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Biomedical subjects

M Carmignani

Publications and source records attributed to M Carmignani.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effects of chronic exposure to arsenate on the cardiovascular function of rats.

Cardiovascular function was studied in anaesthetised male rats which received 50 micrograms/ml of arsenic (as sodium arsenate) in deionised drinking water for 320 days. High urinary excretion of arsenic was found at the end of treatment and the metal accumulated considerably in the kidneys and liver, which both presented slight alterations. No histopathological modifications were evident in other organs. Base line blood pressure, cardiac inotropism, and chronotropism and cardiovascular reactivity to noradrenaline, acetylcholine, angiotensin II, bradykinin, histamine, and serotonin did not differ in exposed or in control animals. In the exposed group, however, there was potentiation of the effects of vascular beta-adrenoceptor stimulation and a reduction in the vascular responsiveness to angiotensin I. Chronic arsenic exposure did not affect the baroreflex sensitivity but was able to induce sympathetic hyperactivity or hypersensitivity, or both, possibly associated with an antivagal action. Our results might help to explain the cardiovascular alterations seen in people chronically exposed to high concentrations of arsenic.

Angiotensin I↗
PubMed1981

Urinary kallikrein and hypertension in cadmium-exposed rats.

Chronic exposure of rats to cadmium (Cd) in drinking water induced elevated systolic and diastolic blood pressure. Heart rate, however, was lowered, suggesting that the hypertension in these rates may be due to an increase of the total peripheral resistance, possibly involving a central nervous system (CNS) component in Cd-induced hypertension. Urinary kallikrein activity was reduced in the exposed animals and may explain the previously reported antinatriuretic effect of Cd, since renal kallikrein is an enzyme responsible for the synthesis of kallidin, a potent vasodilator and natriuretic polypeptide.

Animals↗
PubMed1980

Prostacyclin effects on the blood pressure responses to norepinephrine in rats treated with aspirin or indomethacin.

The atherosclerotic condition is associated with a reduction of PGI2 synthesis; moreover, in the presence of elevated serum cholesterol levels, pressor responses to norepinephrine are potentiated. In order to verify if a complete inhibition of PGI2 production affects the vascular reactivity, it was assayed two cycloxygenase inhibitors (lysine acetylsalicylate and indomethacin) in rats. The two drugs significantly potentiated the blood pressure responses to norepinephrine, and completely inhibited PGI2-like substances production by arterial rings. The prostacyclin infusion (15 ng/kg/min, i.v.) completely reversed such potentiation, without any major modification in the basal blood pressure values. These results show that PGI2 production is responsible for vascular tone modulation and may partially explain the altered vascular reactivity in the atherosclerotic condition.

Animals↗
PubMed1978

Glucocorticoid-binding components in human thymus hyperplasia.

Preliminary experiments on thymocyte suspensions derived from human thymus hyperplasia indicated the presence of specific cytoplasmic receptors binding [3H]-dexamethasone with high affinity and specificity. The receptor was rapidly transferred into the nuclei at 28 degrees but not at 2 degrees. With cell-free preparations and ion-exchange cellulose-impregnated paper filters, thymus cytosol bound [3H]dexamethasone with a dissociation constant of 4.3 x 10(-9) M; the concentration of receptor sites was 9.6 x 10(-14) mole/mg cytosol protein. Cytosol contained binding components that sedimented at approximately 7S and 3.6S (low ionic strength) and at 4S (high ionic strength). Competition studies showed high specificity for glucocorticoids since binding of labeled dexamethasone was inhibited in the presence of 10(-6) M beta-methasone, prednisolone acetate, dexamethasone, corticosterone, cortisol, and cortisone. 17beta-Estradiol, testosterone, and dihydrotestosterone at 10(-6) M did not inhibit specific binding of [3H]dexamethasone. Thus, the dexamethasone-binding components of the human thymus hyperplasia had properties similar to those described for steroid hormone receptors present in target tissues.

Cell Nucleus↗
PubMedDate not supplied

Effects of long-term cadmium exposure on the testis of rabbits: ultrastructural study.

