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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
[Pathogenesis of nasal bleeding in the patients presenting with arterial hypertension]
1Rostov State Medical University, Russian Ministry of Health, Rostov-on-Don, Russia, 3440061.
Abstract:
The objective of the present work was to study the pathogenetic mechanisms underlying nasal bleeding (NB) in the patients presenting with arterial hypertension (AH). A total of 47 patients with AH suffering from NB were available for the examination of whom 28 experienced a single bleeding episode and 19 had recurrent bleeding. 11 of them were treated by endonasal surgical intervention for the achievement of hemostasis. Simultaneously, mucoperichondreal biopsies were taken from the anterior septal portions and used for histological and ultrastructural investigations. The laboratory examination of all the patients has demonstrated hyperfibrinogenemia and the enhanced level of soluble monomeric fibrin complexes in the blood (especially in the patients with recurrent nasal bleeding) despite the normal platelet levels, prothrombin and thrombin times. These findings gave reason to characterize the hemostasiological status of the patients as chronic compensated disseminated intravascular coagulation (DIC) syndrome. The histological study revealed hyaline, erythrocyte-rich and fibrin thrombi in the vessels of the microcirculatory system whereas ultrastructural studies showed desquamation of endothelial cells, massive desendothelization, and disintegration of the basal membrane with the exposure of subendothelium. It is supposed that these changes provoked the development of thrombosis and focal necrosis in nasal mucosa. The authors conclude that the cause of nasal bleeding associated with arterial hypertension is directly related to the lesions of vascular endothelial, microcirculatory disorders, and modification of the blood coagulation processes rather than to the mechanical rupture of blood vessels. These changes are believed to be responsible for the development of local intravascular coagulation.
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