[Molecular and cellular mechanisms of compensation for respiratory failure in nonspecific lung diseases].
Some molecular and cellular mechanisms of compensation for respiratory failure (RF) were examined in 90 patients with nonspecific pulmonary diseases. In acute RF, the content of 2,3-DPH in red blood cells was increased. As RF progressed, the compensatory-adaptation reaction became less marked. In chronic RF, the 2,3-DPH content in red blood cells did not differ from the control values. The disease was characterized by cholesterol a and sphingomyelin accumulation, a reduction in red blood cell ATPase activity, and an increase in microviscosity of red blood cell membranes. Decelerated utilization of ATPases in red blood cells is of a role in the genesis of a rise of the 2,3-DPH content in acute RF.
Landyshev
S Iu
SIu
Borodin
E A
EA
D019794:2,3-Diphosphoglycerate; D000222:Adaptation, Physiological; D000251:Adenosine Triphosphatases / Q000097:blood; D001809:Blood Viscosity; D004163:Diphosphoglyceric Acids / Q000097:blood; D004910:Erythrocyte Membrane / Q000502:physiology; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D007700:Kinetics; D008055:Lipids / Q000097:blood; D008171:Lung Diseases / Q000150:complications / Q000503:physiopathology*; D008564:Membrane Potentials; D012131:Respiratory Insufficiency / Q000503:physiopathology*
D004163:Diphosphoglyceric Acids; D006454:Hemoglobins; D008055:Lipids; D019794:2,3-Diphosphoglycerate; D000251:Adenosine Triphosphatases
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