Six male rabbits received for 9 months drinking water containing 20 micrograms/ml of cadmium (Cd). At the end of the treatment, the Cd contents of kidney and testis were 175 +/- 34 and 0.8 +/- 0.2 micrograms/g wet weight, respectively. Ultrastructural examination by transmission electron microscopy (EM) showed that, in the Sertoli cells, the size of the lysosomes was increased; spermatogenetic cells, vessels and Leydig cells showed no significant alterations. Observations with both transmission and scanning EM did not evidence changes in the blood-testis barrier, but our results do not exclude that male fertility may be affected by chronic exposure to cadmium.

Animals↗
PubMedDate not supplied

Neurobehavioral functions, serum prolactin and plasma renin activity of manganese-exposed workers.

Objective of this study was to assess effects of manganese (Mn) exposure on 56 workers employed in a Mn welding workshop of a machine building factory in Taiyuan (Shanxi Province, P.R. China) for a mean period of 16.1 years. The mean air Mn level in the workshop was 138.4 microg/m3. Neurobehavioral Core Test Battery (NCTB), including the Profile fo Mood States, (POMS), was performed. Blood pressure (BP) increase following immediate stand-up (BP-IS), serum prolactin (PRL) and plasma renin activity (PRA) in supine position were also determine. Most of the NCTB scores of the Mn-exposed workers were lower than those of controls, while the POMS scores were higher, indicating a Mn-induced impairment of neurophysiological functions and a deflection of mood towards negative emotion states. PRL values of the Mn-exposed workers were higher than those of the controls. BP-IS of Mn-exposed workers was significantly lower than that of the controls. PRA of the same workers was augmented more that 200%. In the Mn-exposed workers, the higher PRL values are possibly due to a reduced inhibitory effect on pituitary lactotrope cells by the tubero-infundibular dopamine system; the decreased BP-IS was referred to imbalance between the sympathetic and parasympathetic activities, whereas the higher basal PRA was thought to depend on neuroendocrine changes (including increased central sympathetic tone) and/or on a direct effect of Mn on renal juxta-glomerular cells. On the whole, this study demonstrates that occupational Mn exposure is responsible for neurobehavioral changes coexisting with alterations of neuroendocrine and humoral systems.

Adult↗
PubMedDate not supplied

Clastogenic but not apoptotic effects on human artery endothelial cells by concentrations of inorganic lead inhibiting their nitric oxide production.

Human coronary artery endothelial cells (HCAEC 5156) were cultured as monolayers and exposed to concentrations of lead (as acetate, Pb) in the culture medium similar or lower than those commonly found in the blood of human beings occupationally or environmentally exposed to this element. Only at the concentration of 200 ng/mL, Pb reduced growth rate of HCAEC 5156 cells starting from the 3rd day and up too the 5th day of incubation. On the other hand, Pb (0.2, 2 and 200 ng/mL) increased concentration-dependently micronuclei formation in binucleated HCAEC 5156 cells, as it was shown by the cytokinesis-blocked micronucleus assay (CMBN assay) carried out after 48 hours of exposure to the metal. However Pb was unable, at all the above concentrations to induce apoptosis in the HCAEC 5156 cells following a 48 hour-exposure, as shown by an electorphoretic apoptotic DNA fragmentation test. Moreover, Pb (2 and 200 ng/mL) reduced significantly the concentration of nitric oxide (NO, determined analytically as L-citrulline) in both culture medium and cytosol of HCAEC 5156 cells following a 7 day-exposure to the element. Results were discussed also in relation so evidences of other studies reporting genotoxic and/or apoptotic effects of Pb on various cell types at very elevated dosages of concentrations. The observed clastogenic effects of Pb were explained through a series of mechanisms involving interactions between oxygen reactive species and NO and/or reduced NO synthesis in the endothelium, thus leading to a depressed NO bioavailability. This research first shows that Pb is provided with clastogenic but not apoptotic effects on cultured human endothelial cells. It was emphasized that such effects are induced by Pb concentrations similar to those commonly found in blood and tissues of laboratory animals showing Pb induced cardiovascular and/or neuropsychological alterations.

Apoptosis↗
PubMedDate not supplied

Shock induction by arterial hypoperfusion of the gut involves synergistic interactions between the peripheral enkephalin and nitric oxide systems.

