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Biomedical subjects

P Vic

Publications and source records attributed to P Vic.

At least 55 records · Page 3Linked to original sources
PubMed1991

Increased numbers of hypodense alveolar macrophages in patients with bronchial asthma.

Alveolar macrophages (AM) are among the cells involved in the bronchial inflammation of asthma. It has been shown that AM are a heterogeneous cell population in normal subjects. The heterogeneity of AM from 36 asthmatic patients and 23 normal subjects was studied using Percoll density fractionation. AM recovered from asthmatic patients are mainly in the lower density fractions (1.03 and 1.04 g/ml), whereas AM from normal subjects are in the higher density fractions (1.05 and 1.07 g/ml). Electron microscopic studies showed that low density AM of both asthmatic and normal subjects appear to have morphologic characteristics of activated cells by comparison with high density AM that present characteristics of quiescent cells in both asthmatic and normal subjects. The functional activity of AM fractions of asthmatic and control subjects was assessed using the release of the oxygen free radicals induced by opsonized zymosan and TxB2 generation by A23187. There was no difference between the five fractions of asthmatic or control subjects with regard to oxygen species release. The TxB2 generation was increased in the low density AM from asthmatics when compared with the same fractions of normal subjects. The hypodense cells produced less TxB2 than did cells of higher density in both asthmatic and normal subjects. The density of AM was correlated with the recent instability of the asthma but not with the severity of it. This study shows that AM from asthmatic subjects, when compared with those from control subjects, are heterogeneous, hypodense cells and that they predominate. Hypodense AM did not appear to be hyperresponsive in vitro and may have been already committed into the airways.

Adolescent↗
PubMed1989

Differential effects of amiodarone and propranolol on lipid dynamics and enzymatic activities in cardiac sarcolemmal membranes.

The amphiphilic cationic cardioactive drugs (pindolol, propranolol and amiodarone) were tested for their effects on lipid dynamics (measured by fluorescence depolarization) and on enzymatic activities up to 1 mM in purified cardiac sarcolemmal vesicles from adult rat. The vesicles were enriched 12- to 37-fold (with respect to tissue homogenate) in Na+/K+ ATPase, K+-stimulated p-nitrophenylphosphatase, 5'nucleotidase and adenylate cyclase, all of which are believed to be components of sarcolemma. Phospholipids and cholesterol content were enriched 5- and 13-fold respectively. There was very little contamination of the sarcolemmal vesicles by sarcoplasmic reticulum (as judged by Ca2+ ATPase and glucose-6-phosphatase activities) or mitochondria (as judged by cytochrome-c-oxidase activity). Pindolol had no effect on lipid dynamics and enzyme activities except for the isoproterenol-stimulated adenylate cyclase. The latter was also totally inhibited at 1 microM by propranolol which inhibited Mg2+ ATPase and increased fluidity above 20 microM. Amiodarone affected all the enzyme activities (except Na+/K+ ATPase): isoproterenol-stimulated adenylate (IC50 = 30 microM), Mg2+ ATPase (IC50 = 20 microM) and K+-stimulated-p-nitrophenylphosphatase were inhibited; 5'nucleotidase was activated above 2 microM. By contrast with propranolol, amiodarone decreased lipid mobility. The effect was linear with the concentration of the drug above 1 microM.

4-Nitrophenylphosphatase↗
PubMed1985

Intestinal pathology in the dog induced by sublethal doses of amiodarone.

Amiodarone (A), an unique antiarrhythmic agent and amphiphilic drug, induces at sublethal doses dyslipidic storage in animals. The present work demonstrates a distinct intestinal pathology or "Malabsorption Syndrome" in the dog induced by A. Signs of intestinal pathology were observed in all animals receiving 100 mg/kg, but not in those receiving less than 50 mg/kg, after one month. The malabsorption syndrome was demonstrated by a dynamic study of lipid absorption and pathological lesions (partial villous atrophy and the accumulation of macrophages with dyslipidic inclusions.

Amiodarone↗
PubMed1984

Recovery from amiodarone-induced lipidosis in laboratory animals: a toxicological study.

Numerous amphiphilic cationic drugs cause lipid-lysosomal storage in animal tissues; one of these drugs is amiodarone, a major antiarrhythmic agent. The toxicological effects of amiodarone were studied in three animal species (rats, dogs, and monkeys). It was shown that sublethal dose levels of amiodarone induced lipid storage in a great variety of tissues in rats (Fischer and Sprague-Dawley strains) and dogs. However, this change was not observed in baboons and Wistar rats. This storage, essentially characterized by lamellated inclusions, affected foamy macrophages, and at a later phase multiple cell types. Tissue biochemical analysis provided evidence of the phospholipidic nature of the storage. In addition, amiodarone induced an increased cholesterolemia and marked modifications of the lipoproteinogram. The kinetics of lipid storage was demonstrated following oral administration of amiodarone. After jejunal absorption, lipid storage occurred in the mesenteric lymph nodes followed by widespread deposition in the other lymph nodes and tissues, particularly in the lung. A complete recovery from lipid storage as observed in dogs and rats. Finally, an investigation of a correlation between animal and man by means of long-term experiments is proposed.

Amiodarone↗
PubMed1984

Diffuse interstitial pulmonary disease during amiodarone treatment.

A case of diffuse interstitial pneumopathy which was observed by photonic microscopy and confirmed by electron microscopy is presented in a patient treated with amiodarone only. The iatrogenic origin of this pneumopathy appears certain as clinical and radiological signs improved after amiodarone treatment was withdrawn.

Amiodarone↗
PubMed1982

Somatostatin treatment of psoriasis.

