrees C. The regulation of the PAF concentration in the CSF of SAH patients is discussed.
作者研究了蛛网膜下腔出血(SAH)患者脑脊液(CSF)中血小板活化因子(PAF)和PAF乙酰水解酶的序列变化。SAH发作后,CSF中PAF水平逐渐升高,随后下降。SAH后5至9天,因血管痉挛导致脑梗死的患者CSF中的PAF浓度高于未发生梗死的患者。相反,SAH后PAF乙酰水解酶活性逐渐降低,然后升高。同一时期,发生脑梗死的患者的酶活性低于未发生梗死的患者。两组之间PAF浓度最高值和PAF乙酰水解酶活性最低值出现的天数分布没有显著差异。作为PAF乙酰水解酶活性来源的CSF的表观米氏常数为90.8 microM,最大反应速度为0.2 nmol/分钟/毫克。从CSF中获得的PAF乙酰水解酶活性的最适pH值为6.5。CSF的酶活性随孵育温度升高而增加,范围为25摄氏度至45摄氏度。发现乙二醇四乙酸(1 mM)可抑制SAH患者CSF中的PAF乙酰水解酶活性。添加一份CSF可抑制未改变的PAF乙酰水解酶活性,SAH后最低PAF乙酰水解酶活性降低。在Sephacryl S - 200 HR凝胶过滤中检测到两个抑制活性峰:一个在空体积中洗脱,另一个表观分子量为13 kD。抑制活性非常不稳定,在4摄氏度孵育3天内完全丧失。本文讨论了SAH患者CSF中PAF浓度的调节。