Non-convulsive status epilepticus.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Galletti.
Explore the source record for details and available documents.
A statistical association between hypertension and hyperparathyroidism has been repeatedly reported, but the underlying pathogenetic mechanism has not been elucidated. A 51-year-old woman was hospitalized because of increasing motor disability caused by multiple bone and muscle aches with generalized weakness. She was found to have marked hypercalcemia and hypophosphatemia, increased parathyroid hormone secretion, but normal renal function and blood pressure level. After the identification and removal of a single parathyroid adenoma, the calcium/phosphate metabolism normalized in a relatively short time during which, however, hypertension developed in the absence of any other endocrine or renal dysfunction. A positive, highly significant relationship was observed between the progressive rise in blood pressure and the gradual increase in serum phosphate concentration occurring after the operation, suggesting that, in the hyperparathyroid phase, an underlying trend to hypertension could have been masked by the phosphate depletion, probably through its effects on cardiac and vascular smooth muscle function.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Previous short-term studies of muzolimine (a diuretic with frusemide-like activity) had shown that it did not induce a significant change in the serum potassium concentration. In the present study sodium and potassium handling and other metabolic variables have been compared during 16 weeks of therapy with muzolimine and chlorthalidone, a thiazide-like diuretic. During muzolimine treatment, plasma and red cell potassium concentrations remained unchanged, while a significant fall in potassium occurred with chlorthalidone. Neither drug affected the activity of sodium-potassium cotransport or sodium-lithium countertransport in red cells in vitro. Muzolimine and chlorthalidone had similar effects on arterial pressure and on the other metabolic variables tested.
The antibacterial activity of enoxacin was determined against 1015 strains of Gram-positive and Gram-negative bacteria, mainly freshly isolated from clinical specimens. The minimum inhibitory concentrations (MIC 50-75-90) were determined in comparison to three commonly used antibiotics: ampicillin, cefotaxime and gentamicin. Enoxacin has shown a broad spectrum of action and antibacterial activity in general higher that than of three currently available antibiotics. The antibacterial activity seems similar to that of other quinolones of second generation.
Explore the source record for details and available documents.
A number of abnormalities in the extracellular and intracellular handling of calcium in arterial hypertension, namely an increased urinary calcium excretion, a reduced serum ionized calcium level and an enhanced intracellular free calcium concentration, have previously been reported by this and other laboratories. The present study aimed to investigate the handling of an exogenous calcium load in hypertensive and normotensive subjects in order to detect possible differences with regard to tissue calcium metabolism in vivo. A constant rate intravenous calcium infusion (0.2 mmol 2 h-1 kg-1 body wt.) was carried out in the participants. Serum calcium concentrations were determined at regular intervals during the infusion and in the 4 h after the end of the calcium load. Over the same period, urinary calcium excretion was evaluated in timed urine collections. Hypertensive subjects had lower serum ionized calcium levels compared with normotensive subjects at all the experimental points, a finding suggestive of a faster disappearance of calcium from the circulation. The total body calcium clearance, calculated from the area under the curve of the serum calcium concentrations, was enhanced in hypertensive patients (P less than 0.03). Although the renal calcium excretion was higher in hypertension, the renal calcium clearance accounted for only a minor fraction of the total body clearance, suggesting that the reduced serum calcium levels achieved by the hypertensive patients were not explained by the renal calcium leak. The enhanced total body calcium clearance found in hypertensive subjects is therefore due to an increased tissue calcium uptake. This finding provides indirect evidence of an altered cell calcium handling in hypertension.
Urinary calcium (Ca) excretion and erythrocyte membrane Ca binding and transport were investigated in rats of the Milan hypertensive (MHS) and normotensive strains (MNS). Despite slightly reduced ionized Ca levels in the serum, MHS significantly increased urinary Ca excretion under fasting conditions (P less than 0.01). Urinary Ca was positively related to sodium (Na) excretion in both rat strains; moreover the urinary Ca:Na ratio was significantly enhanced in MHS rats (P less than 0.05). These data suggest that in MHS, Ca reabsorption in the renal tubular cell is reduced independently of disturbances in Na handling. Adenosine triphosphate (ATP)-dependent Ca transport, reflecting the Ca, magnesium (Mg)-ATPase activity (Ca pump), was measured in inside-out vesicles obtained from erythrocyte membranes. This variable was significantly reduced in MHS (P less than 0.01), with no change in the Ca pump affinity constant for Ca. Calcium binding to erythrocyte membranes, measured in the presence of free Ca concentrations comparable with those of the intracellular fluid, was found to be significantly reduced (P less than 0.01) in MHS rats because of the lower number of Ca binding sites. These abnormalities of red blood cell (RBC) Ca handling are in keeping with the increased Ca clearance observed in the kidney. It is not clear whether the disturbances of renal and erythrocyte Ca handling were a genetic primary defect or a secondary change of membrane function.
