Abstract

Introduction. Intracerebral hemorrhage (ICH) is frequently accompanied by respiratory system complications. One of the correction method of post stroke complications is administration of immunosuppressive drug fingolimod. Theobjective of the study is to investigate non-respiratory lung functions in experimental ICH during fingolimod treatment. Materials and methods. Animals were divided into 3 groups: group 1 with ICH, group 2 with ICH receiving fingolimod and group 3 as reference group. Intracranial hemorrhage was modelled by 160 μl autologic blood injection into lateral brain ventricle (P=0.6; D=1.5; V=3.5). Fingolimod (FTY 720, «Sigma») was administered within 1 hour after ICH (intraabdominal, 1 mg/kg). Biochemistry and functional parameters of the lung surfactant in animals were studied. Phospholipids fractions spectrum was assessed by thin-layer chromatography, superficial surfactant activity by Wilhelmi method. Parameters of water metabolism, pulmonary blood filling were studied by gravimetric method. Level of blood nitric oxide was estimated by amount of nitrates and nitrites stable terminal metabolites. Results. We revealed that experimental ICH causes a decrease of alveolar stability index by 9 %, decrease of total alveolar phospholipids content by 25 % and change of its fraction composition, i.e. decrease of major surface active fraction (phosphatidylcholine) by 68 %, increase of phosphatidic acid amount by 151 % and increase of lisophosphatidylcholine by 163 %. Besides that, experimental ICH is followed by lung edema on the lung blood filling background and increase of blood NO. Fingolimod administration does not affect surfactant surface activity but totally corrects water balance, lung blood filling and blood NO content.

Highlights

  • We revealed that experimental Intracerebral hemorrhage (ICH) causes a decrease of alveolar stability index by 9 %, decrease of total alveolar phospholipids content by 25 % and change of its fraction composition, i.e. decrease of major surface active fraction (phosphatidylcholine) by 68 %, increase of phosphatidic acid amount by 151 % and increase of lisophosphatidylcholine by 163 %

  • Воздействие на S1Pрецепторы при введении финголимода также устраняло высокий уровень кровенаполнения легких, индуцированный нарушением мозгового кровотока

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Summary

Introduction

Установлено нарушение нереспираторных функций легких при ВМК [2,3,4]. В экспериментальных исследованиях продемонстрировано корригирующее влияние финголимода на нереспираторные функции легких при рассеянном склерозе, антифосфолипидном синдроме и ишемии головного мозга [6,7,8]. В связи с вышеизложенным, целью нашего исследования стало изучение нереспираторных функций легких при ВМК на фоне применения финголимода.

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