Biomedical subjects
Publications and source records attributed to F Plavsić.
A brief, simple and unexpensive UV spectrophotometric method for theophylline serum level determination is described. Charcoal extraction was performed for theophylline isolation from biological fluids. Coefficients of variation and recovery are similar to other parallel methods.
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Simultaneous and stepwise deprotection of the fully benzylated D-glucosyl esters of 1-benzyl N-benzyloxycarbonyl- and N-tert-butyloxycarbonyl-L-glutamic acid (1 and 5, respectively) have been examined. Catalytic hydrogenation of 1 led to intramolecular aminolysis to give pyroglutamic acid and D-glucose, but similar treatment in the presence of trifluoroacetic acid afforded both anomers of 1-O-(L-gamma-glutamyl)-D-glucopyranose, which were characterized as trifluoroacetates (2alpha and 2beta) and converted into 2,3,4,6-tetra-O-acetyl-1-O-[1-methyl N-(acetyl)-L-glutam-5-oyl]-D-glucopyranose (4) which was also prepared by a definitive method. Hydrogenolysis of 5 gave both anomers of 1-O-[N-(tert-butyloxycarbonyl)-L-gamma-glutamyl]-D-glucopyranose (6), which, upon treatment with trifluoroacetic acid at - 10 degrees, afforded 2alpha and 2beta, respectively. The structure of 6beta was established by its conversion into 2,3,4,6-tetra-O-acetyl-1-O-[1-methyl N-(tert-butyloxycarbonyl)-L-glutam-5-oyl]-beta-D-glucopyranose (7beta), whereas similar treatment of 6alpha gave a mixture of 1,3,4,6-tetra-O-acetyl-2-O-[1-methyl N-(tert-butyloxycarbonyl)-L-glutam-5-oyl]-alpha-D-glucopyranose (9) and 7alpha. A 1 leads to 2 acyl migration occurred during esterification of the aglycon carboxyl group of 6alpha with diazomethane to give 2-O-[1-methyl N-(tert-butyloxycarbonyl)-L-glutam-5-oyl]-alpha-D-glucopyranose (8).
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The effect of food and metoclopramide on the pharmacokinetics of bromocriptine was investigated in 7 healthy subjects. Plasma concentrations of bromocriptine were measured by radioimmunoassay after a single oral dose of 7.5 mg bromocriptine. Maximal plasma concentrations of bromocriptine were slightly lower when the drug was given after breakfast. Bioavailability of the drug was not significantly reduced by food nor by metoclopramide pre-treatment. Side effects of bromocriptine were considerably reduced by metoclopramide pre-treatment (0.5 mg/kg); the decrease was about 83% as estimated from Table II.
During the present war against the Republic of Croatia, chemical weapons have been used by the Yugoslav Federal Army (YFA) against both civilians and Croatian Army soldiers. The use of irritants was suspected (Vukovar, Bogdanovci and Vinkovci, October-November, 1991; Solin in the Split area, September, 1991) and proved (Velika Gorica in the Zagreb area, September, 1991; Cakovec, November, 1991) in many cases. The use of psychochemical incapacitating agents (Bilje near Osijek, July, 1991), as well as of psychostimulants in YFA own soldiers (Zadar, August, 1991) has been suspected on clinical findings or laboratory tests. The use of acetylcholnesterase inhibitors was proved in one aggressor's diversion (Zadar, Krusevo, July, 1991). Phosphorus from projectiles and fuming boxes caused poisoning and skin burns due to incineration (Vukovar, November, 1991). YFA used the civilian's fear of chemical and biological weapons, throwing untoxic substances all over the Croatian territory. Great ecocide problems have occurred with massive industry devastation (Sisak, Osijek, October, 1991-January, 1992), with enumerous amounts of toxic substances released into the soil and river aquatoria.
