Effect of cardiac glycosides on the release of adenylate kinase into cerebrospinal fluid of patients with cerebral arteriosclerosis.
48 patients with cerebral arteriosclerosis were found to have a manifest release of adenylate kinase (AK) into cerebrospinal fluid (CSF). This release was most probably due to an increased leak in the brain cells subsequent to a lowered adenylate charge potential followed by a diminished electrochemical potential in these cells suffering from disturbed oxygen supply. A further increase of AK release into CSF was noted for the 22 patients receiving cardiac glycosides compared to the 26 patients not treated with these drugs. The mean AK value of the former group was 0.119 +/- 0.028 U/l compared to that of the latter group, being 0.089 +/- 0.025 U/l, and this difference was significant (p less than 0.001). The effect of cardiac glycosides is most probably explained by an additional lowering of the membrane electrochemical potential in brain cells of these patients due to the direct action of cardiac glycosides on the Na+- and K+-dependent ATPase system in these cells, resulting in an increased leak in the plasma membrane.
D000263:Adenylate Kinase / Q000134:cerebrospinal fluid*; D000368:Aged; D001772:Blood Cell Count; D001812:Blood-Brain Barrier / Q000187:drug effects*; D002555:Cerebrospinal Fluid / Q000166:cytology; D004074:Digitoxin / Q000627:therapeutic use*; D004077:Digoxin / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000201:enzymology*; D008297:Male; D010770:Phosphotransferases / Q000134:cerebrospinal fluid*
D004077:Digoxin; D004074:Digitoxin; D010770:Phosphotransferases; D000263:Adenylate Kinase