Biomedical subjects
P Preziosi
Publications and source records attributed to P Preziosi.
Is basic red cell ferritin a more specific indicator than serum ferritin in the assessment of iron stores in the elderly?
Iron status was evaluated in 103 elderly institutionalized individuals using haemoglobin concentration, red cell indices, serum iron, serum transferrin, serum ferritin and basic red cell ferritin. Inflammatory processes were identified by measuring concentrations of orosomucoid and C-reactive protein in serum and leukocyte counts. Anaemia was present in 16.5% of the individuals. No serum ferritin values were in the range of depleted iron stores; however 6% of the elderly individuals presented basic red cell ferritin less than 3 attog/cell (3 x 10(-18) g/cell). Serum ferritin was positively correlated with markers of inflammation. Basic red cell ferritin measurement was not influenced by inflammation and may provide a reliable indicator of iron status in the elderly.
Hydroxyurea: relationship between toxicity and centrally-induced adrenal activation.
The anticancer drug hydroxyurea (HU) at doses of 300-800 mg/kg/day causes a dramatic lethality (up to 100% after a 5-day treatment) in hypophysectomized as well as in adrenalectomized rats drinking physiological saline + 5% glucose. Mortality in controls was less than 10% over a 5-day period. Adrenal stimulatory or replacement therapies protect pituitary- or adrenal-ablated rats against HU toxicity. They also counteract white blood cell changes induced by the drug. HU (30-800 mg/kg) induces a dose-dependent increase of plasma corticosterone in normal rats after single or repeated treatments that is not observed in hypophysectomized animals. HU also increases plasma levels of epinephrine, although this finding cannot account for the rise in plasma corticosterone; indeed, it is secondary to a strong rise in plasma corticosterone. The stimulation of the hypothalamic-hypophyseal-adrenal axis induced by HU is responsible for the drug-induced adrenocortical activation. This activation appears to be a valuable defence mechanism protecting intact rats against HU lethality, and its failure causes the dramatic HU lethality in pituitary- or adrenal-ablated animals.
The fate of nursing education funding.
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Nursing education appropriations.
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Physiologic role of the peripheral enkephalinergic system in regulating cardiovascular homeostasis: evidence of interactions with the renin-angiotensin and kallikrein-kinin systems.
On isolated heart preparation, it was found that Leu5-Enkephalin (Leu5-ENK) did not influence the cardiac function. On the other hand, Leu5-ENK induced a specific dose-related inhibition, in the cardiac perfusate, of the activities of kininase II (KII) and angiotensin converting enzyme (ACE) (but not of kininase I-KI). Instead no detectable alterations of the above enzymatic activities with the used concentrations of Leu5-ENK were observed in vitro. This opioid also increased specifically the effects induced by some of the autacoids, related to both renin-angiotensin and kallikrein-kinin systems, on the KII and ACE activities. A specific correlation between these Leu5-ENK-induced modifications and the functional responses of the heart to the same autacoids was observed. Naloxone (NAL) and more significantly ICI 174864 (ICI) opposed or reversed the inhibitory effect of the used opioid whereas they had neither inhibitory nor synergic effect on both KII and ACE activity by themselves. The possible physiologic role of the enkephalins in regulating cardiovascular function by acting peripherally on some humoral systems through modulatory mechanism was discussed.
Renal ultrastructural alterations and cardiovascular functional changes in rats exposed to mercuric chloride.
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Stress hormone changes after toxic doses of new anticancer drugs.
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Lack of stress-induced neuroendocrine changes after prolonged drinking of acid water in the rat.
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Neuropeptide Y increases the inhibitory effects of clonidine on potassium evoked 3H-noradrenaline but not 3H-5-hydroxytryptamine release from synaptosomes of the hypothalamus and the frontoparietal cortex of the male Sprague-Dawley rat.
The release of 3H-noradrenaline (3H-NA) and of 3H-5-hydroxytryptamine (3H-5-HT) evoked by high-K+ (15 mM) was studied in synaptosomes isolated from the hypothalamus and the frontoparietal cortex of the male Sprague-Dawley rat using a superfusion apparatus. Based on concentration-response curves obtained by analyzing the full-time course of the inhibitory effects of clonidine on 3H-NA and on 3H-5-HT release neuropeptide Y (NPY) (1 nM) was shown to significantly increase the ability of clonidine to inhibit 3H-NA release in synaptosomes isolated from the hypothalamus and from the frontoparietal cortex. NPY (1 nM) alone had no effect on K+-evoked 3H-NA release from these regions. In contrast, NPY (1 nM) did not modulate the inhibitory effects of clonidine on 3H-5-HT release in the above mentioned regions. These results indicate that NPY can increase the sensitivity of the alpha 2-autoreceptors belonging to hypothalamic NA and/or to adrenaline nerve terminals and to cortical NA nerve terminals, while the alpha 2-heteroreceptors inhibiting 3H-HT release in the same brain regions appear not to be regulated by high affinity NPY receptors. Thus, alpha 2-autoreceptors and alpha 2-heteroreceptors appear to be differentially controlled by high affinity NPY receptors at least with regard to regulation of 3H-NA and 3H-5-HT release, respectively.
