Morphometric evaluation of murine pulmonary mast cells in experimental hemorrhagic shock

Respiratory failure resulting frequently in death is one of the complications in the course of post-hemorrhagic changes. A systemic inflammatory reaction plays a significant role in the pathogenesis of this syndrome. Mast cells also contribute to this effect. To broaden our knowledge of the pathogenesis of respiratory insufficiency, we evaluated morphometrically lung mast cells in hemorrhagically shocked rats. Lung sections were stained with alcian blue and safranin, and four separate locations were distinguished: under the lung pleura, around the bronchi and the large vessels, and in the interalveolar septa. A decrease in the area and volume of mast cells and an increase in their circularity index in interalveolar septa and around the bronchi was observed. An enlargement of mast cells around lung vessels was also found. There were no changes in the morphometric parameters of mast cells under pleura. The results suggest an activation and degranulation of mast cells and a role in the inflammatory process causing acute lung injury in hemorrhagic shock.     

BN52021 stabilizes the oxidant-antioxidant equilibrium in peritoneal lavage fluid in experimental hemorrhagic shock

The overproduction of highly reactive oxygen metabolites initiates and contributes to the damage to abdominal organs in hemorrhagic shock (HS). Peritoneal environment including free cells located in peritoneal cavity may interact with the inflammatory processes occurring in abdominal organs during HS. Peritoneal lavage was carried out in 48 rats divided into following groups: (1) control, (2) untreated HS for 75 minutes, (3) HS + restoration of blood volume with polyelectrolyte solution (PES) 60 minutes after blood withdrawal, and (4) HS + platelet activating factor (PAF) receptor antagonist BN52021 directly after bleeding + PES after 60 minutes of HS. Peritoneal lavage fluid (PLF) was examined for Cu-, Zn-superoxide dismutase (SOD) activity, sulfhydryl compound (-SH) concentration, and malondialdehyde (MDA) level measured as thiobarbituric acid reactive substances (TBARS). The untreated shock (group 2) as well as HS + PES (group 3), resulted in significant increase in cell numbers in PLF. In groups 2 and 3, the SOD activities were not detected while -SH group levels were significantly higher, than those in the control. The group of shocked rats after blood volume restoration with PES was the only group where the MDA in PLF was found. The highest -SH group concentrations and detectable SOD activities were recorded in shocked rats treated with BN52021 and PES. Systemic hemorrhage may cause significant alterations in the oxidant-antioxidant (O-A) balance in peritoneal cavity, accompanied by significant elevation of number of cells lavaged from peritoneal cavity. There is an escalation of disturbances in O-A balance in peritoneal lavage fluid due to restoration of blood volume. BN52021 may exert beneficial effects stabilizing peritoneal antioxidant system in the hemorrhagic shock.     

The evaluation of quantity and distribution of murine pulmonary mast cells in experimental hemorrhagic shock

Respiratory failure is one of the most serious clinical complications in the course of post-hemorrhagic changes. Cascade-like, systemic inflammatory reaction including the axis: intestines-liver-lung-immune system has a special significance in the pathogenesis of this syndrome. In order to broaden the knowledge of the respiratory insufficiency pathogenesis in hemorrhagic shock, the attempt was made to evaluate quantitatively rat mast cells localized under the pulmonary pleura, around the bronchi, around large vessels and placed in the interalveolar septa. The examinations were conducted on 24 young female Wistar rats, divided into two groups (n=12): (I) sham-operated and (II) shocked. The hemorrhagic shock was evoked by the withdrawal of 25% of the circulating blood. The shock duration was 75 min. The obtained lung sections were stained with toluidine blue and examined in a light microscope. After hemorrhagic shock, sections of lung samples revealed about two-fold increase in mast cell number/mm2 compared to controls. Mast cells were concentrated mostly around the bronchi and blood vessels. Hyperplasia and migration of mast cells may suggest their role in the modulation of inflammatory process causing acute lung injury in the hemorrhagic shock.     

Phospholipids in mitochondrial dysfunction during hemorrhagic shock

Energy deficiency plays a key role in the development of irreversible shock conditions. Therefore, identifying mitochondrial functional disturbances during hemorrhagic shock should be considered a prospective direction for studying its pathogenesis. Phospholipid (PL)-dependent mechanisms of mitochondrial dysfunction in the brain (i.e., in the frontal lobes of the cerebral hemispheres and medulla oblongata) and liver, which, when damaged, leads to an encephalopathy, are examined in this review. These mechanisms show strong regional specificity. Analyzing the data presented in this review suggests that the basis for mitochondrial functional disturbances is cholinergic hyperactivation, accompanied by a choline deficiency and membrane phosphatidylcholine (PC) depletion. Stabilization of the PL composition in mitochondrial membranes using “empty” PC liposomes could be one of the most important methods for eliminating energy deficiency during massive blood loss.