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Biomedical subjects

P Preziosi

Publications and source records attributed to P Preziosi.

At least 181 records · Page 10Linked to original sources
PubMed1988

Effects of the benzazepine SCH 23390 on prolactin release from isolated pituitary.

The benzazepine, SCH 23390 (10(-5) M), is able to block D2 anterior pituitary receptors and their interaction with a maximal concentration of dopamine (10(-7) M) in an experimental setting involving superfused pituitary slices and prolactin release by lactotrophs as a functional model of such receptors; this finding which correlates nicely with binding studies and drug-induced hyperprolactinaemia supports a SCH 23390 D1 dose-related selectivity; given at doses higher than those inducing behavioural changes, the compound may affect D2 receptor-driven functions, e.g. prolactin secretion.

Animals↗
PubMed1988

Nursing: the hospital's competitive edge.

The health care marketplace is becoming increasingly competitive. The hospital has a built-in marketing force with the nursing department, because nurses are in constant, direct contact with the customer. Nursing must identify the case mix profile of the community and focus the hospital product lines to meet community needs. The nursing department should decentralize, change, measure, and innovate the staff mix needed to operationalize these product lines. The development of nursing practice standards for the case mix will help to identify the staff mix needed and create systems to efficiently manage the product lines. Nursing management must become aware of cross-subsidization and downward skill substitution of nursing personnel. Nursing information systems must generate quality reports that invoke cost consciousness on the part of nursing staff. Quality assurance programs must become unit based and complete with frequent audits to correlate length of stay with nursing quality. Correlations must be determined between nursing productivity and case mix to determine the hospital's niche in the marketplace. The transformation of health care into a competitive business industry has created many opportunities for nursing. The health care industry's incentives for efficiency along with the decreasing demand for inpatient hospital services will be the forces driving health care toward a competitive marketplace. The hospital's nursing department should be strategically positioned to become accountable for increasing market share and enhancing quality patient outcomes. The focus has shifted from the theoretical to the tactical, which is a step in the right direction, particularly for nursing. Nursing, if strategically positioned, will not only thrive but will also excel in this chaotic environment by capturing the opportunities and being innovative.

Consumer Behavior↗
PubMed1987

Acid rain: effects on arachidonic acid metabolism in perfused and ventilated guinea-pig lung.

Isolated, perfused and ventilated guinea-pig lungs were exposed for 10 min to acid (sulphuric + nitric acid) aerosol mimicking acid rain at pH 4.5 or 2.5, as well as to a control distilled water aerosol (pH 6.0-6.5). Lung perfusing solution was recovered and thromboxane (TX) B2 and leukotriene (LT) B4 were measured by radioimmunoassay (RIA) techniques. In a series of experiments TXB2 release averaged 0.43 +/- 0.18 (+/- SD) ng/min during exposure to distilled water aerosol and increased to 0.70 +/- 0.30 ng/min during exposure to acid aerosol at pH 4.5 (P less than 0.05). In a second series of experiments TXB2 release was 0.46 +/- 0.18 ng/min and increased to 1.07 +/- 0.51 ng/min (P less than 0.01) after acid aerosol at pH 2.5. In both cases LTB4 release, reflecting lipoxygenase activity, was unchanged. LTC4 levels were not measurable under basal conditions as well as after exposure to acid aerosol. A pneumoconstriction was also observed, being more pronounced after acid aerosol at pH 2.5. Individual sulphuric and nitric acid aerosol component solutions at pH 2.5 evoked TXB2 and airway resistance changes corresponding to those observed with the mixed acid aerosol. LTB4 was not modified. Acid rain inhalation may directly stimulate pathways leading to the bronchoconstrictor and pro-aggregating TXA2 synthesis in isolated guinea-pig lung, without affecting the lipoxygenase pathway of arachidonic acid metabolism.

Aerosols↗
PubMed1987

Electrophysiological studies of the effects of the general anaesthetic etomidate on frog myelinated nerve fibre.

