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Biomedical subjects

P Boscolo

Publications and source records attributed to P Boscolo.

At least 19 recordsLinked to original sources
PubMed1994

Renal toxicity and arterial hypertension in rats chronically exposed to vanadate.

The effects of 1, 10, or 40 micrograms/ml of vanadium, given for six or seven months as sodium metavanadate in drinking water on cardiovascular and biochemical variables and the electrolyte metabolism of male Sprague-Dawley rats were investigated. At the end of the exposure period, all animals exposed to vanadate had increased systolic and diastolic blood pressure. This effect was not dose dependent and heart rate and cardiac inotropism were not affected. The role of defective renal function and electrolyte metabolism in such effects was supported, in the rats exposed to 10 and 40 ppm of vanadium, by the following changes: (a) decreased Na, + K(+)-ATPase activity in the distal tubules of nephrons; (b) increased urinary excretion of potassium; (c) increase in plasma renin activity and urinary kallikrein, kininase I, and kininase II activities; (d) increased plasma aldosterone (only in the rats treated with 10 ppm of vanadium). The alterations in the rats exposed to 1 ppm of vanadium were: (a) reduced urinary calcium excretion; (b) reduced urinary kallikrein activity; (c) reduced plasma aldosterone. These results suggest that blood hypertension in rats exposed to vanadate depends on specific mechanisms of renal toxicity related to the levels of exposure.

Animals↗
PubMed1992

Zinc and copper in tissues of rats with blood hypertension induced by long-term lead exposure.

Male Sprague-Dawley rats received for 14 months 0, 15, 30 and 60 micrograms/ml of lead in drinking water. Both blood pressure and tissue lead were augmented with a dose-response effect, while cardiac inotropism was increased only in the rats treated with 60 ppm of lead. In the exposed animals, zinc and copper were unchanged in kidneys and testicles and augmented in the brain, while copper, but not zinc, was reduced in the heart. These data suggest a possible relation between the modifications of copper and zinc metabolism and the effects of lead on cardiovascular homeostasis.

Administration, Oral↗
PubMed1992

Renal mechanisms in the cardiovascular effects of chronic exposure to inorganic mercury in rats.

Male weanling Wistar rats received 200 micrograms/ml of mercury (Hg), as HgCl2, in drinking water for 180 days. At the end of the treatment, systemic arterial blood pressure was augmented, cardiac inotropism was reduced, and heart rate was unchanged. Light and electron microscopical studies of the kidney showed a mesangial proliferative glomerulonephritis in about 80% of the glomeruli. Tubular cells showed reduction of the acid phosphatase activity, which was related to functional abnormalities of the lysosomes. In the 24 hour urine samples of the Hg exposed rats, there was slight reduction of kallikrein activity, but evident proteinuria was not present in all samples. Plasma renin activity was reduced, that of angiotensin I-converting enzyme was augmented, and plasma aldosterone concentrations were unchanged. Mercury was accumulated mostly in the kidney of the Hg treated animals; and the content of Hg in the heart was higher than in the brain. These data show that chronic exposure to Hg acts on the kidney with complex mechanisms of toxicity; these contribute to modify systemic haemodynamics.

Animals↗
PubMed1988

Ultrastructure of the testis in rats with blood hypertension induced by long-term lead exposure.

Male Sprague-Dawley rats received 60 micrograms/ml of lead (as acetate) in drinking water for 18 months. Their blood pressure and cardiac inotropism were increased. Lead was augmented in blood, kidney and brain, but not in testis. Examination by light microscopy of the organs did not reveal alterations. Ultrastructural examination of the testis with both transmission and scanning electron microscopy (EM) did not evidence modifications in the external part of the seminiferous tubules, in the spermatogenetic cells and in the connective tissue including the Leydig cells; only Sertoli cells presented increased size of lysosomes.

Animals↗
PubMed1988

Neurohumoral blood pressure regulation in lead exposure.

