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Biomedical subjects

G Fabbri

Publications and source records attributed to G Fabbri.

At least 55 records · Page 3Linked to original sources
PubMed1989

Glucocorticoids but not vasopressin or oxytocin inhibit luteinizing hormone secretion in patients with psychogenic amenorrhea.

Activation of the hypothalamus-pituitary-adrenal (HPA) axis is suggested to play a role in the stress-related inhibition of LH secretion. The aim of our study was to investigate the effects of vasopressin and oxytocin, which are increased in pituitary portal plasma in response to stress, and of glucocorticoids, the final product of HPA activation during stress, on basal plasma LH levels and on pituitary LH response to the GnRH test in amenorrheic (n = 33) and fertile (n = 13) women. Plasma LH levels were evaluated by radioimmunoassay in 2 different experimental conditions: 1. Basal secretion; 2. The GnRH test (10 micrograms + 10 micrograms after a 120-minute interval). These 2 evaluations were done in the presence of both placebo and a pharmacological dose of desmopressin (an analogue of vasopressin) (16.6 ngr/minute), oxytocin (0.2 ngr/minute) or hydrocortisone (4.1 mg/minute). None of these drugs modified basal plasma LH levels either in amenorrheic patients or in controls. Hydrocortisone inhibited the GnRH-induced LH increase in amenorrheic women. These data suggest that the glucocorticoids might play a role in LH secretion and indicate a possible participation of the HPA axis in the impairment of the hypothalamus-pituitary-gonadal axis in women with psychogenic amenorrhea.

Adult↗
PubMed1988

Endogenous dopamine (DA) and DA2 receptors: a mechanism limiting excessive sympathetic-adrenal discharge in humans.

We studied the effects of presynaptic dopamine (DA) 2 receptor blockade on the sympathetic-adrenal response to graded exercise in seven normal men. DA2 receptor blockade was achieved by means of domperidone (DMP) administration. The exercise consisted of progressive cycling activity, from 30-80% of the predetermined maximal oxygen consumption for each man. Systolic, diastolic, and mean arterial pressures; heart rate; and plasma norepinephrine (NE), epinephrine (E), PRL, glucose, lactate, FFA, sodium, potassium, cortisol, and PRA were measured at rest, during exercise, and during recovery after placebo or DMP administration. Graded exercise caused significant increases in systolic and mean arterial pressures and plasma NE, E, lactate, sodium, potassium, FFA, cortisol, and PRA. DMP administration before exercise caused a significant increase in plasma PRL (P = 0.0009), a greater increase in plasma NE at the end of the exercise (P = 0.002), and an overall increase in plasma E (P = 0.02) and FFA (P = 0.02) concentrations. These results strongly suggest that endogenous DA limits catecholamine release during sympathetic-adrenal stimulation by activating DA2 receptors.

Adrenal Glands↗
PubMed1988

Bis-arenoxypropanolamines as potential beta-adrenolytics: a reinvestigation.

A number of symmetrical as well as asymmetrical bis-arenoxypropanolamines have been synthesized and evaluated for their beta-adrenolytic properties. The pharmacological characterization of these compounds was performed in vitro by direct studies (3H-dihydroalprenolol was used as the specific ligand for beta-receptors), and by determining the beta-blocking capacity on isoproterenol (ISO)-induced increased heart rate (isolated guinea-pig atrium); and in vivo by evaluating the antagonism on ISO-induced hypotension and tachycardia, as well as the intrinsic sympathomimetic activity (ISA) on reserpinized and vagotomized rats. The best result was observed with the simplest derivative, i.e. the bis-phenoxypropanolamine compound, which shows in vitro and in vivo potencies almost comparable to propranolol and, moreover, significant bronchodilating activity.

Adrenergic beta-Antagonists↗
PubMed1987

Acute effect of furosemide on renal kallikrein and prostaglandin systems in mild to moderate essential hypertension.

