[Initiating young doctors into the physician's work].
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Biomedical subjects
Publications and source records attributed to L Tarssanen.
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The information on the pharmacokinetics of verapamil in overdose is scanty. We report two adults who ingested 3.2 g and 4 g of verapamil, respectively. Both patients had hypotension and a severe bradycardia. The highest plasma verapamil concentration in these patients was about 2200 ng/ml and 2700 ng/ml, respectively. The decline in plasma verapamil and norverapamil concentrations followed first-order kinetics, and the half-life of verapamil was 7.8 h and 15.1 h, respectively. The free fraction of verapamil (non-protein bound) was higher at total concentrations exceeding 2000 ng/ml (12-15%) than at lower concentrations (2-6%). There seems to be no marked saturation of the metabolism of verapamil in acute poisoning. The apparent concentration-dependent changes in the free fraction may be due to therapeutic measures.
Changes in the release of atrial natriuretic peptide (ANP) and vasopressin (VP) may contribute to the final outcome of beta-adrenoceptor blocking therapy. Therefore, we administered 2 hours before a bicycle exercise test (a 30-minute exercise with 100 W work load) in a randomized, double-blind, placebo-controlled crossover study orally 50 mg atenolol, 80 mg propranolol or 10 mg pindolol to 15 healthy volunteers. Hormone release and sympathoadrenal activation were estimated by measuring plasma ANP-, VP-, adrenaline and noradrenaline concentrations. beta-blockade and -antagonism were estimated by measuring the reduction of exercise-induced tachycardia and the extent to which the drugs occupied rabbit lung beta 1- and rat reticulocyte beta 2-adrenoceptors in the circulating plasma. We noticed clear differences in the animal beta 1- and beta 2-receptor occupancy between these agents. The agents and placebo during the exercise augmented plasma ANP level similarly, on average by 34-72%. Pindolol administration enhanced the decline of plasma ANP level after exercise (ANCOVA rep meas, pindolol vs placebo, p < 0.05). Although pindolol increased the mean plasma VP level by 25% (ANCOVA rep meas for the increase, pindolol vs placebo, p < 0.05), drug effects on plasma VP-level were generally negligible. In conclusion, in healthy volunteers beta 1- and beta 2-antagonism by pindolol, atenolol and propranolol do not markedly potentiate plasma ANP- and VP-responses to physical exercise. The responses are, however, slightly influenced presumably by the beta-agonist activity of pindolol.
We randomized 61 patients with paroxysmal atrial fibrillation (AF) ( < 48 hours from onset) to either sotalol or quinidine treatment. Conversion of rhythm was recorded by Holter monitoring. The starting 80 mg dose of sotalol was repeated at 2, 6, and 10 hours if AF persisted (heart rate > 80 beats/min), and if systolic blood was > or = 120 mm Hg. In the quinidine group, if heart rate > 100 beats/min, it was decreased with intravenous digoxin, whereafter 200 mg of oral quinidine sulfate was given maximally 3 times, each dose 2 hours apart. Conversion of AF to sinus rhythm occurred in 17 or 33 patients (52%) taking sotalol, and in 24 of 28 patients (86%) taking quinidine (p < 0.0001). Electric cardioversion was necessary in 39% of the former and in 14% of the latter group. The mean delay from first trial drug to sinus rhythm with the trial medication was 10.2 +/- 7.6 hours in the sotalol group and 4.0 +/- 2.9 hours in the quinidine group (p < 0.01). Treatment was discontinued in 16 patients taking sotalol (48%) because of asymptomatic bradycardia or hypotension, and in 20 taking quinidine (71%) because of rhythm conversion. Asymptomatic wide complex tachycardia (QRS > 0.12 second) was found in 13% and 27% of patients taking sotalol and quinidine, respectively. The longest RR intervals were 6.4 and 3.8 seconds in the sotalol and quinidine groups, respectively. Oral sotalol did not appear as effective as quinidine sulfate treatment in conversion of paroxysmal AF.(ABSTRACT TRUNCATED AT 250 WORDS)
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There is a lack of systematic nephrographic studies on epidemic nephritis (EN). We studied 10 patients with EN using [99Tcm]MAG3 gamma camera nephrography and followed up 9 of them 22-68 days later when they had clinically recovered. Variables for renal clearance of [99Tcm]MAG3 and the retention of radioactivity in the kidneys and blood were calculated. In all patients renal function was impaired acutely. There was marked reconstitution of renal function in the control studies. [99Tcm]MAG3 clearance was inversely related to serum creatinine. On visual inspection the nephrograms showed no focal changes. Nephrography was more sensitive than sonography at identifying renal impairment. [99Tcm]MAG3 nephrography is a sensitive method for identifying renal involvement and reconstitution of renal function in EN. It may be a valuable adjunct to the diagnostic arsenal, especially in nonendemic areas where EN occurs only sporadically and where there may be diagnostic uncertainty in patients presenting acutely with EN.
