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Biomedical subjects

A Borghetti

Publications and source records attributed to A Borghetti.

At least 91 records · Page 5Linked to original sources
PubMed1986

Effect of age on the pharmacokinetics of indobufen.

Eighteen patients of both sexes, aging between 54 and 81 years entered a study on the effects of age on the disposition kinetics of indobufen, a potent inhibitor of platelet aggregation. Plasma levels and urinary excretion of the drug were assayed by HPLC after a single oral dose (200 mg) and after the last dose of a repeated oral schedule (200 mg b.i.d. for 5 days). At steady-state, indobufen plasma levels were about double those after the single dose; plasma level profiles were similar. No significant differences were detected between single dose and steady-state as regards pharmacokinetic parameters of the drug which, at steady-state, were (mean +/- SD, n = 16): Cmax = 32.6 +/- 9.3 micrograms/ml, t 1/2 beta = 12.8 +/- 4.4 h, Pl.Cl. = 14.9 +/- 6.1 ml/min, Vd beta = 223 +/- 63 ml/kg. Evidence of reduced efficiency and rate of indobufen elimination was found in elderly patients compared to young healthy subjects. This is probably because of the age-related decrease in renal function. In the patients of the present study, average Cr.Cl. was about 60 ml/min, corresponding to 50-60% of the normal values in young subjects. A statistically significant correlation was found in patients between drug plasma clearance and Cr.Cl. in agreement with the findings of a previous study on the effects of renal insufficiency on indobufen kinetics. The same dose reduction of indobufen as previously suggested for patients with mild to moderate renal insufficiency should, therefore, be adopted in elderly patients.

Administration, Oral↗
PubMed1985

Low-pressure receptor activity and exaggerated natriuresis in essential hypertension.

Urinary sodium excretion, central hemodynamics, and mean arterial pressure (MAP) were studied in 7 normal subjects and 19 hypertensive patients during both central hypervolemia by water immersion to the neck (NI) and extracellular volume expansion by i.v. saline infusion. During 2-hour NI, 12 out of the 19 hypertensives exhibited a significant fall in MAP (p less than 0.001). Exaggerated natriuresis did not occur in these patients (ns). In the remaining 7 hypertensive patients in whom, during NI, MAP was unchanged, exaggerated natriuresis was found (p less than 0.001). During saline infusion, MAP was either unchanged or increased and exaggerated natriuresis was found in all hypertensive patients (p less than 0.001) previously submitted to NI. Our findings suggest that a high MAP is a major determinant of exaggerated natriuresis in arterial hypertension.

Adolescent↗
PubMed1985

Why is [Ca2+]i increased in blood cells in primary hypertension?

In order to explore a previously observed association between raised blood cell cytosolic calcium [Ca2+]i and primary hypertension, resting levels of [Ca2+]i in the Milan hypertensive rat strain (MHS) were measured. The [Ca2+]i was increased significantly at 7 weeks in MHS (116 +/- 8 versus 93 +/- 6 mumol/l, P < 0.005, n = 7) and non-significantly at 5 weeks (109 +/- 7 versus 85 +/- 9 mumol/l, n = 5). In Okamoto-Aoki spontaneous hypertensive rats (SHR), calcium fluxes were measured with Quin 2 in platelets and lymphocytes. Calcium influx was measured during calcium-pump inhibition either with vanadate or ATP-depletion. Influx was increased in vanadate-treated (but not in ATP-depleted) cells of SHR. This suggests an ATP dependence of calcium influx in blood cells which is more pronounced in SHR. Calcium efflux was determined when the influx was stopped by external EGTA. Calcium efflux was [Ca2+]i-dependent and was moderately increased in SHR. The faster efflux in SHR was due to higher [Ca2+]i. The [Ca2+]i-dependency of calcium efflux was comparable in SHR and Wistar-Kyoto (WKY) rats. These results suggest that a slight but significant rise of cytosolic calcium occurs in blood cells in primary hypertension. In Okamoto-Aoki SHR this rise was due to a higher calcium entry rate.

Aminoquinolines↗
PubMed1985

Intracellular bicarbonate and pH of skeletal muscle in chronic renal failure.

In 11 controls and 10 patients suffering from untreated uraemic acidosis intracellular bicarbonate and skeletal muscle pH (needle biopsy) were determined. In all patients a significant intracellular acidosis, not related to any extracellular indices was found. It is concluded that the chronic proton load is able to effect intracellular buffer composition; moreover the action of other factors such as derangements of cell metabolism and nutritional imbalance could be operating.

Acidosis↗
PubMed1984

Ouabain-resistant, frusemide-sensitive sodium efflux in human lymphocytes: a comparison of normotensive and hypertensive subjects.

