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Biomedical subjects

A Molteni

Publications and source records attributed to A Molteni.

At least 91 records · Page 5Linked to original sources

Detection of alpha-lactalbumin in breast lesions and relationship to estrogen receptors and serum prolactin.

Alpha-lactalbumin, the B protein of lactose synthetase secreted by the mammary epithelial cells, was isolated and purified from fresh human milk and injected into rabbits for antibody production. Indirect immunofluorescence (IIF) was done on various types of breast lesions to assess the relationship, if any, between histologic type and production of alpha-lactalbumin. Fifty percent of fibroadenomas and fibrocystic disease and 63% of infiltrating ductal carcinoma showed positive reaction. No false positives were found on IIF of alpha-lactalbumin of several tumors of nonmammary tissue. These findings suggest that IIF for alpha-lactalbumin may be helpful in ascertaining the site of origin of metastatic breast tumors. However, serum alpha-lactalbumin was detected by radioimmunoassay in only 10% of women with infiltrating ductal carcinoma, indicating that this may not be a useful marker for the presence of breast cancer at least by the method employed. This discrepancy between serum and tissue alpha-lactalbumin may be due to the short half-life of serum alpha-lactalbumin or to the lack of secretion of the protein into the blood. There was no apparent relationship between the presence of estrogen receptors or serum prolactin and alpha-lactalbumin in the 27 mammary carcinomas investigated.

Adenofibroma↗

Effect on an ergoline derivate-nicergoline (Sermion) on methylandrostenediol-induced hypertension in the rat.

The antihypertensive activity of nicergoline (Sermion), an adrenolytic and vasodilator drug, was tested in rats when hypertensive vascular disease was induced by administration of methylandrostenediol (MAD). Nicergoline not only counteracted the effect of MAD on the systolic blood pressure of the rats, but it also prevented the appearance of vascular lesions usually induced by this type of experimental hypertension on arterioles of several organs such as heart, kidney and brain and of the pancreatic mesenteric region. When given alone, the drug was well tolerated. Since the drug did not interfere with the modification induced by MAD on the adrenal steroidogenesis, as seen by EM studies of the zona fasciculata of the androgen-treated animals, it is likely that it may have exerted its adrenolytic effect on the peripheral vessels of the MAD-induced hypertensive rats.

Adrenal Glands↗

Incidence of post burn hypertensive crisis in patients admitted to two burn centers and a community hospital in the United States.

Fortynine patients of 193 admitted (25%) with second and third degree burns to 3 hospitals in different geographical areas of the United States developed a hypertensive crisis within three to four days after admission. The crisis usually lasted from 5 days to about two weeks. Serum sodium levels decreased significantly in hypertensive patients one or two days before the peak of the hypertensive crisis and, in the Center where it was measured, plasma renin activity increased in an opposite trend to the fall of sodium. BUN and creatinine reached their highest levels in hypertensive patients two days after the peak of the crisis. Autopsies were performed on 23 patients who succumbed to the injury: eleven of them (48%) were hypertensive and had marked hypertrophy of left and right heart ventricles and of the adrenal glands when compared to the normotensive burn subjects. The cells of the zona fasciculata and the zona glomerulosa of the adrenal glands were very compact at histologic examination thus suggesting hyperactivity. This data shows that the incidence of hypertension in burn subjects is twice as high as that of the US population. Further studies of the renin-angiotensin-aldosterone system and the adrenal cortical function are indicated by the changes in plasma renin activity and the glandular weight and morphology seen at autopsy.

Adolescent↗

[Hypoxic pulmonary vasoconstriction and angiotensin II blockade in calves (author's transl)].

The pulmonary vascular response to breathing low oxygen containing gas mixture was examined before and during Angiotensin II blockade in five open-chested newborn calves. Angiotensin II blockade was achieved by continuous infusion of Sar1-Ile5-Leu8-Angiotensin II (Saralasin), a competitive inhibitor of Angiotensin II. The hypoxic rise in pulmonary vascular resistance after blockade did not differ from that of control. It is concluded that Angiotensin II does not play a significant role in acute hypoxic pulmonary vasoconstriction in the calf.

Angiotensin II↗

Plasma angiotensin II levels in hypoxic and hypovolemic stress in unanesthetized rabbits.

Plasma levels of angiotensin II were determined by radioimmunoassay in unanesthetized white rabbits exposed to acute hypoxia (FIO2 10% for 10 min), chronic hypoxia (0.5 atm up to 16 days), or hypovolemic stress (bleeding 20 ml/kg). Angiotensin II levels significantly decreased after 10 min of acute hypoxia in normal rabbits and significantly increased when the same procedure was applied to animals previously exposed to hypoxia by 6-8 days of permanence in the hypobaric chamber or sodium deprivation. Chronic hypoxia resulted in a temporary increase of angiotensin II already evident on the 3rd day, but maximal at the 9th day with return to normal values within 16 days. Hypovolemic stress resulted in the expected rise of angiotensin II levels 10 min postbleeding both in normal and acclimatized rabbits. The response of the renin-angiotensin-aldosterone system to hypoxic and hypovolemic stress is different. The direction and magnitude of the response to hypoxia depends on the underlying state of activation of the system and the cardiovascular condition of the animal at the time of hypoxic stress.

Adaptation, Physiological↗

Angiotensin I-converting enzyme and angiotensin II levels in women receiving an oral contraceptive.