Previous human studies demonstrated that lead exposure may modify the metabolism of catecholamines and of hormones controlled by the hypothalamo-pituitary axis and may affect the kallikrein-kinin system. This paper reports unpublished data on the plasma renin activity of lead-exposed workers; these results are in agreement with those of previous human and experimental studies suggesting that the synthesis or release of renin is increased after short and moderate exposure to inorganic lead and reduced whenever the exposure is prolonged. Previous experimental investigations demonstrated that lead may act on the cardiovascular system, with effects on the renin-angiotensin system, on the reactivity to stimulation of peripheral catecholaminergic receptors, on sympathetic and vagal tone, and on reactivity to the stimulation of baroreceptors. This paper reports the results of a study on male Sprague-Dawley rats that received 0, 15, 30, and 60 micrograms/mL of lead in drinking water for 18 months. Blood pressure was increased in the rats receiving 30 and 60 ppm of lead; cardiac inotropism was augmented only in those receiving the higher dose of the metal, and heart rate was not modified. Cardiovascular responses to agonists indicated that lead exposure affects the renin-angiotensin system and induces sympathetic hyperactivity by acting on central and peripheral sympathetic junctions increasing the responsiveness to stimulation of alpha 2-adrenoreceptors and by increasing the reactivity to stimulation of cardiac and vascular beta-adrenergic and dopaminergic receptors. The cAMP-dependent availability of Ca2+ for contractile mechanisms of the cardiovascular muscle cells was affected by lead.

Animals↗
PubMed1988

[Health status of journalists and organization of work in a national daily newspaper].

A multidisciplinary investigation was performed on 173 reporters (53 men and 20 women) of a newspaper. The microclimate and illumination conditions of the main seat, in which the use of VDT was beginning, were satisfactory, although not all the instruments were correctly adjusted. A very low percentage of reporters working in the main center was suffering from arterial hypertension indicating the presence of the "healthy worker effect". The values of plasma cortisol and arterial blood pressure of 10 reporters of the main seat, except two cases, changed normally during the evening hours. It is to point out that among the reporters there was significant correlation between spondylosis and astigmatism. The psychological investigation evidenced that the reporters were aggressive, eager of success and with constant attention. The EMG biofeedback demonstrated in the reporters with a more prolonged period of employment nervous tension and difficulty in relaxing. Particularly, in the reporters of the main center, the Stait-Trait Anxiety Inventory was more altered than in those of the peripheral seats.

Adult↗
PubMed1988

[Postoperative radiotherapy in the treatment of breast tumors. Evaluation of a 5-year case series].

Between January 1981 and December 1985, 364 female patients underwent surgical treatment for breast cancer in Mestre General Hospital. The pathological stage of the disease was stage I in 60 patients, stage II in 215 patients, stage III A in 30 patients, stage III B in 44 patients and stage IV in 15 patients. The patients with T1-T2 N0 lesions located in the outer quadrants received no additional treatment after surgery, while the others received adjuvant therapy. The patients with stage-IV disease (M+) were treated with chemo and/or hormonotherapy. All patients were followed for an average of 33 months up to December 1986 (range 1-71 months). Local-regional relapses developed in 17 patients, 15 on the chest wall and 2 in the drainage lymph nodes (only 7 within the previously-treated area). A 5-year actuarial survival rate was observed of about 78%, and 66% of relapse-free survival, in the whole group of patients (100% and 92% in stage I; 92.5% and 76% in stage II; 51% and 33% in stage III A; 32% and 19% in stage III B; 31% in stage IV, respectively). As far as our series of patients is concerned, the massive involvement of axillary lymph nodes seems to be the most adverse prognostic factor in survival rates. Even though the short follow-up does not allow definitive conclusions to be drawn, the authors believe such loco-regional treatments as surgery and radiation therapy to be extremely important in the local control of breast cancers, as well as in the patients' survival in the long run.