To determine whether critical splanchnic artery hypoperfusion can provoke systemic shock and to identify the roles of the peripheral opioid and nitric oxide (NO) systems in this process, various degrees of superior mesenteric artery hypoperfusion (SMA-H) were produced in anesthetized adult rabbits (n=40), and hemodynamic and metabolic indices were measured. Metabolic acidosis and irreversible hypodynamic shock occurred with SMA-H at levels representing 25-20% of mean baseline SMA blood flow. In 112 other rabbits subjected to SMA-H at 20% (SMA-H20%), we studied plasma NO and enkephalin (ENK) levels, cardiovascular reactivity to selected physiological agonists, effects of ENKs on plasma NO levels, and effects of peripheral opioid receptor blockade and inducible NO synthase (iNOS) inhibition. SMA-H20% progressively increased systemic blood levels of NO and ENKs. Exogenous ENK administration accentuated SMA-H20%-induced increases in plasma NO levels, and their cardiovascular depressing effects were significantly greater when they were administered during SMA-H20% (vs. administration under baseline conditions). Selective blockade of cardiovascular delta-opioid receptors improved hemodynamics, prevented shock irreversibility and reduced plasma NO levels; similar effects were obtained by selective iNOS inhibition. These findings demonstrate that critical arterial hypoperfusion of the gut can induce hypodynamic systemic shock through ENK-induced hyperactivation of cardiovascular delta-opioid receptors, which leads to increased plasma levels of NO related in part to increased iNOS activity. Since pronounced splanchnic artery hypoperfusion occurs in all advanced systemic shock states, selective delta-opioid receptor antagonists and/or iNOS inhibitors may prove to be useful in improving shock hemodynamics and metabolic derangements and/or preventing progression toward irreversibility.

Animals↗
PubMedDate not supplied

[Chronic exposure to arsenic in rats: morphological and functional findings].

Male Sprague-Dawley rats, who had received 50 micrograms/ml of arsenic (as sodium arsenate) in drinking water for 320 days, showed high urinary excretion of this element. Arsenic was accumulated in tissues, mostly in the kidney and in the liver. In the kidney were evident slight focal alterations in tubules and glameruli; some of the tubules contained casts of amorphous hyaline material. The hepatocytes close to the centrolobular veins were swollen and showed ultrastructural alterations. The seric GOT, GPT and LDH activities were normal, while the alkaline phosphatase alto have been found in the brain, sciatic nerve, lung, heart and arteries. No significant changes of systolic and diastolic blood pressure levels were observed. Similarly, cardiac inotropism and chronotropism were unchanged. The electrocardiogram, also, was normal. The cardiovascular reactivity to noradrenaline, acetylcholine, histamine, serotonin, bradykinin and angiotensin II was unchanged. However, the vascular reactivity to the beta-stimulation was increased, while it was decreased to the angiotensin I. On the whole, our results suggest that chronic arsenic exposure produces focal alterations in the kidney and characteristic modifications in the hepatic structure and in the cardiovascular reactivity.

Animals↗
PubMedDate not supplied

Vanadate and cardiovascular system.

Rats were given 1, 10, 40, or 100 ppm of vanadium in drinking water for seven months, while rabbits received 1 ppm of vanadium (as sodium metavanadate, NaVO3) in drinking water for twelve months. Rats developed arterial hypertension through complex effects of vanadium on central neurogenic pathways, central and periferal catecholaminergic mechanisms, specific autacoidal systems (kallikrein-kinin, reninangiotensin-aldosterone, enkephalin ones), and effectors (vessels and heart). The above effects of vanadium were in part confirmed in the rabbits which, however, did not show arterial hypertension since the increase of vascular resistance was counteracted by a reduction of both cardiac inotropism and cardiac output. Vanadium was accumulated in tissues as vanadyl; higher levels were found in the bone and in the kidney, but relevant amounts were determined in aorta, heart and brain. There was evidence, in the rabbits, that vanadium reduces synthesis and/or release of nitric oxide, the endothelium-derived vasodilating factor, likely through a reduced formation from bradykinin. The functional, analytical and morphological results obtained in this study show that chronic exposure to vanadium induces arterial hypertension by mechanisms only in part related to the levels and times of exposure, and to the species.

Animals↗