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M Prosdocimi

Publications and source records attributed to M Prosdocimi.

86 records · Page 5Linked to original sources
PubMed1977

Multiple symmetric lipomatosis: a defect in adrenergic-stimulated lipolysis.

The cellularity of normal and lipomatous adipose tissue and its response to different lipolytic agents have been studied in a group of 10 patients with multiple symmetric lipomatosis (MSL). In MSL patients, fat cells from lipomatous tissue are smaller than normal, uninvolved adipocytes. Fat cells from lipomata show minimal variations in size following conspicuous increase of lipomatous masses. These findings suggest that the growth of lipomata can be attributed to the neoformation of adipocytes rather than to an enlargement in the single fat cells. The incidence of reduced glucose tolerance and of hyperlipoproteinemia is similar in MSL patients and in controls. A significant reduction in plasma free fatty acids was observed in MSL patients after a 24-h fast as well as after noradrenaline infusion. A specific insensitivity of lipomatous tissue to the lipolytic effect of noradrenaline and isoprenaline was observed in vitro, as indicated by glycerol release in the medium, whereas response to theophylline and to dibutyryl cyclic AMP was retained. The lipolytic response to catecholamines was retained. The lipolytic response to catecholamines was normal in the nonlipomatous adipose tissue of MSL patients. In basal conditions ATP concentrations were similar in normal and in lipomatous adipose tissue. However, incubation with noradrenaline induced a significant fall in intracellular ATP levels in normal tissue, whereas no variations were observed in lipomatous tissue. Theophylline, instead, induced a prompt and significant decrease in intracellular ATP levels in lipomatous tissue. These observations indicate that the block in catecholamine-stimulated lipolysis in lipomatous tissue of MSL patients can be localized at a level preceding the formation of cyclic AMP.

Adenosine Triphosphate↗
PubMedDate not supplied

Atrial bioenergetic variations in moderate hypoxia: danger or protective defense?

The effects of hypoxia on contractile tension and on tissue adenylate pool content, nicotinamide adenine nucleotide, NAD, nicotinamide adenine dinucleotide phosphate, NADP, and creatine phosphate, CrP, were investigated in isolated, spontaneously beating, guinea pig atria. When two different degrees of hypoxia were induced by lowering oxygen tension from 95% O2 (control) to 40% (moderate hypoxia) and 20% (severe hypoxia) for 30 min, contractile tension slowly decreased to 60% and 40% of control, respectively. In 40% O2 hypoxic atria, ATP was not significantly decreased, AMP slightly increased, TAN (total adenylate nucleotides) and adenylate energy charge [(ATP + 0.5 ADP)/(ATP + ADP + AMP)] did not change and creatine phosphate was decreased down to 53%. Hypoxic atria in 20% O2 showed a significant decrease of 26% in ATP, while ADP and AMP increased four and seven times, respectively. The adenylate energy-charge value was reduced from 0.93 to 0.70. Creatine phosphate decreased to below the analytical detection limit. Moderate hypoxia (40% O2), which induced a significant decrease of contractile tension but only minor changes of energetic tissue metabolism, was further investigated 2, 5, and 10 min after low oxygen tension was applied. Two stages of variations were evident during 30 min of experimental hypoxia. Within the first 10 min, concomitantly with atrial tension decrease, ATP, NAD, NADP, ATP/AMP, ATP/ADP, and TAN decreased, CrP began to decrease, inosine and xanthine showed no significant change. During the following 20 min of hypoxia, all parameters returned to the control levels with the exception of creatine phosphate. Adenylate energy charge did not change. The electrophysiological analysis of atrial cells did not show any major change in action potential configuration and resting potential, during 40% O2 hypoxia. The differences at metabolic level between moderate and more severe hypoxia suggest that the energetic state may be extremely unbalanced, in atrial tissue, as long as hypoxia is aggravated. Moreover, the time-course study, during 30 min of 40% O2, suggests that the early decrease of contractile tension does not depend on lowered energy availability, instead it might be, at least in part, a preventive measure to maintain energy balance in myocardial tissue to counteract hypoxic damage and, in this mechanism of defense, creatine phosphate shuttle seems to play a relevant role.

