{"title":"缺氧对人血小板聚集和血栓素A2形成的刺激","authors":"K. Pönicke , R. Sternitzky , H.-J. Mest","doi":"10.1016/0262-1746(87)90096-5","DOIUrl":null,"url":null,"abstract":"<div><p>The influence of hypoxia on the spontaneous platelet aggregation (SPA) and thromboxane formation was studied. The analysis of aggregation curve was carried out according to Breddin.</p><p>The hypoxia enhanced the aggregayility from Q<sub>2</sub>norm = 2.46 ±0.40 (normoxia) to Q<sub>2</sub>hyp = 4.39±0.39 (hypoxia), n = 52, p < 0.001. 10 samples of those showed no SPA under equilibration with air but the hypoxic stimulus provoked SPA (Q<sub>2</sub>norm = 0, Q<sub>2</sub>hyp = 1.19±60, n = 10, p < 0.001).</p><p>When the results were arranged according to the degree of the stimulation of SPA, two groups could be separated with low and high response to hypoxic.</p><p>The hypoxia caused also an augmentation of the TXB<sub>2</sub> level in comparison to normoxia. The stronger enhancement of the TXB<sub>2</sub> formation during the incubation under hypoxic conditions was independent of the fact whether SPA took place or not.</p><p>The present study suggests that hypoxic conditions alone may be a reason for a stimulated TXA<sub>2</sub> formation of the platelets and that the enhanced TXA2 formation caused by hypoxic is possibly inducing or reinforcing the SPA.</p></div>","PeriodicalId":20720,"journal":{"name":"Prostaglandins, leukotrienes, and medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1987-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0262-1746(87)90096-5","citationCount":"23","resultStr":"{\"title\":\"Stimulation of aggregation and thromboxane A2 formation of human platelets by hypoxia\",\"authors\":\"K. Pönicke , R. Sternitzky , H.-J. Mest\",\"doi\":\"10.1016/0262-1746(87)90096-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>The influence of hypoxia on the spontaneous platelet aggregation (SPA) and thromboxane formation was studied. The analysis of aggregation curve was carried out according to Breddin.</p><p>The hypoxia enhanced the aggregayility from Q<sub>2</sub>norm = 2.46 ±0.40 (normoxia) to Q<sub>2</sub>hyp = 4.39±0.39 (hypoxia), n = 52, p < 0.001. 10 samples of those showed no SPA under equilibration with air but the hypoxic stimulus provoked SPA (Q<sub>2</sub>norm = 0, Q<sub>2</sub>hyp = 1.19±60, n = 10, p < 0.001).</p><p>When the results were arranged according to the degree of the stimulation of SPA, two groups could be separated with low and high response to hypoxic.</p><p>The hypoxia caused also an augmentation of the TXB<sub>2</sub> level in comparison to normoxia. The stronger enhancement of the TXB<sub>2</sub> formation during the incubation under hypoxic conditions was independent of the fact whether SPA took place or not.</p><p>The present study suggests that hypoxic conditions alone may be a reason for a stimulated TXA<sub>2</sub> formation of the platelets and that the enhanced TXA2 formation caused by hypoxic is possibly inducing or reinforcing the SPA.</p></div>\",\"PeriodicalId\":20720,\"journal\":{\"name\":\"Prostaglandins, leukotrienes, and medicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1987-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0262-1746(87)90096-5\",\"citationCount\":\"23\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Prostaglandins, leukotrienes, and medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0262174687900965\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins, leukotrienes, and medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0262174687900965","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 23
摘要
研究了缺氧对血小板自发聚集(SPA)和血栓素形成的影响。根据布雷丁法对聚合曲线进行了分析。低氧增强了Q2norm = 2.46±0.40(常氧)至Q2hyp = 4.39±0.39(低氧)，n = 52, p <0.001. 其中10个样本在空气平衡下无SPA，但缺氧刺激引起SPA (Q2norm = 0, Q2hyp = 1.19±60,n = 10, p <0.001)。将结果按SPA刺激程度排序，可分为低、高缺氧反应两组。与正常缺氧相比，缺氧也引起TXB2水平的升高。在低氧条件下培养期间，TXB2形成的增强与是否发生SPA无关。本研究提示，缺氧条件本身可能是刺激血小板TXA2形成的一个原因，而缺氧引起的TXA2形成的增强可能是诱导或加强SPA。
Stimulation of aggregation and thromboxane A2 formation of human platelets by hypoxia
The influence of hypoxia on the spontaneous platelet aggregation (SPA) and thromboxane formation was studied. The analysis of aggregation curve was carried out according to Breddin.
The hypoxia enhanced the aggregayility from Q2norm = 2.46 ±0.40 (normoxia) to Q2hyp = 4.39±0.39 (hypoxia), n = 52, p < 0.001. 10 samples of those showed no SPA under equilibration with air but the hypoxic stimulus provoked SPA (Q2norm = 0, Q2hyp = 1.19±60, n = 10, p < 0.001).
When the results were arranged according to the degree of the stimulation of SPA, two groups could be separated with low and high response to hypoxic.
The hypoxia caused also an augmentation of the TXB2 level in comparison to normoxia. The stronger enhancement of the TXB2 formation during the incubation under hypoxic conditions was independent of the fact whether SPA took place or not.
The present study suggests that hypoxic conditions alone may be a reason for a stimulated TXA2 formation of the platelets and that the enhanced TXA2 formation caused by hypoxic is possibly inducing or reinforcing the SPA.
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