In 11 healthy, normotensive young women taking contraceptive medication (Enovid) for at least one year, plasma levels of angiotensin II were significantly higher than in healthy male and female controls. No significant difference was seen in the serum activity of angiotensin I-converting enzyme measured in vitro. Although serum angiotensin I converting enzyme activity is stimulated in several conditions in which other components of renin-angiotensin-aldosterone system are increased, this is not the case during administration of estrogens.

Adult↗

The effect of changes in dietary sodium on lung and serum antiotensin-I-converting enzyme in the rat.

Three groups of rats were fed a sodium-deficient diet, a normal sodium diet, and a diet high in sodium for up to 8 weeks. Animals on a sodium-deficient diet had a significant decrease of serum sodium levels with a concomitant increase of renal renin granules. The reverse was true in rats on a high sodium diet whereas no significant changes in renin granulation were seen in rats fed a normal sodium diet. The changes in serum sodium levels and in number of renal renin granules were not associated with changes in lung or serum angiotensin-I-converting enzyme activity which did not vary significantly in any of the three groups of rats throughout the experiment. It is, therefore, suggested that such activity is independent of changes in sodium balance sufficient to affect the renal renin content.

Animals↗

Deveolpment of hypertension in rats maintained on a sodium deficient diet and bearing a mammotropic tumor (MtTF4).

Implantation of a mammotropic tumor (MtTF4), secreting growth hormone, prolactin, and corticotropin, in female rats of Fischer F344 strain causes hypertension, vasculitis, renal and cardiac hypertrophy, and extensive renal and cardiac lesions. When rats of the same strain were implanted with the MtTF4 tumor but sodium was withheld from the diet, systolic blood pressure rose more slowly but by six weeks reached the same values recorded in the animals implanted with the tumor and allowed to consume sodium ad libitum. In the rats, on sodium deficient diet, however, the vascular damage as well as the renal and cardiac lesions were minimal or absent. Implantation of the tumor caused adrenal cortical dysfunction, and elevated levels of deoxycorticosterone were seen in the peripheral plasma of the rats of all three groups. Nonetheless, plasma deoxycorticosterone was significantly lower in rats on a sodium deficient diet as compared with those having sodium added to the diet. Light microscopic and ultrastructural studies of the adrenal glands revealed that the lack of dietary sodium largely prevented the extensive damage of the zona fasciculata cells usually seen in the tumor-bearing rats, consuming sodium ad libitum. Both hypertensive MtT tumor-bearing animals and normotensive controls on a sodium deficient diet had a conspicuous increase of renal content of renin. It is evident that hypertension may be produced in rats bearing the MtTF4 tumor even in the virtual absence of dietary sodium. It does not appear that the hypersecretion of renal renin sustains the hypertension in these rats, since high levels of this substance were seen in the kidney of normotensive controls on the same sodium deficient diet. Elevated levels of plasma DOC may possibly explain the hypertension. In addition, it is likely that the animals may also have elevated levels of glucocorticoids.

Adrenal Cortex↗

Angiotensin-I-converting enzyme activity in idiopathic respiratory distress syndrome of the newborn infant and in experimental alveolar hypoxia in mice.

Serum angiotensin-I-converting enzyme activity was found to be elevated in infants with idiopathic respiratory distress syndrome when compared with healthy premature infants, normal infants, and acutely ill full-term infants. Serum and lung CE activity has been found to be elevated in mice exposed to hypobaric alveolar hypoxia which also stimulated renal renin production. These findings suggest that alveolar hypoxia stimulates the renin-angiotensin-aldosterone system and this system may be involved in the response to the stress of IRDS.

Age Factors↗

Resistance of W/Fu rats to adrenal regeneration hypertension.

The procedure for producing adrenal regeneration hypertension did not cause an increase in the systolic blood pressure of W/Fu animals. The regenerating adrenal gland in W/Fu animals was not restored to normal; reduced numbers of mitochondrial cristae were seen and the mitochondria were smaller in size; regeneration was complete in Sprague-Dawley rats of the Holtzman strain and there was a severe form of hypertensive, cardiovascular disease.

Adrenal Cortex↗

Prevention of pulmonary vascular changes of chronic alveolar hypoxia by inhibition of angiotensin I-converting enzyme in the rat.

To test the hypothesis that the renin-angiotensin system is involved in the development of the pulmonary vascular patholigic changes of chronic alveolar hypoxia, two groups of rats were exposed to 0.5 atm. for 21 days. One group received SQ 20,881 (2 mg. per kg.) every 8 hours subcutaneously and the second group received normal saline. A third group of rats was maintained at normobaria. Rats receiving SQ 20,881 had significantly less pulmonary arterial hypertrophy and right ventricular hypertrophy than hypobaric animals. SQ 20,881-treated rats showed a significant increase in adrenal weight but a marked reduction in the thickness of the zona glomerulosa, as compared with the other groups. Our findings indicate that angiotensin II is necessary in the development of the pulmonary vascular structural changes of chronic alveolar hypoxia.

Adrenal Glands↗

Hypertension and narrowing of the renal arteries in infancy.

The clinical histories of two infants who had severe hypertension and stenoses of the renal arteries are reported. In both children blood pressure fell significantly after surgical correction of renal ischemia. However, both infants had persistent mild hypertension for several months after surgical treatment. Similar results were found in other infants with renovascular hypertension, reported previously (11 cases). The mortality rate in this total group of 13 infants reviewed was high if renal ischemia was not corrected surgically (4/4). The reason why some infants have persistent hypertension after apparently adequate surgical relief of renal ischemia is not known.

Female↗