Brain cell membrane modification following hypercapnia and recovery in newborn piglets.
The effect of hypercapnia on brain cell membrane structure and function was studied in anesthetized newborn piglets. Lipid peroxidation products (conjugated dienes and fluorescent compounds), Na+,K(+)-ATPase activity and enzyme affinity to ATP (substrate), K+ and Na+ ions (activators), and strophanthidin (inhibitor) were measured in three groups of animals: controls, those exposed to 90 minutes of PaCO2 > 80 mmHg (hypercapnia) and those exposed the same way, following restoration of normal PaCO2 (recovery). Enzyme activity was unchanged by hypercapnia, but enzyme affinity was altered as indicated by an increase in ATP affinity. Affinities to Na+, K+, and strophanthidin were unchanged. Restoration of normal PaCO2 resulted in an increase in conjugated dienes. The data demonstrate that hypercapnia followed by restoration of normal PaCO2 in healthy term newborn piglets is associated with mild modification of brain cell membrane Na+,K(+)-ATPase, possibly due to lipid peroxidation.
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia.
R
R
Schneiderman
J
J
Kubin
O P
OP
Mishra
M
M
Delivoria-Papadopoulos
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000503:physiopathology* / Q000648:ultrastructure*; D002462:Cell Membrane / Q000502:physiology / Q000648:ultrastructure; D004789:Enzyme Activation; D006935:Hypercapnia / Q000503:physiopathology*; D016014:Linear Models; D050356:Lipid Metabolism; D015227:Lipid Peroxidation / Q000502:physiology; D008564:Membrane Potentials; D015221:Potassium Channels / Q000502:physiology*; D015222:Sodium Channels / Q000502:physiology*; D013050:Spectrometry, Fluorescence; D013327:Strophanthidin / Q000494:pharmacology; D013552:Swine
D015221:Potassium Channels; D015222:Sodium Channels; D013327:Strophanthidin; D000255:Adenosine Triphosphate