The effects of the general anaesthetic etomidate (0.1 to 1 mM) upon the node of Ranvier of frog isolated nerve fibres were investigated under current and voltage clamp conditions. When added to the external solution, etomidate reversibly decreased the amplitude of the action potential. The action potential block, induced by the drug, was reversed by increasing the membrane potential. Etomidate rapidly and reversibly blocked the Na current with an apparent dissociation constant of 0.6 mM. In the presence of the drug, the steady-state inactivation-voltage curve of the Na current was shifted towards negative voltages. The block of Na current by etomidate was partially removed by repetitive depolarization preceded by a 50 ms period of hyperpolarization. In contrast, the block was enhanced when the repetitive depolarization was not preceded by hyperpolarization. This suggests that Na channels were preferentially blocked by the drug in the inactivated state. The K current was reversibly blocked by etomidate with an apparent dissociation constant of 0.2 mM. In the presence of the drug, the K current showed an apparent fast inactivation suggesting that K channels were blocked in the open state. We conclude that at higher concentrations than those attainable in the mammalian brain following single anaesthetic doses the general anaesthetic etomidate has a "local anaesthetic-like' action on the peripheral nervous system.

Action Potentials↗
PubMed1986

[Echographic study in evaluating gastrointestinal pathology].

The echographic study of the gastrointestinal tract is hampered by the presence of gas that prevents the long-range penetration of the ultrasound beam. However the presence of a mass with a central echogenic region surrounded by a sonolucent wall of over 1.5 cm is characteristic of intestinal pathologies. A study of 23 patients with gastrointestinal disorders in whom echography revealed specific pictures is presented.

Appendicitis↗
PubMed1986

Perfused and ventilated guinea-pig lung: a method for evaluating xenobiotic effects on arachidonic acid using formaldehyde.

Lipoxygenase as well as cyclooxygenase pathways of arachidonic acid (AA) metabolism are involved in antigen-induced bronchoconstriction in ovalbumin-sensitized guinea-pig lungs. Chemical lung challenge induced by aerosol containing formaldehyde (5 ppm up to 20 ppm) was effective in increasing thromboxane (TX) B2 release in a dose-dependent manner, without affecting leukotriene (LT) release. This suggests that xenobiotics acting by non-immunologic mechanisms on bronchial mucosa may stimulate the cyclooxygenase pathway of AA metabolism, which, in turn, might cause bronchial and/or lung parenchymal effects of pathophysiological relevance.

Animals↗
PubMed1986

Neuropeptide Y enhances the inhibitory effects of clonidine on 3H-noradrenaline release in synaptosomes isolated from the medulla oblongata of the male rat.

In studies on superfused synaptosomes from the rat medulla oblongata, the inhibitory effects of the alpha 2-adrenergic agonist clonidine (0.1 microM) on potassium (15 mM K+) induced 3H-noradrenaline (NA) release was potentiated by 20%, when neuropeptide Y was added to the system. The effect of NPY was detectable at low concentrations (1 nM) and was not dose-dependent. Neuropeptide Y alone produced no significant effects on 3H-NA release. The results may indicate the existence of a presynaptic NPY receptor on the noradrenaline and/or adrenaline nerve terminals, which may enhance the presynaptic alpha 2-adrenoreceptor function to inhibit 3H-NA release.

Animals↗
PubMed1985

Rat brain alpha 2-pre- and postsynaptic receptors are different or differently modulated?

In order to get better characterization of alpha 2-pre- and postsynaptic noradrenergic receptors in the rat brain, we investigated the alpha 2-receptor changes which take place during a 12-day treatment with the alpha 2-antagonists yohimbine (4 mg/kg) and mianserin (10 mg/kg). These treatments caused a significant increase in the sensitivity of hypothalamic synaptosomes to the inhibitory action of the noradrenergic agonist clonidine on the 3H-noradrenaline release elicited by K depolarization. Frontal cortex alpha 2-autoreceptors were not affected by drug treatments. However, the 3H-p-aminoclonidine (3H-PAC) binding to membranes from hypothalamus or frontal cortex from treated animals was the same as in controls. Changes in neural firing, elicited by the alpha 2-antagonists on noradrenergic neurons, could explain our results. The presynaptic autoreceptors may thus become hypersensitive to counteract the enhanced neurotransmitter release in the hypothalamus, where the noradrenaline is accumulated at the synaptic cleft. In the frontal cortex, where it seems that only 5% of the noradrenergic terminals make synaptic contacts with postsynaptic elements, the alpha 2-autoreceptors are less sensitive to an enhanced neurotransmitter release. Alternatively, they have scarce functional importance because the noradrenaline release is effectively modulated by the inhibitory recurrent locus coeruleus collaterals. At the postsynaptic level, the receptor down-regulation might be prevented by chronic presence of the antagonist drug. Thus the different behavior between pre- and postysynaptic alpha 2-receptors and between alpha 2-receptors of different brain areas may be ascribed to a different modulation rather than to different molecular arrangements.

