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Biomedical subjects

A Molteni

Publications and source records attributed to A Molteni.

At least 109 records · Page 6Linked to original sources
PubMed1972

Irreversibility of methylandrostenediol-induced hypertension in the rat after suspension of the androgen treatment.

Administration of 10 mg of methylandrostenediol for 10 weeks to uninephrectomized, salt drinking, female Sprague Dawley rats caused severe hypertension with extensive renal and cardiovascular damage. The hypertension was accompanied by increased consumption of sodium, high sodium levels in peripheral plasma, decreased weight of the pituitary, thymus, adrenals and ovaries and decreased content of renal renin. Methylandrostenediol treatment also produced impairment of normal adrenal steroidogenesis, reflected in elevated production in vitro of 11-deoxycorticosterone during incubation of adrenal gland homogenates with (14)C-progesterone. Such increased production of deoxycorticosterone is probably responsible for the development of the hypertensive disease. If the methylandrostenediol-treated animals were kept alive for 12 additional weeks after suspension of the treatment with the androgen, the hypertension, as well as the high sodium consumption, high plasma sodium concentrations and low levels of renal renin, persisted to the end of the experiment. The cardiovascular and renal lesions in these animals, killed 12 weeks after suspension of the androgen administration, were similar to those seen in the rats receiving methylandrostenediol but killed at the tenth week of the treatment. Suspension of methylandrostenediol administration, however, resulted in a return to normal weight of the pituitary, thymus, adrenals and ovaries within 12 weeks. Normal amounts of deoxycorticosterone were formed in vitro by the adrenal glands of these rats and the return to normal structure was also confirmed by a electron microscopic study. Thus, contrary to a previous experiment where methylandrostenediol was given for a shorter period of time and the hypertension was reversible, it was shown in this study that metacorticoid hypertension is induced by methylandrostenediol administration, as it is with treatment with deoxycorticosterone. Since adrenal steroidogenesis returned to normal, some other mechanisms must be involved in maintaining the hypertension. It is very likely that these factors are consequent to the extensive and irreversible renal and cardiovascular damage.

Adrenal Glands↗
PubMed1971

Recovery of adrenal ultrastructure after cessation of androgen treatment.

Female, uninephrectomized rats injected with methylandrostenediol became hypertensive by 4 weeks of treatment. After cessation of treatment, blood pressure continued to rise during the first week but gradually decreased below the borderline of hypertension by 5 weeks. After methylandrostenediol treatment for 4 weeks and after 1 week of recovery, adrenocortical fine structure exhibited a number of abnormalities including reduced numbers of mitochondrial cristae, hypertrophic smooth endoplasmic reticulum, microfilaments and large lipid vacuoles within zona reticularis cells. During an intermediate period of recovery (2 weeks), mitochondrial cristae increased in number, although animals remained hypertensive. After 2 weeks, all of the ultrastructural abnormalities seen at early and intermediate periods of recovery were fully reversed, concomitant with a return of systolic blood pressure to below hypertensive levels.

Adrenal Glands↗
PubMedDate not supplied

Plasma copper and iron changes in sheep after left lung inhalation injury: effect of the thromboxane antagonist BM 13.177 (Solutroban).

A significant decline in plasma concentrations of copper and iron were observed in sheep exposed to preferential smoke inhalation of the left lung. The decline was evident 30 minutes after smoke inhalation, and the levels of both trace metals persisted at quite low levels for up to the 18-hour time interval after injury. From that time a gradual recover for copper but not for iron levels was observed so that by 24 hours the levels of copper were in the same range of those at baseline. Copper and iron levels showed an inverse correlation to airway peak and plateau pressures and left lung vascular resistance index and a direct correlation to left lung blood flow. Administration of BM 13.177 (Solutroban), a thromboxane antagonist, before exposure to smoke inhalation protected the sheep from the decline of copper and iron levels in plasma. In these animals airway peak and plateau pressure, left lung vascular resistance, and blood flow were also unmodified. Lipid peroxidation of the lung tissue by oxygen free radicals were lower than in those animals that did not receive BM 13.177. There was likewise a tendency of a decreased wet-to-dry weight ratios in the animals treated with BM 13.177. BM 13.177 treatment in an inhalation injury model might partly protect lung damage and parallels unchanged plasma copper and iron levels. The plasma copper and iron may therefore be an indicator of acute lung damage.

Analysis of Variance↗
PubMedDate not supplied

Angiotensin-1-converting enzyme activity as index of pulmonary damage in thermal injury with or without smoke inhalation.

Serum angiotensin-converting enzyme (ACE) activity, plasma renin activity (PRA), and serum aldosterone levels were measured up to four weeks in a population of adults exposed to thermal injury, with or without concomitant exposure to smoke inhalation. In 10 patients, plasma levels of angiotensin-2 and ACE activity in bronchial lavage were also evaluated. Patients with severe burn injury had a significant decline of serum ACE activity while the concentrations of aldosterone and PRA were markedly elevated. Smoke inhalation seemed to counterbalance the decline of serum ACE activity, and, in the last group of patients, ACE concentrations were higher than those recorded in patients suffering only from cutaneous burn. The ACE activity was evidenced in bronchial lavage of patients exposed to smoke inhalation with the highest values present in the first day after the injury. The same patients had also very elevated levels of plasma angiotensin 2. In conclusion, serum ACE activity decreases in burn patients according to the severity of the cutaneous burn; smoke inhalation influences serum levels of the enzyme with concentration values opposite to the low ones present in cutaneous burn. Finally, the enzyme activity has an independent pattern from that of the other components of the renin angiotensin aldosterone system. The evaluation of ACE activity may be a marker of pulmonary damage in smoke inhalation.

Adolescent↗