digoxin and Brain-Injuries

This review mainly summarizes selected aspects of the present knowledge of drug elimination kinetics independent of developmental changes, with special attention given to clinical situations. The effects of different disease states, drug interactions, changes in urinary pH, induction of microsomal enzymes, competition for renal excretory mechanisms, possible enterohepatic recirculation, binding of drugs to tissues, effects of a drug on another drug's metabolizing organ, and dose-dependent elimination, on increase or decrease of drug elimination rates in children, have been presented. Based on the available data it seems that one may postulate the following conclusions: (1) that the distribution factors as well as changes in drug elimination capacities seem to play a role, perhaps with differing relative importance, during each of the maturational periods; (2) that the physicochemical properties of a drug and its dosage, as well as changes in the volume of distribution in children, in the course of certain disease states may have a significant effect on kinetics of drug disposition in the body; (3) that systemic clearance, a model independent parameter, rather than elimination half-life, a hybrid pharmacokinetic parameter, more accurately reflects elimination of some drugs from the body; (4) that each drug and every clinical situation may require the evaluation of the direct effect on pharmacokinetic processes, since general principles may not always apply; (5) that drug disposition studies should also be performed, if possible, on patients under actual clinical situations and receiving the usual therapeutic regime, and (6) that the half-life of colistin is independent of postnatal age which should serve as a warning not to generalize about drug excretion in the young infant.

Topics: Adult; Anti-Bacterial Agents; Brain Injuries; Child; Child, Preschool; Colistin; Cystic Fibrosis; Digoxin; Dose-Response Relationship, Drug; Drug Interactions; Female; Half-Life; Heart Failure; Humans; Hydrogen-Ion Concentration; Hypothermia, Induced; Infant; Infant, Newborn; Kidney; Kinetics; Liver; Nephrotic Syndrome; Nutrition Disorders; Pharmaceutical Preparations; Phenobarbital; Reye Syndrome; Serum Albumin; Urine

Brain injury may induce hypertension. Because serum ouabain-like compound (OLC) has vasoconstrictor activity, digoxin antibody antihypertensive effects were evaluated using an intracerebroventricular (ICV) hemorrhage rat model.. Four ICV infused Wistar rat groups were studied: control; blood; blood plus digoxin antibody, and cerebrospinal fluid-like solution. Tail-cuff blood pressure, cumulative sodium balance, and serum OLC were measured.. The ICV blood infusion increased blood pressure (BP) and OLC without sodium balance change. Digoxin antibody prevented BP and OLC rise. Blood pressure was positively correlated with OLC in blood and blood plus digoxin antibody rats (R = 0.63; P <.05).. Cerebral hemorrhage increased OLC and BP, which were reversed by digoxin antibody administration.

Topics: Animals; Antibodies; Blood Pressure; Brain Injuries; Cardenolides; Digoxin; Immunoglobulin Fab Fragments; Infusions, Parenteral; Intracranial Hemorrhage, Hypertensive; Male; Models, Animal; Rats; Rats, Wistar; Saponins; Sodium-Potassium-Exchanging ATPase

Topics: Accidental Falls; Age Factors; Aged; Aged, 80 and over; Anti-Arrhythmia Agents; Brain Injuries; Digoxin; Drug Overdose; Electrocardiography; Female; Humans

An endogenous ouabain-like factor (EOLF) was measured in brain tissue of cats 12 and 24 hrs after cold injury-induced edema. EOLF was assayed via its inhibition of 86Rb+ uptake in human red blood cells in a fraction which was obtained from brain tissue by methanol extraction, chloroform treatment and purification of the water phase by C-18 HPLC. As compared to the contralateral hemispheres with an EOLF concentration of 605 +/- 71 pmol ouabain equivalents per g wet weight, the edematous hemisphere had significantly higher concentrations: 12 hours after cold injury it was 2600 +/- 1762 pmol (p < 0.03) and fell to 857 +/- 160 pmol ouabain equivalents/g wet weight after 24 hrs. Similar kinetics were evident for the EOLF concentrations in cerebrospinal fluid. It is suggested that the increase of EOLF in the edematous brain hemisphere may participate as a mediator in the development of vasogenic brain edema in the disturbance of the sodium metabolism.

Topics: Animals; Biological Factors; Blood-Brain Barrier; Brain Edema; Brain Injuries; Cardenolides; Cats; Chromatography, High Pressure Liquid; Digoxin; Erythrocytes; Freezing; Humans; Saponins; Sodium; Sodium-Potassium-Exchanging ATPase; Water-Electrolyte Balance

Topics: Adolescent; Adult; Brain Injuries; Diagnosis, Differential; Digoxin; Electroconvulsive Therapy; Encephalitis; Extrapyramidal Tracts; Female; Humans; Hyperkinesis; Hysteria; Male; Meclofenoxate; Middle Aged; Parkinson Disease, Postencephalitic; Schizophrenia; Time Factors; Tranquilizing Agents