Composition changes of membranes phospholipids in pathogenesis of brain mitochondrial function during hemorrhagic shock in cats

  • G. F. Leskova Institute of General Pathology and Pathophysiology, Moscow, Russian Federation; Research Institute of Space Medicine of All-Russian Center for Disaster Medicine “Protection” of the Federal Biomedical Agency of Russia, Moscow, Russian Federation
Keywords: phospholipides, mitochondrial membranes, brain, mechanisms of apoptose, hemorrhagic shock

Abstract

In experiments on cats it has been established, that composition changes of membranes phospholipids can be the basic pathogenic factors of brain mitochondrial dysfunctions under hemorrhagic shock. The decrease of membrane phosphatidylcholine content in mitochondria of medulla oblongata represents one of the basic mechanisms of mitochondrial еnergy-formation function decrease and intensification of cellular apoptose. The key mechanism of apoptose – the mitochondria aggregation – in medulla oblongata under hemorrhagic shock is connected with superfluous concentration of membrane phosphatidic acid. In mitochondria of cerebral hemispheres frontal lobes a specific falling of membrane phosphatidylethanolamine conсеntration indicate on a significant way of еnergy-formation disturbances during hemorrhagic shock. The decrease of membrane

phosphatidylinositol content can be considered as a way of apoptose intensification. The increase of membrane lysophosphatidylcholine level is the general mechanism of mitochondrial functions disturbances in the studied departments of a brain. Promoting formation of special protein channels, this phospholipid stimulate a mitochondrial capture of Са2+. Lysophosphatidylcholine participates in mechanisms of intensive formation of reactive oxygen species, and also in activation of apoptose.

Published
2023-03-02
How to Cite
Leskova, G. F. (2023). Composition changes of membranes phospholipids in pathogenesis of brain mitochondrial function during hemorrhagic shock in cats. Patogenez (Pathogenesis), 12(4), 17-20. Retrieved from https://pathogenesis.pro/index.php/pathogenesis/article/view/607
Section
Original investigations