Blood endothelin-1, t-PA, and PAI-1 in patients with cerebral thrombosis Evaluation of measurements at the acute and chronic phases, and the venous occlusion test.

DOI 3 Citations 21 References
  • Ichino Takeshi
    Second Department of Internal Medicine, St. Marianna University School of Medicine
  • Sugihara Hiroshi
    Second Department of Internal Medicine, St. Marianna University School of Medicine
  • Kamogawa Asahi
    Second Department of Internal Medicine, St. Marianna University School of Medicine
  • Narita Nobuyoshi
    Second Department of Internal Medicine, St. Marianna University School of Medicine
  • Shimizu Tooru
    Second Department of Internal Medicine, St. Marianna University School of Medicine

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Other Title
  • 脳血栓症における血中エンドセリン１，ｔ‐ＰＡおよびＰＡＩ‐１　急性期，慢性期の測定値および静脈うっ滞試験からの検討
  • Evaluation of measurements at the acute and chronic phases, and the venous occlusion test
  • 急性期, 慢性期の測定値および静脈うっ滞試験からの検討

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Abstract

To investigate the effects of various factors derived from vascular endothelial cells on the pathology of cerebral thrombosis, we measured the blood levels of the putative thrombogenic factor, endothelin-1 (ET-1), the fibrinolytic factor, tissue plasminogen activator (t-PA), and its inhibitor, plasminogen activator inhibitor (PAI-1). Determinations were made at both the acute and chronic phases in patients with lacunar stroke (LAC) or atherothrombotic stroke (ATH). Venous occlusion tests were also carried out in these patients during the chronic phase. In patients with cerebral thrombosis, the ET-1 level decreased from the lower limit of normal over the course of the first 7 days after thrombosis, whereas the t-PA level tended to increase in the patients over the same time period. The changes were more significant in patients with ATH, in whom the t-PA level was higher than those measured in a group of normal healthy subjects and patients with LAC. The total PAI-1 level was high in patients with LAC or ATH; however, no temporal fluctuation was noted. The changes in ET-1 and t-PA levels in patients with LAC or ATH can be explained by a tendency for ET-1 release to decrease and t-PA release from vascular endothelial cells to increase during the venous occlusion test, when there is high basal release of PAT-1. The t-PA level increases as an adjustment reaction, and subsequent release of ET-1 is inhibited. In order to clarify the significance of vascular endothelial cells in the pathophysiology of cerebral thrombosis, it is important to determine the temporal relationships of these factors.

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