The activity of basal 24-hour urinary kallikrein activity (UKA), prostaglandin E2 (U. PGE2) and thromboxane B2 (U. TxB2) and their relationship to natriuresis (U. Sodium), urinary aldosterone (U. Aldosterone) and plasma renin activity (in supine position: PRA1; in standing position: PRA2) were evaluated in 20 patients with early-moderate hemodynamically defined (first pass and gate blood pool radionuclide angiocardiography) essential hypertension (H) and in 13 age-matched normotensive patients (N). In basal conditions, UKA and PRA2 were significantly reduced (p less than 0.005 and p less than 0.05, respectively) in H compared with N. However, no differences between N and H were found for U. TxB2, U. PGE2, U. Aldosterone, U. Sodium, and PRA1. All parameters were also evaluated both in H and N before and after the administration of furosemide (40 mg i.v.). In H, but not in N, furosemide induced an increase of UKA (p less than 0.05), U. TxB2 (p less than 0.05) and U. Sodium (p less than 0.001). In both H and N furosemide caused a significant rise of PRA1 (p less than 0.001 in H and p less than 0.01 in N) and PRA2 (p less than 0.001 in H and p less than 0.05 in N). In H a significant correlation was found between percent increases of U. Sodium and U. Kallikrein (r = 0.54, p less than 0.01) and between percent differences of PGE2 and TxB2 (r = 0.59, p less than 0.01). It is proposed that reduction of basal UKA may be an early evidence of the first stages of hypertension, i.e., in absence of renal and cardiovascular alteration. The finding is not accompanied by significant changes in urinary excretion of arachidonic acid metabolites and aldosterone. Finally, any relation between UKA values and systemic hemodynamics is lacking.

Aldosterone↗
PubMed1984

Hemodynamics in borderline hypertension: acute effect of furosemide.

In order to identify the hemodynamics of borderline essential hypertension, radionuclide angiography was performed before and after bolus injection of furosemide (40 mg i.v.) both at 3 min (i.e. before diuretic effect) and at 30 min (i.e. after diuretic effect) in 16 borderline (B) patients and in 14 age-matched WHO classification I-II essential hypertensives (H) patients. 14 age-matched normotensive (N) subjects were used as controls. B patients were further subdivided into two subgroups according to a cardiac index under or above 3 liter/min/m2 in basal conditions. Baseline hemodynamic characteristics showed higher values of mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) in both H and B patients when compared with N subjects (p less than 0.001). Furthermore, B and H patients exhibited lower values of left ventricular peak filling rate (PFR) than seen in N subjects (p less than 0.01 and p less than 0.05, respectively). H patients demonstrated higher peak systolic blood pressure/endsystolic volume ratio (PSP/ESV) than seen in N subjects (p less than 0.05). PFR positively correlated with peak emptying rate (PER) only in N and B patients (p less than 0.05). After furosemide administration, even though differences were observed in the absolute values, B and H patients showed similar hemodynamic patterns. Only the B subgroup with cardiac index (CI) greater than 3 liter ('volume-dependent' patients) showed a decrease in left ventricular end-diastolic volume index (LVEDVI) at 30 min associated with a lowering of stroke index (SI; p less than 0.005 for both), when compared with pre-drug values. In B patients with CI less than 3 liter ('afterload-dependent' patients) no differences were observed either at 3 min or at 30 min in comparison with values obtained prior to drug administration. Moreover, in this subgroup, like in H patients, there was a negative correlation (p less than 0.01) between 3-min percent change of SVRI and 3-min percent change of SI. Our data suggest that in 'borderline' hypertension: (a) there may be an increase in peripheral resistance, as in established hypertension, especially when age-matched groups are considered; (b) the earliest sign of compromised left ventricular function is the reduction in diastolic PFR but, unlike established hypertension, this index is still correlated with systolic function; (c) cardiac output might be even somewhat reduced and also negatively correlated with vascular resistance ('afterload-dependent' hearts); (d) furosemide (acute administration) might contribute to a better definition of hemodynamic behavior.

Adult↗