Action Potentials↗
PubMedDate not supplied

Effects of long-term diabetes and treatment with gangliosides on cardiac sympathetic innervation: a biochemical and functional study in mice.

The effect of long-term diabetes on cardiac sympathetic innervation was investigated in genetically obese diabetic mice (db/db). Previous studies have shown the presence of a peripheral neuropathy starting a few months after birth, and we recently reported a significant reduction of myocardial norepinephrine (NE) levels in the hearts of diabetic mice at the age of 6 months. In the present study, histofluorescence analysis of comparable sections of cardiac tissue of both control and diabetic animals confirmed the picture of a sympathetic denervated heart in this experimental model. Furthermore, functional studies in isolated atria revealed a difference between the two groups of animals: in fact heart rate increases induced by transmural stimulation were significantly lower in diabetic mice. Since a bovine brain ganglioside mixture (Cronassial) has been extensively studied for its effect on peripheral diabetic neuropathy, a group of diabetic mice was treated throughout the sixth month with this drug (10 mg/kg/day i.p.). The ganglioside treated animals showed a marked recovery of atrial function and cardiac NE concentration. The above results clearly indicate sympathetic neural damage in db/db animals, likely related to an autonomic diabetic neuropathy and a possible protection by ganglioside of adrenergic nerves from this alteration.

Animals↗
PubMedDate not supplied

Endothelium as a therapeutical target in peripheral occlusive arterial diseases: consideration for pharmacological interventions.

The aim of this review is to consider the role of endothelium in the establishment of injury induced by ischaemia and reperfusion with particular emphasis on the vascular beds of the legs. We review the main abnormalities found in the macro- and microcirculation in these conditions and discuss the various theories put forward to explain the mechanism by which endothelial injury is induced. Endothelial cells play a key role in maintaining patent and functional capillaries. When blood vessels are damaged they become unresponsive to vasodilatory stimuli and intraluminal thrombosis may occur. The relative contribution of platelets and leukocytes in the formation of final ischaemic damage is widely discussed. Furthermore, the role of reperfusion in causing damage to post-ischaemic vascular beds is considered as well. The degree to which post-ischaemic injury is reversible might define the opportunity for therapeutic interventions.

Animals↗
PubMedDate not supplied

Urine retention due to intra-spinal cord injection of colchicine in rats: improved recovery of bladder function by monosialoganglioside GM1 and nerve growth factor administration.

Intra-spinal cord injection of a low dose of colchicine (2 micrograms/rat) at the lumbar level affects the micturition reflex leading to voiding suppression, bladder hypertrophy and overflow incontinence which lasts about four weeks. The administration of nerve growth factor and monosialoganglioside GM1 normalizes urine output within 3 days and improves recovery of the bladder contraction tested by a cystometric analysis.

Animals↗
PubMedDate not supplied

Diabetic autonomic neuropathy and bladder function: pharmacological use of gangliosides and insulin.

This paper briefly describes experimental evidence indicating that bladder dysfunction observed in diabetic rats is due in part to hyperdiuresis and in part to autonomic nerves alterations. The latter, in analogy with somatic nerves alteration, can be ameliorated by treatment of diabetic animals with gangliosides. The use of this agent in the autonomic nerve dysfunction of diabetic origin is discussed.

Animals↗
PubMedDate not supplied

Alterations of the vegetative nervous system, experimental diabetes and pharmacological use of gangliosides.

We studied in diabetic animals several variables related to the vegetative innervation of the heart and the urinary bladder. Cardiac content of norepinephrine was lower in the heart of the diabetic mice (db/db) as compared to the heart of their heterozygote littermates (db/m). Bladder responses were clearly altered in alloxan treated rats as compared to normal rats, as shown by an increased vesical weight, an increased threshold for micturition reflex and a reduced rate of rhythmic contraction. Ganglioside administration was able to prevent partly or completely these alterations observed in the diabetic animals.

Alloxan↗