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Biomedical subjects

M Bardelli

Publications and source records attributed to M Bardelli.

50 records · Page 3Linked to original sources
PubMed1978

Experimental progressive muscular dystrophy and its treatment with high doses anabolizing agents.

We are still a long way from discovering an unequivocal pathogenetic interpretation of progressive muscular dystrophy in man. Noteworthy efforts have been made in the experimental field; a recessive autosomic form found in the mouse seems to bear the closest resemblance to the human form from the genetic point of view. Myopathy due to lack of vitamin E and myopathy induced by certain viruses have much in common anatomically and pathologically with the human form. The authors induced myodystrophy in the rat by giving it a diet lacking in vitamin E. The pharmacological characteristics of vitamin E and the degenerative changes brought about by its deficiency, especially in the muscles, are illustrated. It is thus confirmed that the histological characteristics of myopathic rat muscle induced experimentally are extraordinarily similar to those of human myopathy as confirmed during biopsies performed at the Orthopaedic Traumatological Centre, Florence. The encouraging results obtained in various authoratative departments in myopathic patients by using anabolizing steroids have encouraged the authors to investigate the beneficial effects of one anabolizing agent (Dianabol, CIBA) at high doses in rats rendered myopathic by a diet deficient in vitamin E. In this way they obtained appreciable changes in body weight (increased from 50 to 70 g after forty days at a dose of 5 mg per day of anabolizing agent), but most of all they found histological changes due to "regenerative" changes in the muscle tissue, which however maintained its myopathic characteristics in the control animals that were not treated with the anabolizing agent. The authors conclude by affirming the undoubted efficacy of the anabolizing steroids in experimental myopathic disease, but they have reservations as to the transfer of the results into the human field, where high dosage cannot be carried out continuously because of the effects of the drug on virility; because the tissue injury too often occurs at an irreversible stage vis-a-vis the "regeneration" of the muscle tissue; and finally because the dystrophic injurious agent is certainly not the lack of vitamin E but something as yet unknown.

Anabolic Agents↗
PubMedDate not supplied

Effects of central alpha 2-adrenergic agonists on systemic haemodynamics and on baroreceptor reflex sensitivity in spontaneously hypertensive rats.

Clonidine, an imidazoline derivative, is a widely used antihypertensive agent which acts by stimulating the alpha 2-adrenergic receptors at the central nervous system. Clonidine also seems to exert beneficial effects on baroreceptor reflex sensitivity which is usually altered by arterial systemic hypertension and arteriosclerosis. Aim of the study was to compare acute and chronic hypotensive response and the effects on baroreflex sensitivity of a newly synthesized central alpha 2-adrenergic agonist, guanfacine, with those induced by clonidine. The effects of acute and chronic treatment were studied by evaluating blood pressure modifications through intraarterial or sphygmomanometric detection. Baroreflex sensitivity was studied before and after acute treatment with the two drugs. Our results show that guanfacine and clonidine may induce comparable effects, both reducing arterial blood pressure levels and heart rate with an order of potency for guanfacine 10 times lower than clonidine. After chronic treatment the effect of guanfacine on blood pressure was more pronounced than that observed after clonidine administration. Both drugs may enhance baroreflex sensitivity, with a more evident effect of guanfacine than clonidine in response to a sudden decrease of blood pressure. This suggests that guanfacine could afford a more effective cardiovascular adaptation during acute hypotension (i.e. during orthostatic hypotension), particularly in the elderly hypertensive patients.

Adrenergic alpha-2 Receptor Agonists↗