| Platelet activating factor(PAF), a widely studied cytokine, has extensive biological activities. It can induce cerebral thrombosis, cerebral ischemia, calcium ion influx into brain cells, excitatory toxicity, DNA damage and neuron apoptosis. Role of PAP in the pathogenesis of ischemic hear* disease and thiombosis Ha< hecn elucidated. To discuss the role of PAF in the physiology of cerebral vascular disease is very important. Thus, we observed the dynamic change of PAF in the patients with cerebral vascular disease.Subject and Method1. Subjects(1). Patients: We examined 120 patients with cerebral vascular disease(from Jan 1999 to Aug 2000) hospitalized in Neurological department of Zhejiang University Medical School. Patients were diagnosed by the standard from 4th National Congress for Cerebral Vascular Disease. Patients with bronchial asthma, diabetes mellitus, ischemic heart disease were excluded. There were 43 patients withischemic cerebral vascular disease in acute stage (<72hrs) or in stage of recovery (>15 days), the average age is 65.8?0.7 yrs(42-83), 25 was male, and 18 was female. In 7 patients (4 males and 3 females), PAF was detected on the 1* 3rd, 7th , 15th ,21th, and 28* day after onset for dynamic observation. There were 21 patients(12 male and 9 female ) with cerebral hemorrhage, the aberage age was 61.3 + 12.2yrs(41-79yrs). (2).Disease controls: Totally there were 32 non-cerebrovascular disease patients(16 male and 16 female) including 7 sciatica, 6 cervical syndrome, 4 acute myelitis, 6 GBS, 5 epilepsy, 2 Parkinson's disease, 2 spasmodic torticollis, the average age was 54.1 + 10.9yrs(41-77yrs). (3).Healthy controls: There were 46 healthy controls( 27 male and 19 female), the average age was 60.3 ?11.5yrs(41-80yrs).2. Method.Got the venous biood at 72 hrs and 15 days after the onset, and deteci the PAF. The standard PAF was bought from Sigma company, silica ge G was produced by Shanghai Huamei bioengineering company.PAF was detected by thin-layer chromatography. The 2 ml venous blood was immediately put into the test tube with 3ml Chloroform and 6 ml methyl alcohol, then centrifugation(1200g, 15min), got the supernatant, adding 6ml Chloroform and 9.6 ml methyl alcohol, left in room temperature for 1 hrs, then centrifugation(1200g, 15min), got the Chloroform phase, then water bath(37癈). Prepare the plate using silica ge G and water, baking(120癈,120min)> and cooling to room temperature. Adding samples and standard PAF. Outspreaded them by chloroform : methyl alcohol:water(65:35:6,v/v/v). Cooling it. Mist spray using 10% phosphomolybdate(80*C, 30min) until the blot appearing blue. Scrapingdown the chromatography zone with same Rf value as standard PAP, resolve it by 200ml 0.25%BSA, get rid of the sendimentation, color matching and quantu.Results1. In the ischemic cerebral vasculardisease group, PAP in the acute stage was higher than that of recovery stage. But PAP in the hemorrhagic and non-cerebral vascular disease group had same PAP value in the acute and recovery stages. In the acute stage, there were significant difference among the group of cerebral ischemia, cerebral hemorrhage, non-cerebrovascular disease and healthy control, except between healthy control and non-cerebrovascular disease. In the recovery stage, PAP of cerebral ischemia and cerebral hemorrhage group was higher than that of non-cerebrovascular disease and healthy control group.2. In 7 patients with cerebral ischemia, PAP level was observed dynamically, PAP didn't changed significantly at the 1-3 days after the onset of disease, and did decrease at 3-28 days after onset, but it was still higher than that of healthy control and non-cerebrovascular disease.ConclusionFrom the results above, PAP level was significantly elevated in cerebral ischmic disease, it was highest at 72 hrs after onset, and could persist for a long period of time. Detection of PAP is helpful for understanding the pathogenesis and diagnosis of stro...
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