Paracetamol.
Reduces the effectiveness of uricosuric medicines (LS). The concomitant use of paracetamol in high doses increases the effect of anticoagulant drugs (a decrease in the synthesis of procoagulant factors in the liver). Inductors of microsomal oxidation in the liver (phenytoin, barbiturates, rifampicin, phenylbutazone, tricyclic antidepressants), ethanol and hepatotoxic drugs increase the production of hydroxylated active metabolites, which allows the development of severe intoxication even with a slight overdose.
Long-term use of barbiturates reduces the effectiveness of paracetamol.
Ethanol promotes the development of acute pancreatitis.
Inhibitors of microsomal oxidation (incl. cimetidine) reduce the risk hepatotoxic action.
Prolonged sharing of paracetamol and other NSAIDs increases the risk of developing "analgesic" nephropathy and renal papillary necrosis, the onset of the terminal stage of renal failure. Simultaneous long-term administration of paracetamol in high doses and salicylates increases the risk of developing kidney or bladder cancer. Diflunisal increases the plasma concentration of paracetamol by 50% - the risk of developing hepatotoxicity.
Myelotoxic drugs increase the manifestation of hematotoxicity of the drug.
Phenylephrine.
Reduces the hypotensive effect of diuretics and antihypertensive drugs (in t.ch. methyldopa, meqamylamine, guanadrel, guanethidine).
Phenothiazines, alpha-adrenoblockers (phentolamine), furosemide and other diuretics reduce the hypertensive effect.
MAO inhibitors (including furubbish, procarbazine, selegilim), oxytocin, ergot alkaloids, tricyclic antidepressants, methylphenidate, adrenostimulants enhance the pressor effect and arrhythmogenicity of phenylephrine.
Beta-adrenoblockers reduce cardiostimulating activity against the background of a reservepin possible arterial hypertension depletion of stocks catecholamines in adrenergic endings increases sensitivity to adrenomimetics).
Inhalation anesthetics (including chloroform, enflurane, halothane, isoflurane, methoxyflurane) increase the risk of severe atrial and ventricular arrhythmia, as sharply increase the sensitivity of the myocardium to sympathomimetics.
Ergometrine, ergotamine, methylergomethrin, oxytocin, doxapram increase the severity of the vasoconstrictor effect.
Reduces the antianginal effect of nitrates, which in turn can reduce the pressor effect of sympathomimetics and the risk of arterial hypotension (simultaneous use is allowed depending on the achievement of the necessary therapeutic effect). Thyroid hormones increase (mutually) the effect and the associated risk of coronary insufficiency (especially in coronary atherosclerosis).
Ascorbic acid.
Increases the concentration in the blood of benzylpenicillin and tetracyclines; in a dose of 1 g / day increases the bioavailability of ethinyl estradiol (including those included in oral contraceptives).
Improves absorption in the intestines of iron preparations (converts trivalent iron into bivalent); can increase the excretion of iron with simultaneous use with deferoxamine.
Reduces the effectiveness of heparin and indirect anticoagulants. Acetylsalicylic acid (ASA), oral contraceptives, fresh juices and alkaline drink reduce absorption and absorption.
With simultaneous application with ASA, urinary excretion of ascorbic acid increases and the excretion of ASA decreases.
ASA reduces the absorption of ascorbic acid by about 30%.
Increases the risk of developing crystalluria in the treatment of salicylates and sulfonamides short-acting, slows the excretion of the kidneys, increases the excretion of drugs that have an alkaline reaction (including alkaloids), reduces the concentration of oral contraceptives in the blood.
Increases the total clearance of ethanol, which in turn reduces the concentration of ascorbic acid in the body.
Quinoline drugs, calcium chloride, salicylates, glucocorticosteroids. When long-term use depletes the supply of ascorbic acid.
With simultaneous use reduces the chronotropic effect of isoprenaline.
With prolonged use or use in high doses, it can interfere with the interaction of disulfiram and ethanol.
In high doses increases the excretion of mexiletine by the kidneys.
Barbiturates and primidon increase inExcretion of ascorbic acid with urine. Reduces the therapeutic effect of antipsychotic drugs (neuroleptics) - phenothiazine derivatives, tubular reabsorption of amphetamine and tricyclic antidepressants.