title: Effects of electric footshock and water immersion restraint stresses on fibrinolytic parameters in the plasma of rats.
abstract: Wistar rats were exposed to electric footshock (ES) or water immersion restraint stress (WS). Blood was taken immediately after, 24, or 48 hours after the stress. The stomachs of rats taken 1 hour after stress application indicate that there were many bleeding spots in the stomachs of WS rats, but practically no visible bleeding spots in the stomachs of ES rats. Plasma levels of t-PA antigens increased in ES rats up to 24 hours after the stress, but the t-PA antigen levels decreased up to 48 hours in ES rats. There were no changes in t-PA activities in plasma of WS rats, but the levels in ES rats decreased immediately and 48 hours after the stress. PAI activity did not change immediately after WS but increased 24 hours after the stress. There was no change in PAI activity in ES rats up to 48 hours. ELT did not change in ES rats, but prolonged in WS rats at 24 hours after the stress. There were significant negative correlations between t-PA antigen levels or activities and ELT in control rats. No correlation was observed in ES or WS rats between t-PA antigen levels and ELT, and no correlation was shown in WS rats between t-PA activities and ELT. Plasma levels of catecholamines increased at the 20-minute period during ES, which may not explain the delayed effects of ES on hemostatic balance. Plasma levels of arginine vasopressin increased significantly immediately after the shock up to 2 hours, indicating that the stress was conveyed to the hypothalamus during the stress application. These results may indicate that some stressors induce an increase or decrease in the local balance of fibrinolytic activities, resulting in bleeding or thrombosis in the local vessels. Such changes may not be detected in the general circulation due to the neutralization of locally induced fibrinolytic changes or the involvement of other hepatically originated hemostatic factors induced by stressors.
authors.affiliation: Department of Pathophysiology, Hamamatsu University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Takada
authors.forename: T
authors.initials: T
authors.lastname: Urano
authors.forename: H
authors.initials: H
authors.lastname: Takahashi
authors.forename: N
authors.initials: N
authors.lastname: Nagai
authors.forename: A
authors.initials: A
authors.lastname: Takada
mesh_terms: D000818:Animals; D002395:Catecholamines / Q000097:blood; D005342:Fibrinolysis; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D012712:Serum Globulins / Q000032:analysis; D012774:Shock, Traumatic / Q000097:blood*; D013312:Stress, Physiological / Q000097:blood*; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D002395:Catecholamines; D017395:Plasminogen Activator Inhibitor 1; D012712:Serum Globulins; D010959:Tissue Plasminogen Activator