Adrenergic alpha-Agonists↗
PubMed1985

Combined ultrasounds and CEA in preoperative assessment of hepatic metastases from gastrointestinal malignancies.

A consecutive series of 100 patients affected by gastrointestinal malignancies entered a prospective controlled study of liver metastases performed by ultrasound echography, CEA, hepatic enzymes (only alkaline phosphatase (AP) was found to be somehow significant). Laparotomic inspection and palpation were taken as objective control of ultrasound scan. Eighteen out of the 100 patients showed diffuse hepatic metastases at surgery (all controlled histologically). Hepatic echography correctly diagnosed liver metastases in 15 out of these 18 patients (= 83.8% sensitivity); two more cases (hepatic fibroangiomas) were interpreted as metastases (= 89.9% specificity). CEA-RIA assay was pathologic (greater than 10 ng/ml) in all of the 18 patients with liver metastases; 21 out of the 82 without liver metastases were CEA positive (difference of mean values statistically significant at P less than 0.01). The only significant hepatic enzyme was AP, which was pathologic in 12 out of 18 patients with liver metastases. The comparative evaluation of the three tests showed that ultrasound scanning missed three cases of diffuse hepatic metastases, which, however, were CEA positive, while AP could not help to correct such misdiagnosis.

Adult↗
PubMed1985

Hepatic staging in operable breast cancer: a reappraisal from a prospective study.

A consecutive series of 100 patients affected by breast cancer and referred for surgical treatment were studied for the eventual spread of the tumour to the liver (echography, carcinoembryonic antigen [CEA], hepatic enzymes). Hepatic echography was positive in five cases: two also had bone and skin metastases at the time of diagnosis, and one was a case of remastectomy (these three patients died rather quickly of the disease); the remaining two patients are free of the disease 24 months after surgery and thus should be considered false-positive cases. Hepatic enzymes were not significant. The same was true for CEA except in nine cases with levels much greater than 20 ng/ml (six of these had early local and/or distant metastases). It is concluded that the usefulness of routine hepatic echography before locoregional treatment of breast cancer is rather limited. CEA much greater than 20 ng/ml may be useful prognostically.

Alanine Transaminase↗
PubMed1985

Possible adrenal involvement in hydroxyurea toxicity defense mechanisms.

Changes in blood biochemistry, resembling adrenocortical hyperfunction, induced by oral administration with hydroxyurea (HYD) at a dosage of 800 mg/Kg/d for 5 days (K+ and total protein decrease, total cholesterol increase) are not modified or enhanced (total protein) by adrenalectomy. Adrenalectomy dramatically enhanced the decrease of WBC and neutrophils normally induced by HYD. Replacement therapy with corticosterone attenuated and/or delayed the above changes. Normally-functioning adrenocortical tissue may play a role in protection against HYD haematological toxicity in the rat and the drug-induced hypothalamus pituitary mediated adrenocortical activation seems to represent a mechanism capable of counteracting drug toxicity.

Adrenalectomy↗
PubMed1985

Replacement therapy against increased hydroxyurea toxicity in pituitary or adrenal ablated rats.

The main rat adrenocortical hormone, corticosterone, the mineralocorticoid, 11-deoxycorticosterone (DCA) acetate given alone or together (2:1 ratio) twice daily at doses of 2-4 and 1-8 mg/kg, DCA enanthate given in a single injection of 20 mg/kg 0-3 days before the beginning of the experiments and a highly-concentrated injectable extract of the adrenal cortex (4 mg/kg as hydrocortisone twice a day) given by the intramuscular route, delay and partially protect against the increased toxicity following administration of the anticancer drug, hydroxyurea (800 mg/kg/day for 5 days) in adrenalectomized or hypophysectomized animals (80-100% lethality; in control non ablated rats 0-10% lethality). ACTH1-24 (tetracosactide) also proved effective in pituitary ablated rats. The best protection was afforded with the joint administration of corticosterone and DCA (2-4 and 1-2 mg/kg twice a day) or with corticosterone alone at doses (4 mg/kg twice a day) capable of giving plasma levels, six hours after administration on the third day, similar to those observed in non ablated rats receiving HYD in the morning. The adrenocortical hormones may replace a possible unique defense mechanism against drug toxicity, which is lacking in pituitary or adrenal ablated rats.

