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Biomedical subjects

A Lanari

Publications and source records attributed to A Lanari.

At least 19 recordsLinked to original sources

[Propafenone and verapamil poisoning. Report of 2 clinical cases].

We described the self-poisoning of two young adolescents who took improper doses of two major cardiovascular drugs: propafenone and verapamil. The young girls developed markedly different clinical patterns: ECG abnormalities without clinical consequences were found in one case progressively ingravescent ECG abnormalities leading to cardiac arrest in the other. These differences are probably due to varying doses taken and metabolic states. Conventional detoxication and resuscitation techniques proved successful in both cases.

Adolescent

Local renin-angiotensin system in human adrenals and aldosteronomas.

The local renin-angiotensin system may regulate adrenal cell growth and function. Angiotensinogen, renin, and angiotensin converting enzyme gene expression were studied in four normal adrenal glands (removed from patients with renal carcinomas) and five aldosterone-secreting adenomas. Northern blot analysis showed expression of angiotensinogen messenger RNA (mRNA) in normal adrenals at levels approximately 35-fold lower than liver and sixfold lower than kidney. Similar angiotensinogen mRNA levels were present in two aldosteronomas, whereas a third had levels approximately 50% of those found in kidney. Renin mRNA was detectable in most normal adrenals and in three adenomas, one of which had relatively high renin mRNA levels. Angiotensin converting enzyme gene was expressed in adrenal tissue and in three adenomas. Portions from these normal adrenals and two of these aldosteronomas, as well as samples from two other adrenals and three aldosteronomas, were also studied in an in vitro superfusion system coupled with active renin radioimmunometric assay, angiotensin II/III, and aldosterone radioimmunoassay. Total amounts of active renin and angiotensin II/III released from normal adrenals during 270 minutes of superfusion were higher than the amounts released from aldosteronomas (312 +/- 35 versus 187 +/- 43 and 823 +/- 100 versus 436 +/- 55 pg/100 mg tissue, respectively; mean +/- SEM, p less than 0.05), whereas aldosterone release from the adenomatous tissue was approximately threefold higher (320 +/- 21 versus 115 +/- 18 ng/100 mg tissue; mean +/- SEM, p less than 0.01). Total amounts of active renin and angiotensin II/III released by normal or adenomatous adrenal samples exceeded threefold to fourfold the amounts extracted from similar samples of the same surgical specimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Neoplasms

[Hepatic fibrosis and progesterone].

To study the progesterone (Prog.) action on the hepatic fibrosis, we produced fibrosis on 55 New Zealand male rabbits, by oral ingestion of carbon tetrachloride (Cl4C) and ethanol. They developed it in six months. All the animals received the toxic. A group of these animals also received the Prog since the onset (0.66 mg/3 times a week, IM) and the rest received it 180 days after the beginning of the experiment. We could see in the biopsies of the animals who received Prog since the beginning or after 180 days: protection of the hepatocytes, no vacuolization of the cell, no inflammatory infiltrate, no fat metamorphosis, very thin fibrous hands. If one of these alterations had appeared with the toxic, the Prog action would have diminished it gradually until its disappearance. Between the groups who received only toxic and the groups that received th Prog (at the beginning or deferred), the laboratory results showed a high significative difference (p less than o.01) especially in the transferases (ASAT-ALAT) in the 60-180 days period. The Prog in the fibroblasts culture and in the treatment of desmoid tumours, on operative adhesions, destroy the fibroblasts and for this action diminished the volume of the tumour and the adhesions. Perhaps the incomplete resolution of the cirrhosis (though the hands of fibrosis diminished considerably) could be explained by the activity of another kind of fibroblast (the myofibroblast), which provokes the retraction of cirrhotic hepatic tissue.

Alanine Transaminase

Growth inhibition of fibroblasts by progesterone and medroxyprogesterone in vitro.

This study was carried out to evaluate in vitro the beneficial effects observed in various aggressive fibromatoses (mediastinal, retroperitoneal, paraneoplastic fibrosis and desmoid tumors) after treatment with progesterone. Primary cultures of fibroblasts were prepared from fetuses of Swiss strain mice. Continuous fibroblast lines LM and Vero were also used. Moreover, cultures of non-fetal human fibroblast from skin and lung were employed. Epithelial tumor cell line HeLa was used as a control. All cultures were incubated with various doses of progesterone at concentrations from 1.4 X 10(-4) to 1.4 X 10(-3) M. Human cells and monolayers of fetal murine fibroblast were submitted to the action of medroxyprogesterone solution at the same concentrations as used for progesterone. Other steroids (estrone, estriol, testosterone and prednisolone) were used at the identical concentrations in the same vehicles. Progesterone affected all lines of fibroblasts studied and destroyed them within either 2-4 or 24-48 h depending on the steroid concentrations used. Medroxyprogesterone had a comparable effect on human cell lines and monolayers of fetal murine fibroblasts provided that the same ratio between the hormone concentration and the time of exposure was maintained. With higher medium concentrations shorter times of incubation were required for the destruction of fibroblast. However, to observe a degree of lysis similar to that elicited by progesterone, it was necessary to use 4 times higher concentrations of medroxyprogesterone. No effect on HeLa epithelial cells was observed nor were the controls affected by the steroids or diluents used at the appropriate concentrations. Results from incubation studies using monolayers of murine fibroblast and 14C-progesterone suggested that the cells were destroyed by the progesterone and not by a bioproduct of its metabolism.

Animals

Respiratory changes after intraarterial acetylcholine and abdominal concussion.

In 50 dogs anesthetized with chloralose the respiratory changes produced by intraarterial acetylcholine (ACh) and after an abdominal blow, were studied. Intraarterial ACh produced expiratory apnea when it was injected in the superior and inferior mesenteric artery, splenic and left gastric artery. This apnea disappeared when the splanchnic nerves were severed and disappeared or decreased after atropine sulfate was injected. The duration of the apnea coincides with the contraction of the gut smooth muscle recorded, with a small balloon placed in the jejunum or in the ileum. The ACh did not produce respiratory changes when it was injected in the hepatic artery and pulmonary trunk. In the peripheral arteries, especially in the subclavian, ACh injection produced a respiratory stimulation which could be caused by the pain which accompanied the muscular contraction. After a blow in the abdominal wall, an expiratory apnea was also obtained, similar to that observed by the injection of ACh in the gastrointestinal arteries. This apnea disappeared when splanchnic nerves were severed or when atropine sulfate was injected. Smooth muscle contraction was also observed, suggesting that the expiratory apnea was originated in the smooth muscle receptors.

Abdominal Injuries