A randomized, double-blind, placebo-controlled crossover trial of oral calcium supplementation was carried out in 18 patients with uncomplicated essential hypertension. After 15 weeks of oral calcium supplementation, 1 g/day, of the patients' habitual diet, the only blood pressure change (compared with the results of placebo treatment) was in the average standing systolic blood pressure, which was significantly reduced (-8.6 mm Hg; p less than 0.01). The 24-hour urinary calcium excretion and the total serum calcium concentration increased significantly during calcium supplementation (p less than 0.05), indicating good compliance with the treatment. The individual blood pressure changes with high calcium intake were found to be inversely related to basal 24-hour urinary calcium excretion (r = -0.69, p less than 0.001 for standing systolic pressure; r = -0.55, p less than 0.002 for standing diastolic pressure). This correlation was independent of age, basal blood pressure, serum calcium concentration, basal 24-hour urinary sodium excretion, and body weight changes during the trial. In particular, a subgroup of six patients, who had a basal 24-hour urinary calcium excretion higher than the mean + 2 SD of a reference healthy population previously described, showed a substantial average blood pressure fall at variance with the other patients in the study. These results do not support the usefulness of an oral calcium supplement in the majority of subjects with mild essential hypertension; however, they suggest that a group of patients with a previously reported abnormality of calcium metabolism may be responsive to this therapeutic measure.
The bioavailability and pharmacokinetics of acetylsalicylic acid were studied in 6 volunteers, under a cross-over design, using plain compressed aspirin, two buffered preparations and an enteric-coated tablet. Absorption, calculated from urinary excretion, was complete for all the formulations. The buffered forms gave higher peak concentrations and AUC for acetylsalicylic acid than the other forms. Absorption from the enteric-coated tablet was the slowest. Acetylsalicylic acid was not measurable in plasma (less than 0.1 micrograms/ml) at any time in 3 subjects after plain and in 2 after enteric-coated aspirin. Acetylsalicylic acid was no longer measurable in plasma after 4 hours, irrespective of the preparation given.
Explore the source record for details and available documents.
Six healthy male volunteers received aspirin (ASA) in a compressed (320 mg) and an enteric-coated (800 mg) formulation as single oral doses ten days apart. Ten plasma samples were obtained from each volunteer between 5 and 120 min after compressed ASA, and seven between 10 and 240 min after enteric-coated ASA. ASA was undetectable (less than 100 ng/ml) in plasma from three subjects receiving compressed ASA and two receiving the enteric-coated preparation. Plasma levels and kinetic parameters of salicylate were the same in subjects with undetectable and detectable ASA plasma levels. More than 98% inhibition of pre-drug serum TXB2 was noted in all samples collected one and four hours after either ASA preparation. TXB2 generation recovered on average by 3.5% at 24 hr with both preparations. Thus inhibition of platelet TXB2 generation occurred independently of the amount of ASA reaching the peripheral circulation. If this is due to inhibition of platelet function in the enterohepatic circulation followed by extensive first-pass deacetylation of ASA, vascular PGI2 synthesis could be spared. A better knowledge of the kinetic parameters of ASA for each of the formulations used in thrombosis prevention trials might help in solving the "aspirin dilemma".
Altered regulation of serum calcium level was proposed to be associated with arterial hypertension and to be dependent on a renal calcium leak or an altered calcium binding to plasma proteins and cell membrane described in human and experimental hypertension. The aim of this study was to analyze the regulation of serum total and ionized calcium levels during an intravenous calcium infusion (0.25 mmol calcium/kg body weight/hr for 2 hours) in a group of untreated essential hypertensives and a comparable normotensive group. Basal serum calcium concentrations did not differ between the two groups, whereas parathyroid activity and urinary calcium were significantly increased in hypertensive subjects. During the calcium load, serum calcium rose almost linearly in all subjects but with a reduced slope in the hypertensive group, which showed serum total and ionized calcium levels significantly lower than those of the controls at the end of the infusion. Our data indicate that hypertensive patients have an altered regulation of serum calcium concentrations, probably due to a different body distribution of calcium, rather than to an altered calcium binding to plasma proteins.
Explore the source record for details and available documents.
On the basis of general pharmacological information (blood cells/plasma partition, plasma protein binding) and using HPLC as the principal analytical method, we investigated the kinetics and metabolism of theobromine (a caffeine metabolite) in male rats after a single dose and after a 2 week chronic application. Doses in both conditions varied between 1 and 100 mg/kg. In in vitro and in vivo the fraction of theobromine unbound to plasma proteins averaged 0.90 over a wide range of concentrations. No significant difference was found in the pharmacokinetic profile of the drug after acute or chronic treatment at different doses except for a reduction in the absorption rate constant as the dose increased. AUC values increased in proportion to the dose. The 2 treatment schedules were also similar as regards metabolism, at least 50% of the administered dose of theobromine being excreted unchanged, and 25% as 6-amino-5-[N-methyl- formylamino ]1-methyluracil. Only at the highest doses was there a tendency for theobromine to accumulate at the expense of its major metabolite (a uracil compound).
Explore the source record for details and available documents.
Data are reported on the analytical and physicochemical characteristics of amiodarone, for use in identifying and/or assaying this antiarrhythmic agent. The drug is highly soluble in chloroform and poorly soluble in water. Its acid-base constant (pKa) is 6.56, and its maximal lipid solubility range is from pH 3.5 to 5.5.