Adrenalectomy↗
PubMed1984

Long-term treatment with clonidine and alpha-receptors in the brain of normotensive rats.

The aim of the present study was to investigate whether or not changes in rat brain alpha-adrenoceptors take place during chronic treatment with a low dose of clonidine. Male Wistar normotensive rats were treated with clonidine (0.1 mg/kg)i.p. twice daily for 12 days. This treatment caused a significant increase in [3H]clonidine and in [3H]WB4101 binding, respectively, to alpha 2- and to alpha 1-adrenoceptors of the frontal cortex; the levels were 30% for [3H]clonidine and 20% for [3H]WB4101. The Scatchard analysis of data obtained in binding studies indicated that the enhanced binding of two ligands to membranes prepared from chronically clonidine-treated animals, was due to an apparent increase in the number of binding sites. These changes were seen 4 h after administration of the last treatment, before the appearance of the withdrawal syndrome. However, noradrenergic alpha 2-autoreceptors of synaptosomes, from the frontal cortex and hypothalamus of treated animals, were sensitive to the regulatory action of clonidine or of noradrenaline on the [3H]noradrenaline overflow elicited by high K+ as well as on the control animals. On the contrary, the alpha 2-receptors on the serotoninergic nerve terminals from the frontal cortex of treated animals were more sensitive than those of control animals to the action of clonidine or of noradrenaline in counteracting the [3H]5-hydroxytryptamine overflow elicited by high K+. These results suggest that during treatment with clonidine no autoreceptor hyposensitivity to the regulatory action of clonidine or noradrenaline on [3H]noradrenaline overflow elicited by high K+ takes place, but, as a consequence of the diminished noradrenaline availability at the synaptic cleft, the binding of [3H]WBA101 to alpha 1-receptors and of [3H]clonidine to pre- and postsynaptic alpha 2-receptors were significantly elevated in the frontal cortex, a brain areas where the alpha-2-receptors are mainly postsynaptic. Thus, the neurotransmitter concentration in the synaptic cleft may be responsible for the trans-synaptic modulation of the alpha 2-adrenoceptor postsynaptic population. In fact, the alpha 2-adrenoceptors which are presynaptically located on the serotoninergic terminals, but are postsynaptic in relation to the noradrenergic neurons, also show increased sensitivity after chronic clonidine treatment.

Animals↗
PubMed1984

Antitumour drug toxicity in pituitary or adrenal-ablated rats.

Hypophysectomy or adrenalectomy increase the toxicity of the antitumour drug hydroxyurea (HYD) given by the oral route at daily doses/kg over 5 days, 10 times higher (10 Htd) than that employed in daily schedules for humans (100% and 85% lethality against 0% in intact controls). No differences were found between intact or hypophysectomized rats in their ability to tolerate a 5-day treatment with 1 Htd HYD given orally, 1-10 Htd of procarbazine (i.v.) and cisplatinum (i.v.) at a dose per kg/day equivalent to that recommended for protocols providing daily drug schedules in humans. L-asparaginase (10 Htd) induce 45% lethality in adrenalectomized animals. All the above drugs in intact rats induce significant (p less than 0.01) adrenocortical activation after single, and in the case of hydroxyurea after 5-days, treatment at the above dosages. Replacement therapy with corticosterone may reduce HYD toxicity in adrenalectomized (20% lethality) but less so (90% lethality) in hypophysectomized rats.

Adrenalectomy↗
PubMed1984

Tolerance to pituitary-adrenal axis activation by anticancer drugs in normal and tumour-bearing rats.

Cisplatinum given intravenously (i.v.), hydroxyurea given orally (os), procarbazine (os) and L-asparaginase (i.v.), on a decreasing scale, produce significant (p less than 0.01) adrenocortical activation over 4-h period at a single dose per kg 10 times higher than those employed in human therapy. Only hydroxyurea retained this activity after a 5-day treatment both in normal and Walker carcinosarcoma-bearing rats. Adrenocortical activation depends on the presence of pituitary ACTH both after single or repeated treatments.

Adrenal Cortex↗