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Updated: May 5, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Changes in the coagulation and fibrinolytic system of patients with subarachnoid hemorrhage
Yong Ji1, Qin-Hu Meng, Zhi-Gang Wang
1Department of Neurosurgery, The Second Hospital of Shandong University.
The aim of this study was to investigate the dynamic changes in the coagulation and fibrinolytic system with subarachnoid hemorrhage. The blood coagulation enzyme-AT complex (TAT), anticoagulant enzyme (AT), tissue plasminogen activator (tPA), plasminogen activin inhibitor (PAI-1), and mean blood flow velocity were measured. The TAT level was significantly higher 6 h after subarachnoid hemorrhage (SAH), whereas AT was significantly lower. These changes were maintained at 12 h to 1 d after SAH, returned to normal at 3 d, significantly changed again at 7 d to 14 d. The tPA level gradually increased after SAH and peaked at 14 d, and then returned to normal at 21 d. The PAI-1 levels were significantly lower than those in the control group 1 d after SAH gradually increased, and returned to normal at 21 d. In the cerebral vasospasm (CVS) groups, the levels of TAT, and AT significantly changed compared to the non-CVS groups after SAH. The PAI-1 levels were higher at 7 d and 14 d, but the changes were not significant. In groups Fisher III and IV as well as Hunt III to V, the TAT, AT, tPA, and PAI-1 levels were significantly higher than those in both Fisher and Hunt I and II 6 h, 12 h, 1 d, 7 d, and 14 d after SAH. The changes in the coagulation and fibrinolytic system of patients with SAH are correlated with the progress and symptoms of SAH as well as the blood content and CVS.
The aim of this study was to investigate the dynamic changes in the coagulation and fibrinolytic system with subarachnoid hemorrhage. The blood coagulation enzyme-AT complex (TAT), anticoagulant enzyme (AT), tissue plasminogen activator (tPA), plasminogen activin inhibitor (PAI-1), and mean blood flow velocity were measured. The TAT level was significantly higher 6 h after subarachnoid hemorrhage (SAH), whereas AT was significantly lower. These changes were maintained at 12 h to 1 d after SAH, returned to normal at 3 d, significantly changed again at 7 d to 14 d. The tPA level gradually increased after SAH and peaked at 14 d, and then returned to normal at 21 d. The PAI-1 levels were significantly lower than those in the control group 1 d after SAH gradually increased, and returned to normal at 21 d. In the cerebral vasospasm (CVS) groups, the levels of TAT, and AT significantly changed compared to the non-CVS groups after SAH. The PAI-1 levels were higher at 7 d and 14 d, but the changes were not significant. In groups Fisher III and IV as well as Hunt III to V, the TAT, AT, tPA, and PAI-1 levels were significantly higher than those in both Fisher and Hunt I and II 6 h, 12 h, 1 d, 7 d, and 14 d after SAH. The changes in the coagulation and fibrinolytic system of patients with SAH are correlated with the progress and symptoms of SAH as well as the blood content and CVS.
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