Adult↗
PubMed1986

Mechanisms of cardiovascular regulation in male rabbits chronically exposed to cadmium.

Male rabbits received 20 micrograms/ml of cadmium in drinking water for nine months. At the end of the treatment aortic vascular resistance was increased, whereas maximum rate of increase in left ventricular pressure, aortic blood flow, stroke volume, cardiac output, left ventricular minute work, and left ventricular stroke work were reduced. Arterial blood pressure, heart rate, and the index of myocardial oxygen consumption were not modified. The exposed rabbits also showed reduced pressor responses to vagotomy, increased cardiovascular responses to angiotensin I and II and isoprenaline, and lower responses to serotonin and guanethidine; the bradycardia induced by clonidine was augmented; the cardiovascular effects of bilateral carotid occlusion, hexamethonium, phenylephrine, histamine, acetylcholine, tyramine, papaverine and verapamil were unaltered. In the treated rabbits cadmium was appreciably higher in the kidney than in the heart; however, renal concentrations of cadmium were lower than those reported as critical for workers exposed to cadmium. Zinc was increased in the kidney but not in the heart, whereas copper remained unchanged in the examined organs. In rabbits treated with cadmium the increased aortic vascular resistance and the reduced myocardial contractility contribute to preserve a haemodynamic equilibrium without alteration of blood pressure and heart rate; the question of whether a similar condition may be present in people exposed to cadmium with normal cardiovascular parameters is discussed.

Animals↗
PubMed1985

Metabolic fate and cardiovascular effects of arsenic in rats and rabbits chronically exposed to trivalent and pentavalent arsenic.

Male rats and female rabbits exposed for eighteen and ten months, respectively, to 50 micrograms/ml of trivalent arsenic (As III) in drinking water showed reduction of stroke volume (SV) and cardiac output (CO) and increase of vascular resistance (VR), while no cardiovascular change was observed in male rats receiving 50 micrograms/ml of pentavalent arsenic (As V) for eighteen months. The exposed animals showed specific alterations in some neurohumoral and effector mechanisms regulating cardiovascular function (CF). Elevated levels of urinary As were found in all treated groups. However, there were significant differences in the urinary levels of dimethylarsenic acid (DMA), monomethylarsenic acid (MMA) and inorganic As, which depended on both animal species and the valency state of As. Thus, As(III) was methylated to a greater extent than As(V) in rats, with less elimination of inorganic As, while rabbits had a lower capacity to methylate As and to retain As in tissues than rats. Either cardiovascular effects or metabolism of As seemed to depend on its valency state and animal species.

Animals↗
PubMed1985

Long-term exposure to cadmium and cardiovascular alterations in the rabbit.

Some mechanisms regulating cardiovascular function (CF) were investigated in male rabbits exposed for ten months to 20 micrograms/ml of cadmium (Cd) in drinking water. Cd reduced cardiac inotropism (CI), increased aortic vascular resistance (AVR) and altered cardiovascular reactivity by acting on renin-angiotensin, serotonin, sympathetic and vagal parasympathetic systems. Cd levels were higher in the aorta than in the heart. Renal Cd content was lower than that reported as critical for Cd-exposed workers. Zinc (Zn) was increased only in the kidney and copper (Cu) was unchanged in the organs studied. It was shown that humoral, neurogenic and metabolic mechanisms are involved in the Cd-induced alterations of CF.

Animals↗
PubMed1984

Cardiovascular responsiveness to physiological agonists of male rats made hypertensive by long-term exposure to cadmium.