The paper deals with the course of the illness in a 66 years old male, who had taken an amount of 0.2 mg of medigoxin for an unknown period of time, because of chronic heart failure due to atherosclerotic heart disease and chronic atrial fibrillation. He have had a cholelithiasis also and reduced renal reserve. He was admitted by an emergency admittance because of nausea, vomiting, color vision disturbances: blue colored vision, and with other signs of digitalis toxicity: diffuse abdominal pain, an absolute arrhythmia with a slow ventricular rate, and with a short corrected Q-T interval in an electrocardiogram of 0.315 seconds and with high serum digoxin level reacted 3.8 nmol/L. After stopping of a digitalis treatment, in a period of time of four days, all signs of digitalis toxicity including blue color vision disturbances disappeared. In the paper that rare sign of digitalis toxicity is discussed.
Rationality of digitalis use in 20 elderly patients in long term-care institution was analysed using the method of correlation of the past medical history, clinical examination and basic laboratory findings. After consultation of clinical pharmacologist, general practitioner and medical biochemist it was possible to stop the digoxin therapy in 6 (30%) of the patients. Four (20%) patients were hypersaturated with digoxin. Lack of indication was the reason for stopping the digitalis in one of them. Therapy was modified in 3 patients. Use of digitalis was rational in 10 (50%) of the patients. The results suggest that digitalis was prescribed too often in this sample of the elderly patients.
The course of illness in a 76-year-old woman with a history of dyspnea being treated with medigoxin, 0.1 mg daily, is presented. Five days before the symptoms of acute psychosis developed she had used medigoxin, 0.2 mg per day. On the fifth day of that therapy, the patient developed acute psychosis and was admitted to the Department of Psychiatry. An electrocardiogram recorded monomorphous ventricular premature beats at a frequency of 50%, the S-T segment depression of the anterolateral location with the diphasic T-wave and the corrected Q-T interval of 0.377 to 0.355 seconds. Five days after the discontinuation of medigoxin therapy, serum digoxin concentration was 2.2 nmol/L, out of which follows that two days after digitalis was stopped it was 4.0 nmol/L and that concentration was probably higher at the moment when acute psychosis developed. The patient was free of symptoms of acute psychosis after a single promazine dose and discontinuation of medigoxin.
In this paper, a course of the disease of a 68-year-old patient treated with medigoxin for congestive heart failure is presented. After being withdrawn from his treatment at the hospital, the patient was administered spironolactone and furosemide. The plasma digoxin level at entry was 1.1 nmol/L, after five days it reached 3.2 nmol/L, and after ten days it was 2.3 nmol/L. The patient had a normal renal function. The interference of spironolactone and its metabolites with the digoxin radioimmunoassay was discussed as a possible explanation for this phenomenon.
In a group of 84 patients aged 65 to 89 years with the high serum digoxin levels, electrocardiograms, as well as serum creatinine and serum potassium levels were analysed. In an electrocardiogram, a rhythm and conduction disturbances, PR interval, PTQ index, corrected QT interval, both a corrected QT interval I using the second root from a heart frequency and a corrected QT interval II using the third root from a heart frequency were studied. A rhythm disturbances were seen in 37% and a conduction disturbances in 39% of the patients, but no changes were observed in 24% of the patients. There was no correlation between serum digoxin levels and the PR interval. There was a slight correlation between serum digoxin levels and the PTQ index, and no correlation could be demonstrated between serum digoxin levels and a corrected QT interval I as well as a corrected QT interval II. Also, no correlation was evident between serum digoxin levels and serum creatinine levels, although many of those patients suffered from chronic renal failure. In an analysis of the influence of digoxin on the heart, electrocardiographic changes together with serum digoxin levels and serum potassium levels have to be followed. Only one of these parameters is not enough for the analysis of the effect of digoxin on the heart. It is concluded that clinical examination is most important in the analysis of digoxin action.
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Kidney and liver diseases induce alterations in drug binding to plasma proteins. These alterations are caused by qualitative and quantitative changes of plasma proteins and the presence of endogenous substances which act as competitive inhibitors of drug binding to plasma proteins. These changes are the most prominent in nephrotic syndrome and uremia among kidney diseases and in cirrhosis among liver diseases. The more important drugs in which the free fraction is changed in these entities are listed in the tables. The changes in drug distribution caused by plasma protein alterations may induce significant changes in entire drug pharmacokinetics. Discussed are theoretically expected and experimentally proven changes in plasma proteins in kidney and liver diseases and their influence to drug action and dosing regimen.