Somatostatin treatment was administered to 20 psoriatic patients according to the following protocol: Continuous infusion (250 micrograms/h) for at least 2 days followed either by short infusions (1 h) at 8 A.M. and 8 P.M. (12 cases) or by repeating the initial 2-day infusion (eight patients). Before treatment (day 0) and on day 6, biopsy specimens were taken for routine examination (12 patients) and for ultrastructure (seven patients). In vitro immunological studies were carried out on peripheral blood lymphocytes (six patients) on day 0 and day 8. In two patients, somatostatin was stopped because of serious side effects. Thus, clinical results were evaluated in 18 patients, on day 30. In ten of them no improvement whatsoever occurred, two had a partial clearing and an almost complete remission was achieved in six others. Ultrastructural studies showed, on day 6, enlargement of the intercellular spaces with deposits of granular material of glucidic composition, associated with features of cellular damage. Percentages of T and B cells were unmodified but a significant depression of mitogenic stimulation by PHA and ConA was clearly observed on day 8. Even if somatostatin treatment may have a beneficial effect in some patients it seems much less valid than other well-known therapies for psoriasis.

Adult↗
PubMed1982

[Terminolateral portacaval shunt does not prevent hepatic regeneration after 65% hepatectomy in the dog. Value of parenteral nutritional support].

Lack of portal blood supply to the liver induced by end to side porto-caval shunt leads to liver atrophy but does not prevent hepatic regeneration after 65% hepatectomy in the dog. This work demonstrates the usefulness of parenteral nutritive support with a branched-chain amino acids enriched essential amino-acids solution in helping hepatic function restoration by comparison of three groups of animals which were fed either parenterally (two groups) or per os (1 group).

Amino Acids, Essential↗
PubMed1982

Effect of estradiol on the ultrastructure of the MCF7 human breast cancer cells in culture.

We have analyzed the effect of estradiol and of two classes of antiestrogens on the morphology of the MCF7 human breast cancer cell line by scanning and transmission electron microscopy. Estradiol progressively increased the number and the length of microvilli at the cell surface. The density of the microvilli network increased between 2 and 11 days of estrogen treatment, while the cells became more granular and less tightly attached to the surface of the dish. Estradiol also progressively transformed cells into secretory cells containing, at Day 2, large, clear mitochondria and, at Day 4, rough endoplasmic reticulum and Golgi complex. At Day 6, secretory granules (diameter, 0.2 microM), which mainly contained glycoproteins, were first developed in the cytoplasm. By Day 8, they were concentrated at the cell membrane and being liberated into the medium. Larger granules (diameter, 0.8 microM), which probably contained lipids, were obtained later (Day 11). Cell cultures in 10% fetal calf serum not treated by charcoal contained secretory granules. The modifications were induced by physiological concentrations of estradiol but not 5 alpha-dihydrotestosterone. Progesterone (10 nM for 8 days) completely inhibited the effect of estradiol on the microvilli and secretory activity. Tamoxifen or hydroxy-tamoxifen did not induce secretory activity but did alter the cell morphology compared to control cells. The effects of estradiol were observed in other estrogen receptor-positive breast cancer cell lines (ZR 75-1, T 47 D) but not in an estrogen receptor-negative cell line (BT 20). This morphological evidence that estrogens modify the cell surface of breast cancer cells in culture and transform them into "secretory cells" complements evidence that a molecular weight of approximately 50,000 into the culture medium (Cell, 24: 352-362, 1980). (The molecular weight was found first to be 46,000. It seems to be closer to 52,000 in a 10% polyacrylamide gel and by using the NEN-labeled proteins as molecular weight markers.

Breast Neoplasms↗
PubMed1981

[Comparative hepatic toxicity of perhexiline maleate and griseofulvin in mice].

Hepatic toxicity was observed in mice which had received Griseofulvin or Perhexilin Maleate over a period of several months. Treatment of griseofulvin alone gave rise to hepatitis with the presence of Mallory bodies (MB) whereas the same length of treatment with Perhexilin Maleate was associated with steatonecrosis with an absence of MB. When treatment was followed by a one month rest period hepatic lesions disappeared with no trace of sequelae. Cross-treatment studies showed that one week of Perhexiline Maleate was sufficient to induce MB in mice pretreated with Griseofulvin. Similarly, Griseofulvin administered to mice pretreated with Perhexilin Maleate gave rise to MB formation after one week as opposed to the usual two months incubation time (DENK et al.). The histological nature and mode of formation of these MB was identical to that encountered in acute alcoholic hepatitis. On addition, combined drug therapy employing Perhexilin Maleate suggests a particular hepatic toxicity in man in cases where the liver has become predisposed due to other therapeutic.

Animals↗
PubMed1980

Early effect of estrogen on chromatin ultrastructure in endometrial nuclei.

The effect of estradiol on chromatin ultrastructure in interphase nuclei was studied in immature rat and lamb endometrium. Physiological doses of estradiol within the first hour transformed the condensed chromatin into dispersed chromatin both in vivo and in vitro. These ultrastructural modifications were specifically induced by hormones translocating the estrogen receptor to the nucleus of estrogen-responsive tissues. Conversely, the antiestrogen tamoxifen gave a hypercondensation of chromatin. The addition of actinomycin D, cordycepin or alpha-amanitin, but not of cycloheximide, prevented the effect of estradiol both on the ultrastructural change and on [3H]uridine incorporation, suggesting that chromatin decondensation was closely related to transcriptional activity. These results indicate that in endometrium, estrogen rapidly provokes a large and extended modification of chromatin ultrastructure, which suggest a general effect on chromatin function rather than a selective activation of a limited number of genes.

Animals↗