Abstract
Aim of the research is to evaluate the structure changes of the capillaries, arterioles, venules and intra and extravascular alterations in myocardium of rats after traumatic brain injury (TBI). Material and methods. Experiments were performed in 18 white male noninbred rats. Midline thoracotomy was performed, and the heart excised under intraperitoneal anesthesia (sodium thiopental) on 3, 7 and 12 days after TBI. Myocardial tissue of the left ventricle was examined under light and electron microscopy. The results showed that following brain trauma there were changes of microvascular wall characterized by alterations of permeability, paracellular oedema, outgrowths of vessel endothelium, swelling, edema, and thinning of endothelial cells, intussusceptions, vacuolization of cytoplasm with fragmentation within the myocardium of the rats with TBI. Intravascular changes were manifested by the formation of hyaline thrombi, microaggregates and sludge of red blood cells in the lumen, altered vascular membrane structures, bubbles or even complete absence of circulation in capillaries (noreflow). Alterations outside of the vascular wall were manifested by the formation of diapedetic hemorrhage and development of a strongly pronounced perivascular edema. The injury of microvessels and the microrelief of the luminal surface of endothelial cells appeared to be important factors of activation of vascularplatelet mechanism of hemostasis. Conclusion. Treatment of traumatic disease should consider the need in timely correction of nonspecific alter ations associated with TBI to optimize the restructuring of cytoskeleton of endothelial cells, abrogate endothelial dysfunction and prevent microcirculatory complications.
Highlights
Известно, что острый период тяжелой череп но мозговой травмы (ЧМТ) характеризуется ак тивацией сосудисто тромбоцитарного гемостаза [1], главным образом в системе микроциркуляции [2,3,4]
Procoagulant patterns appearing in stimulated endothelial cells activate the con sumption of platelets duringof the vascular platelet hemostasis
Adhesion and aggregation of blood cells may demonstrate a consequence of a decreased synthe sis of endothelial relaxing factor nitric oxide (NO)
Summary
Experiments were performed in 18 white male non inbred rats. The heart excised under intraperitoneal anesthesia (sodium thiopental) on 3, 7 and 12 days after TBI. The results showed that following brain trauma there were changes of microvascular wall characterized by alterations of permeability, paracellular oedema, outgrowths of vessel endothelium, swelling, edema, and thinning of endothelial cells, intussusceptions, vacuolization of cytoplasm with fragmentation within the myocardium of the rats with TBI. Intravascular changes were manifested by the formation of hyaline thrombi, microaggregates and sludge of red blood cells in the lumen, altered vascular membrane structures, bubbles or even complete absence of circulation in capillaries (no reflow). Alterations outside of the vascular wall were manifested by the formation of diapedetic hemorrhage and development of a strongly pronounced perivascular edema. The injury of microvessels and the microrelief of the luminal surface of endothelial cells appeared to be important factors of activation of vas cular platelet mechanism of hemostasis
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