The mechanisms by which cadmium may affect cardiovascular regulation are controversial. In this study, we investigated haemodynamics and cardiovascular reactivity to various physiological agonists in anaesthetized male Sprague-Dawley rats which received, for 190 days, deionized drinking water containing 0 (control), 10 and 20 micrograms/ml of cadmium (as acetate). Systolic and diastolic blood pressure, as well as cardiac inotropism, were increased in a similar manner in the two groups of treated rats. Heart rate was reduced in the rats exposed to the higher dose of cadmium, while no electrocardiographic alteration was demonstrated. Cadmium exposure reduced the pressor responses following intravenous norepinephrine (0.25-1 microgram/kg), angiotensin I (0.25-1 microgram/kg) and higher doses of epinephrine (0.50 and 1 microgram/kg) as well as the depressor responses to bradykinin (0.40-1.6 microgram/kg). On the other hand, the exposed rats showed an increased vascular responsiveness to the beta-adrenoceptor stimulating effects of lower doses of epinephrine (0.125 and 0.25 microgram/kg). Moreover, the effects on blood pressure, heart rate and cardiac inotropism of graduated doses of intravenous acetylcholine, angiotensin II, histamine and serotonin were unchanged. Cadmium was accumulated in the kidney of the treated rats at levels similar to those found in exposed humans. Renal copper and zinc were also augmented, possibly in relation to the cadmium-induced synthesis of metallothionein, a protein able to bind different metals. On the whole, this study suggests that cadmium affects several neurohumoral mechanisms that regulate cardiovascular function. It is likely that the changes in these mechanisms have additive effects, under a possible influence of genetic and/or environmental variables, in determining cardiovascular alterations.

Acetylcholine↗
PubMed1984

Cardiovascular homeostasis in rats chronically exposed to mercuric chloride.

Two groups of male Sprague-Dawley rats received from weaning 50 micrograms/ml of mercury as mercuric chloride (HgCl2) in drinking water for 320 and 350 days. Hg exposure increased cardiac inotropism, without chronotropic changes, in both groups, and induced arterial hypertension in the rats exposed for 350 days. In the exposed rats, cardiovascular responses to the stimulation of peripheral alpha and beta adrenoceptors were decreased and increased, respectively, possibly through a reduced intracellular availability of calcium ions for contractile mechanisms. Hg exposure did not affect either vagal or sympathetic activity or cardiovascular reactivity to several physiological agonists. On the other hand, Hg exposure induced baroreflex hyposensitivity and produced a drastic alteration of the levels of copper and zinc in brain and kidney.

Animals↗
PubMed1983

Mechanisms in cardiovascular regulation following chronic exposure of male rats to inorganic mercury.

In this study we verified the possibility that chronic exposure to inorganic mercury may induce hemodynamic changes in the rat by affecting some neurogenic and/or humoral mechanisms regulating cardiovascular function. For this reason, aortic blood pressure, maximum rate of rise of the left ventricular pressure, heart rate, and electrocardiogram were monitored under pentothal anesthesia in rats which received 50 micrograms/ml of mercury (as HgCL2) in drinking water for 320 days and in control rats. No pressor or electrocardiographic changes were found in mercury-treated animals, which showed increase of cardiac inotropism and decrease of the pressor and inotropic responses to bilateral carotid occlusion. Cardiovascular responses to bilateral vagotomy and iv hexamethonium under vagotomy were unchanged in the mercury-exposed rats. In these animals both pressor and inotropic responses to iv norepinephrine and to higher doses of epinephrine were reduced, while the vascular beta-adrenergic response to 0.125 micrograms/kg of iv epinephrine was potentiated. Cardiovascular responses to acetylcholine, angiotensin I, angiotensin II, bradykinin, histamine, and serotonin did not differ in the two groups of rats. These results indicated that chronic mercury exposure affects cardiovascular function by interfering with the baroreflex mechanisms and/or the reactivity to catecholamines. Higher amounts of mercury were found in kidney, but the metal was significantly accumulated also in urine, blood, and brain. Mercury exposure greatly increased the levels of copper and zinc, but not that of iron, in brain and kidney. The increased accumulation of copper and zinc in tissues may be related in part to the mercury-induced synthesis of metallothionein, a protein able to bind these essential metals. It may be suggested that zinc and copper interact with mercury in inducing cardiovascular changes.

Animals↗
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↗