Peripheral blood lymphocytes were isolated at room temperature in a low sodium medium in 17 normotensive control subjects (NC) and 13 patients with essential hypertension (EHP). Lymphocyte sodium content was not significantly different between NC and EHP (3.1 +/- 0.5, n = 11, and 3.6 +/- 0.5, n = 10, respectively; means +/- SEM). The effect of frusemide on the ouabain-resistant rate constant of sodium efflux (KNao) from these lymphocytes into a sodium-free medium was measured. The frusemide-sensitive efflux rate constant was 75 +/- mus (n = 17) in controls and significantly lower in EHP (32 +/- 7 mus, n = 13, P less than 0.001). In human lymphocytes there is a ouabain-resistant, frusemide-sensitive fraction of sodium efflux into a sodium-free medium; this fraction may be reasonably attributed to a sodium-potassium cotransport system. This sodium transport pathway seems to be reduced in lymphocytes from EHP.

Adult↗
PubMed1984

Effects of 'central hypervolemia' by Water immersion on renin-aldosterone system and ACTH-cortisol axis in hemodialyzed patients.

Water immersion up to the neck (WI) results in a central hypervolemia; the increased atrial pressure, evoked by this maneuver, stimulates low pressure receptors (LPR) which exert tonic inhibition on sympathetic activity and suppresses both the renin (PRA)-aldosterone (PA) system and the ACTH-cortisol axis in normal man. In hemodialyzed patients (HP), in whom autonomic neuropathy has been frequently found, PRA and ACTH were not suppressed during WI while plasma cortisol and PA were reduced. Other modulators, like dopamine, are supposed to be involved in regulating cortisol and PA levels in HP.

Adrenocorticotropic Hormone↗
PubMed1984

Erythrocyte sodium transport in acute hypophosphatemia in man.

In 21 patients with acute hypophosphatemia (AHPP), we measured red cell intracellular Na concentration (Nai) and either total (T), ouabain-sensitive (OS) or ouabain-resistant (OR) efflux rate constant of Na (0K Na) in a 'physiological' Na medium. High Nai, normal 0K Na T, reduced 0K Na OS and normal 0K Na OR were found. Total OS and OR unidirectional Na effluxes were increased, normal and increased, respectively. The findings suggest that high Nai in AHPP is due to an impairment of active (OS) red cell Na transport; the increase of total Na efflux is only supported by the OR Na efflux, which, under physiological conditions, is mediated mostly by the 1 Na:1 Na exchange diffusion.

Acute Disease↗
PubMed1984

Skeletal muscle cell abnormalities in acute hypophosphatemia during total parenteral nutrition.

Muscle tissue H2O, Na, K, Mg, Cl and total P were studied in 23 patients with acute hypophosphatemia during P-deficient total parenteral nutrition. Increased muscle extracellular water and low intracellular K and Mg with high intracellular Na were found. These abnormalities were detected either in previously underfed patients with low muscle P or in well-nourished, acutely ill subjects with muscle P near to normal. These findings show that acute depletion of extracellular inorganic P is associated with changes of muscle cell composition independently of muscle cell P content.

Acute Disease↗
PubMed1983

Extracellular water, electrolyte and nitrogen balance after postoperative parenteral nutrition and intracellular involvement in muscle.

Brief periods of fasting or moderate trauma were previously shown to give rise to malnutrition characterized by negative nitrogen balance, reduction of lean body mass and relative increase of body water. The present study aimed to assess the possibility that brief low-calorie, low-protein parenteral fluid regimen after relatively moderate surgical trauma can modify the muscle metabolism and alter the water, electrolyte and protein composition. Well-nourished patients undergoing elective cholecystectomy were studied. During the first four postoperative days, seven patients (group I) received parenteral nutrition adequate as regards water, sodium and potassium but deficient in carbohydrates and without amino acids, while six patients (group II) had adequate parenteral supply of calories and nitrogen. The extracellular balance in regard to water, sodium, potassium, calcium, phosphorus, magnesium and urea was assessed in all 13 patients. Needle biopsy of muscle was performed during surgery and at the end of the observation period in six patients from group I and five from group II, in order to assess the total and the intracellular and extracellular water content and also sodium, chloride, potassium, magnesium, phosphorus and alkali-soluble protein nitrogen. In group I, but not in group II, there was weight loss and negative extracellular balance of all parameters, in particular potassium and nitrogen, and reduction of muscle potassium. The analyses of balance and of muscle cell composition showed considerable loss of lean body mass and indicated 'true' electrolyte disturbance, although clinical symptoms were absent and serum parameters remained normal.

Adult↗