Hemostatic disorders and alterations in erythrocyte deformability in experimental acute ischemic stroke

Abstract

Background. Acute ischemic stroke is one of the leading causes of mortality and disability worldwide. Hemostatic disorders and alterations in blood rheology play a pivotal role in the pathogenesis of cerebral ischemia by promoting thrombosis, microvascular dysfunction, and impaired tissue perfusion. However, the dynamics of vascular-platelet hemostasis and erythrocyte deformability during ischemic brain injury remain insufficiently characterized.

The aim. To investigate changes in vascular-platelet hemostasis and erythrocyte deformability in rats with experimentally induced focal cerebral ischemia.

Materials and Methods. Experimental focal cerebral ischemia was induced in white non-linear rats by middle cerebral artery occlusion according to the Longa model. Platelet count was determined using the Fonio method. Platelet aggregation was assessed using ADP, adrenaline, and collagen as aggregation inducers. Erythrocyte deformability was evaluated spectrophotometrically by measuring fluctuations in optical density of erythrocyte suspensions. The parameters were assessed on days 1 and 14 after ischemia induction. Statistical analysis was performed using Student’s t-test, and differences were considered significant at p<0.05.

Results. Experimental cerebral ischemia resulted in significant activation of the vascular-platelet component of hemostasis. On day 1, platelet count increased by 1.5-fold (p<0.05) compared with intact animals and remained elevated by 1.8-fold (p<0.05) on day 14. Platelet aggregation induced by ADP, adrenaline, and collagen increased by 1.2-, 1.3-, and 1.2-fold (p<0.05), respectively, during the acute phase and remained significantly elevated throughout the observation period. Assessment of erythrocyte deformability revealed marked alterations in blood rheology. On day 1, erythrocyte deformability in plasma increased by 1.4-fold (p<0.05), while in physiological saline it increased by 1.5-fold (p<0.05) compared with intact controls. By day 14, these parameters decreased slightly but remained significantly higher than control values, exceeding them by 1.2-fold and 1.3-fold (p<0.05), respectively.

Conclusions. Experimental focal cerebral ischemia is accompanied by persistent platelet activation, increased thrombogenic potential, and significant alterations in erythrocyte rheological properties. Enhanced platelet aggregation and changes in erythrocyte deformability contribute to microcirculatory dysfunction and may aggravate ischemic brain injury. These findings highlight the important role of hemostatic and hemorheological disturbances in the pathogenesis and progression of acute ischemic stroke.