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The effects of ethanol on blood rheology were studied in twelve healthy male volunteers each serving as his own control. They drank 1.5 g (33 mmol) of ethanol per kg body weight in fruit juice over 2.5 h under controlled laboratory conditions. Blood and plasma viscosity, packed cell volume and erythrocyte flexibility were measured before and 3, 12 and 16 h after ethanol ingestion began, and again during a second session equal volumes of fruit juice were consumed. Packed cell volume varied similarly after ingestion of juice with or without ethanol. Blood viscosity remained almost unchanged after ethanol, while drinking of juice caused an initial decrease followed by a significant (P less than 0.05) increase from 4.04 (SEM 0.06) to 4.32 (SEM 0.18) mPa.s. The juice also caused more significant fluctuations in erythrocyte rigidity (whole blood) than ethanol, which had parallel but insignificant effects. We conclude that a blood ethanol concentration of 28 mmol l-1 failed to induce any marked changes in blood rheology.
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Plasma viscosity, haemoglobin-oxygen affinity and red cell flexibility were determined in 16 patients who had angina pectoris but no objective evidence for spasms or obstructions in the coronary arteries. Reference data were obtained from healthy controls and from a group of patients with angina pectoris and multivessel coronary artery disease. In the non-coronary angina group mean plasma viscosity (+/- SD) was in the normal range (1.3 leads to 0.06 centipoise). The same was true for haemoglobin-oxygen affinity (P50: 25.9 +/- 1.7 mmHg). Both red cell rigidity (71 +/- 20 mmHg) and red cell fragility (142 +/- 95 mg/l) were significantly higher (p les than 0.0025) than in the control group (54 +/- 10 mmHg and 63 +/- 29 mg/l, respectively). The group with coronary artery obstructions did not differ from the controls. Thus rigid red cells appear to be related to the syndrome of angina pectoris despite normal coronary arteries. In the light of previous findings of local perfusion abnormalities in these patients, inflexible erythrocytes could be an additional factor compromising myocardial capillary flow.
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We present three aged female patients who fulfil the criteria of a syndrome that we call "amiloride hyponatremia". They became hyponatremic during amiloride + hydrochlorothiazide therapy. They needed diuretic therapy and tolerated well hydrochlorothiazide with potassium supplementation as potassium chloride. Patients with hyponatremia during diuretic therapy for cardiovascular diseases can be allocated to three groups: 1) Patients with edema and water retention due to severe impairment of cardiac function and decreased water clearance. They need diuretic therapy and water restriction. 2) Patients with "normal diuretic hyponatremia". Hypokalemia and extracellular volume contraction seem to be associated with this phenomenon, and the therapy involves discontinuing the necessary diuretic treatment. 3) Patients with "amiloride hyponatremia". They need diuretic treatment and tolerated thiazide therapy, but the hyponatremia can be corrected by changing amiloride to potassium supplementation. "Amiloride hyponatremia" is suggested to be due to a direct effect of amiloride + hydrochlorothiazide on the distal nephrons. The combination amiloride + hydrochlorothiazide must be used cautiously in elderly patients and the possibility of hyponatremia should be born in mind cases of vague symptoms and CNS disturbances.
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Three patients ate different amounts of a common northern mushroom, brown fly agaric, Amanita regalis. All of them believed they had eaten delicious parasol mushrooms, Macrolepiota procera. The symptoms of poisoning began 1--2 hours after ingestion of the mushrooms. All the patients had marked gastrointestinal symptoms: nausea and heavy vomiting. Two had central nervous system manifestations and cholinergic symptoms: hallucinations, confusion, or loss of consciousness as well as copious salivation, or sweating. All patients recovered within 4--24 hours without any damage to liver, kidneys or central nervous system. It seems that cooking the mushrooms does not completely neutralize the toxic agents of Amanita regalis. The analysis of fried mushrooms shows that it may be possible to identify mushrooms reliably from the remains of a meal.