Effect of methyl-β-cyclodextrin and its complex with cholesterol on lung hydration and osmotic resistance of erythrocytes in experimental pulmonary edema

Abstract

Background. Methyl-β-cyclodextrin (MβC) is a cyclic oligosaccharide. It is hydrophilic and low-toxic, and can encapsulate various insoluble molecules, including hydrophobic ones, which allows its use for targeted delivery of cholesterol to damaged cell membranes.

Aim: To study indicators of lung hydration and osmotic resistance of the erythrocyte membrane in a model of hemodynamic pulmonary edema in adult rats administered with "pure" MβC and its water-soluble complex with cholesterol.

Materials and methods. The study was conducted on 40 adults male Wistar rats. Animals were divided into a control group (n=10) and 3 experimental groups, each with 10 animals. In the experimental groups, pulmonary edema was simulated by intravenous administration of a 1% solution of Mesaton (phenylephrine), followed by administration of MβC or cholesterol-methyl-β-cyclodextrin (ChMβC). 50 minutes after the administration of Mesaton, blood was withdrawn, and the lungs were isolated from rats of all study groups. The degree of lung hydration was determined by the lung coefficient and the dry residue. The osmotic stability of the erythrocyte membrane was assessed by percentage of hemolysis in serial dilutions of sodium chloride solution.

Results. Administration of "pure" MβC not containing cholesterol to rats with experimental pulmonary edema increased lung hydration and reduced osmotic resistance of erythrocytes. Administration of ChMβC to rats with experimental pulmonary edema significantly reduced lung hydration and increased osmotic resistance of erythrocytes.

Conclusion. Indicators of lung hydration and erythrocyte resistance change in opposite directions during the treatment of MβC and ChMβC. This confirms that cholesterol is the leading factor in the pathogenesis of pulmonary alveolar edema.