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R Ripa

Publications and source records attributed to R Ripa.

61 records · Page 4Linked to original sources
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Are failured cardiomyopathies a zinc-deficit related disease? A study on Zn and Cu in patients with chronic failured dilated and hypertrophic cardiomyopathies.

BACKGROUND: Muscle zinc deficit may be important in cardiac failure pathogenesis. We studied whether Zn deficit is present in dilated (DCM) and hypertrophic (HCM) cardiomyopathies with chronic cardiac failure. The aim was to find out whether it might be a diagnostic and prognostic marker. METHODS: Zn and Cu values were measured in plasma, urine and red blood cells by flame atomic absorption spectrophotometer in normal subjects, in 15 patients with DCM and in 11 patients with HCM in chronic cardiac failure. RESULTS: There is a statistically important increase of zincuria as well as low plasmatic and erythrocytic zinc in DCM; low plasmatic and erythrocytic zinc was found in HCM. CONCLUSIONS: It is likely that chronic cardiac failure, by atrial natriuretic peptide activation, increases zincuria and involves a secondary loss of plasmatic and erythrocytic zinc. Primitive or secondary zinc deficit causes marked structural and functional myocardial cell impairment. Hypozinchemia from increased zincuria seems to represent an important diagnostic and prognostic marker in chronic failured cardiomyopathies. Dilated cardiomyopathy, particularly in elder subjects, may be considered as a primitive or a secondary Zn-deficit myocardial disease. In the essay, the possible pathogenetic mechanisms underlying hypozinchemia and determining functional and structural myocardial cell changes are discussed. The main consequence of present results is pharmacological Zn administration as a new pathogenetic therapy in chronic failured cardiomyopathies.

Aged↗
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Zinc and immune function.

Zinc and immune function relationship has been extensively studied. Both in experimentally induced mineral deficit and in genetically determined deficit observable in acrodermatitis enteropathica and in enteropathy of Danish A-46 cattle, a B and T dependent antibody response decrease, a T dependent cytolytic response decrease and a natural killer cytotoxic activity decrease are present noteviously. Serious reduction of the immune function is present, in proportion to the value of low zinc plasmatic level, in elderly patients, in malnourished and seriously zinc deficient children, in patients subjected to total parenteral supply, in HIV infections and especially in evident AIDS: in this condition the plasmatic zinc level can be considered, together with the CD4+ lymphocytes amount and the B2-microglobulin value, a disease progression marker. Zinc immunostimulating action mechanisms are complex, although thymic hormone (of which zinc is essential cofactor) stimulation seems to be most important. Zinc supplementation, also parenterally, can be useful in immunodeficiency (in the elderly, in the post-surgical patients, in genetically determined or alimentary induced deficit, in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Zinc cellular traffic: physiopathological considerations.

Zinc cellular traffic is reviewed in both influx and efflux stages. Zinc influx happens through three different modalities: 1) anionic exchange channels, with the metal cotransported in complex form with anions, often as anionic monovalent complex (Zn [HCO3)2Cl]. Bicarbonate-ions, chloro-ions and thiocyanate-ions can stimulate zinc << uptake >>, while phosphate and sulphate-ions are inhibitory. 2) facilitated diffusion through amino acids which, by passing into cells, carry zinc (particularly cysteine and histidine) with them. 3) transferrin receptor route, very important for cellular uptake of iron and zinc. Various mitogenic factors cause increased synthesis of transferrin receptors and increase of metal uptake. Zinc efflux happens through zinc/calcium exchange (zinc efflux coupled with calcium influx). Calcium is then expelled from cells by means of calcium pump (with energy consumption), regulated by membrane Ca-ATPase. Impairment of this ionic exchange process may cause an intracellular accumulation (as may be seen in SHR rats).

Amino Acids↗
PubMedDate not supplied

[Zinc and the growth hormone system].

Chronic zinc nutritional deficiency constantly causes delay in pondero-statural growth. The mineral controls GH synthesis and secretion, but its administration acts on physical growth also after hypophysectomy: zinc supplementation causes a significant increase in liver synthesis of IGF-I (somatomedin C), which, in chronic mineral nutritional deficiency, is remarkably reduced. In men, in this condition, GH response to its releasing factor (GRF) is normal: a demonstration of the less important role of the pituitary gland in this situation. Therefore, in chronic zinc deficiency, reduced liver production of IGF-I is responsible for reduced physical growth; moreover in this situation receptor resistance to IGF-I (in addition to GH), that fades away after dietetic supplementation of the mineral, has been demonstrated. Therefore zinc play an important role at receptor level, throughout various mechanisms (including a proven increase in receptor number, due to its aggregating membrane direct induced effect).

Animals↗