Shortening of the bleeding time in rabbits by hydrocortisone caused by inhibition of prostacyclin generation by the vessel wall.
Shortening of the bleeding time in rabbits by hydrocortisone caused by inhibition of prostacyclin generation by the vessel wall.
复制标题
氢化可的松通过抑制血管壁产生前列环素而缩短家兔的出血时间。
DOI：
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发表时间：
1979
影响因子：
15.9
通讯作者：
J. Mustard
中科院分区：
文献类型：
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作者：
M. Blajchman;A. Senyi;J. Hirsh;Y. Surya;M. Buchanan;J. Mustard
采用颈静脉出血时间技术和微血管出血时间技术研究了氢化可的松对家兔缺血性出血的影响。在X射线照射或注射异源血小板抗血清致血小板减少的家兔中，两种方法的出血时间与血小板计数呈反比关系。氢化可的松单次大剂量静脉给药（25-100 mg/kg）和每日剂量（6 mg/kg）肌内给药可缩短失血性休克动物的出血时间，将氢化可的松应用于颈静脉外或腔内滴入静脉可缩短颈静脉出血时间。在正常动物中也观察到这种效应。对血小板减少性出血的影响与剂量相关。每日给药时，氢化可的松连续给药10 d的效果比连续给药5 d的效果好。吲哚美辛和反苯环丙胺也减少了颈静脉出血时间时，注入颈静脉腔内，而外源性提供花生四烯酸逆转氢化可的松的效果，但没有逆转吲哚美辛或反苯环丙胺的效果。外源提供的亚油酸没有任何影响。用前列环素（PGI（2））灌注血管段可逆转腔内注射氢化可的松、吲哚美辛和反苯环丙胺的作用。类似地，氢化可的松、吲哚美辛和反苯环丙胺都降低了标准伤口在离体血管中的液体流失率，该离体血管在恒定压力下排空血液并灌注生理盐水。PGI（2）可逆转这三种药物的作用，而花生四烯酸仅逆转氢化可的松的作用，不能逆转吲哚美辛和反苯环丙胺的作用。通过预先将动物或血管壁暴露于氢化可的松，可以防止颈静脉条产生PGI（2）样物质和6-酮-野牡丹素F（1）α。这些结果与以下假设是一致的，即血管壁在受伤时释放平滑肌松弛素，并且氢化可的松抑制前列腺素形成通过维持血管收缩来增强止血。
The effect of hydrocortisone on thrombocytopenic bleeding has been studied in rabbits using a jugular vein bleeding-time technique and a microvascular bleeding-time technique. An inverse relationship was found between the bleeding time and platelet count with both techniques in rabbits made thrombocytopenic by either X-irradiation or injection of heterologous platelet antiserum. Hydrocortisone shortened both bleeding times in thrombocytopenic animals when given in single large doses intravenously (25-100 mg/kg), in daily doses (6 mg/kg) intramuscularly, and shortened the jugular bleeding time when applied to the outside of the jugular vein or instilled intraluminally into the vein. This effect was also noted in normal animals. The effect on thrombocytopenic bleeding was dose related. When given daily, the effect was greater when hydrocortisone was given for 10 d than for 5 d. Both indomethacin and tranylcypromine also reduced the jugular vein bleeding time when instilled intraluminally into the jugular vein, whereas exogenously provided arachidonic acid reversed the effect of hydrocortisone but did not reverse the effect of indomethacin or tranylcypromine. Exogenously provided linoleic acid did not have any effect. Perfusion of the vessel segment with prostacyclin (PGI(2)) reversed the effect of intraluminally administered hydrocortisone, indomethacin, and tranylcypromine. Similarly, hydrocortisone, indomethacin, and tranylcypromine all reduced the rate of loss of fluid from a standard wound in isolated vessels emptied of blood and perfused with saline under constant pressure. PGI(2) reversed the action of these three agents, however, arachidonic acid reversed only the effect of hydrocortisone and did not reverse the effect of indomethacin and tranylcypromine. The generation of PGI(2)-like material and 6-keto-prostaglandinF(1) alpha from jugular vein strips was prevented by prior exposure of the animals or vessel wall to hydrocortisone. These results are compatible with the hypothesis that the vessel wall releases smooth muscle-relaxing prostaglandins when injured and that inhibition of prostaglandin formation by hydrocortisone enhances hemostasis by allowing vasoconstriction to be maintained.