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抗坏血酸对血小板结构和功能的影响。

The influence of ascorbic acid on platelet structure and function.

作者信息

Cowan D H, Graham R C, Shook P, Griffin R

出版信息

Thromb Diath Haemorrh. 1975 Sep 30;34(1):50-62.

PMID:242092
Abstract

To determine the effect on platelet behavior of transient exposure of platelets to ascorbic acid, studies of platelet function and ultrastructure were done before exposure to ascorbic acid at pH 6.5, during exposure to pH 6.5, and after restoration of pH to pre-acidification levels. The effect of ascorbic acid (A.A.) was compared to that of HCl and citric acid (C.A.). ADP- and collagen-induced aggregation of normal platelets were significantly impaired by both A.A. and C.A. but were less affected by HCl. The release of 14C-serotonin was significantly reduced by each agent. The ultrastructure of normal platelets brought to pH 6.5 by A.A. was normal. After neutralization, there was marked dilatation of the open channel system and loss of the disc shape. When platelets were brought to pH 6.5 by A.A., then neutralized, the aggregates which formed after stimulation by ADP or collagen were smaller than normal, the platelets were less closely approximated, and degranulation was less complete. The data show that exposure of platelets to ascorbic acid for short intervals impairs their function when measured after restoration of pH to levels compatible with maximal responses. Platelet survival studies using autologous platelets labelled with 51Cr in the presence or absence of ascorbic acid showed that the recovery of normal platelets was unaffected by ascorbic acid, whereas recovery of platelets from patients with idiopathic thrombocytopenic purpura, idiopathic thrombocythemia, and alcohol-related thrombocytopenia was markedly reduced. The injury resulting from the use of ascorbic acid in preparing platelets for studies of platelet survival in patients with disorders affecting platelets may impair the recovery of the cells, resulting in artifactual changes in the survival studies.

摘要

为了确定血小板短暂暴露于抗坏血酸对血小板行为的影响,在血小板暴露于pH 6.5的抗坏血酸之前、暴露于pH 6.5期间以及pH恢复到酸化前水平之后,进行了血小板功能和超微结构研究。将抗坏血酸(A.A.)的作用与盐酸和柠檬酸(C.A.)的作用进行了比较。ADP和胶原诱导的正常血小板聚集均受到A.A.和C.A.的显著损害,但受盐酸的影响较小。每种试剂均显著降低了14C - 5羟色胺的释放。由A.A.使pH达到6.5的正常血小板的超微结构正常。中和后,开放通道系统明显扩张,盘状形态丧失。当血小板由A.A.使其达到pH 6.5然后中和时,ADP或胶原刺激后形成的聚集体比正常情况小,血小板彼此贴附不紧密,脱颗粒也不完全。数据表明,在pH恢复到与最大反应相容的水平后测量时,血小板短时间暴露于抗坏血酸会损害其功能。使用51Cr标记的自体血小板在有或没有抗坏血酸存在的情况下进行的血小板存活研究表明,正常血小板的恢复不受抗坏血酸影响,而特发性血小板减少性紫癜、原发性血小板增多症和酒精相关性血小板减少症患者的血小板恢复则明显降低。在为影响血小板的疾病患者进行血小板存活研究而制备血小板时使用抗坏血酸所导致的损伤可能会损害细胞的恢复,从而在存活研究中产生人为变化。

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