Different regulation of serotonin receptors following adrenal hormone imbalance in the rat hippocampus and hypothalamus.
Adrenal influence on serotonin (5-HT) transmission in the hippocampal and hypothalamic areas was studied in adrenalectomized rats receiving or not corticosterone replacement. After adrenalectomy, the 5-HT presynaptic receptors were desensitized both in hippocampus and hypothalamus: a significant increase in 5-HT 1 and 5-HT 2 receptor binding numbers took place in membranes from the hippocampus, but not in hypothalamus, while no changes in affinity of receptors to radioligands were observed in either brain area. Corticosterone treatment restored the adrenalectomy-impaired 5-HT autoreceptor sensitivity in hippocampus and hypothalamus and 5-HT density receptor sites in the hippocampus. Serotonin autoreceptor down-regulation following adrenalectomy may increase 5-HT release to maintain the constancy of serotonergic transmission in the brain and 5-HT modulated CRH-ACTH release to compensate the plasma corticosteroid drop. Corticosterone seems to display a distinct tonic control on serotonin transmission in both hippocampus and hypothalamus, the diversity being due to the different roles played by the hormone in these brain regions.
Reduced inhibitory effects of clonidine and neuropeptide Y on 3H-noradrenaline release from synaptosomes of the medulla oblongata of the spontaneously hypertensive rat.
The release of 3H-noradrenaline (3H-NA) evoked by high-K+ (15 mM) was studied in synaptosomes isolated from the medulla oblongata of the normotensive Wistar-Kyoto and spontaneously hypertensive male rat (14 weeks old) using a superfusion apparatus. Based on concentration-response curves clonidine was shown to have a reduced ability to inhibit 3H-NA release in synaptosomes isolated from the spontaneously hypertensive rat (SHR) versus the normotensive rat. Furthermore, only a high concentration of NPY (100 nM) had the ability to enhance the inhibitory effects of clonidine on 3H-NA release in synaptosomes isolated from the medulla oblongata of the SH male rat, while 1 nM of NPY was effective in synaptosomes isolated from the medulla oblongata of the normotensive Wistar-Kyoto rat. These results may indicate a reduced presynaptic alpha 2-adrenoceptor and NPY receptor function to inhibit 3H-NA release from NA and/or adrenaline (A) nerve terminals in the medulla oblongata of the adult 14 weeks old SHR.
Long-term care: the cost/quality debate continues.
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Prolactin-lowering ability of (+/-)-idazoxan may be linked to a central noradrenergic-serotonergic interplay.
2-[2-(1,4-benzodioxanyl)-2-imidazoline] (idazoxan) sometimes lowers basal prolactin levels in the male adult rat, but strongly inhibits hyperprolactinemia in suckling rats. A possible antido paminergic drug effect is not involved, due to its inability to modify prolactin release from superfused pituitary in vitro as well as rat haloperidol hyperprolactinemia in vivo. On the contrary, in the rat idazoxan counteracts hyperprolactinemias due to central presynaptic serotonergic neurotransmission increase (5-hydroxytryptophan, D-fenfluramine and fluoxetine) but not those related to direct agonists at 5-hydroxytryptamine (5-HT) receptor (6-chloro-2-[1-piperazinyl] pyrazine, MK 212; 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane, DOI). (+/-)-Idazoxan does not modify [3H]-5-HT release from isolated hypothalamic synaptosomes. It displays an affinity for alpha-2 adrenergic autoreceptors about 250-fold more than for alpha-2 heteroreceptors located on 5-HT nerve terminals in the central nervous system (pA2 value 9.99, equivalent to a Kb of 0.1 nM vs. pA2 7.60 equivalent to a Kb of 2.5 nM). The noradrenergic outflow selectively induced by idazoxan in the brain may negatively modulate the 5-HT release from the relevant nerve endings, thus preventing prolactin release due to an activation of presynaptic serotonergic axons induced both physiologically (lactation) and pharmacologically (5-hydroxytryptophan, D-fenfluramine and fluoxetine) without influencing hyperprolactinemias related to a direct activation of serotonergic receptors (MK 212 and DOI). Other blocking agents, strong but less selective than (+/-)-idazoxan for noradrenergic brain neurotransmission, do not modify or increase blood prolactin.(ABSTRACT TRUNCATED AT 250 WORDS)
Alpha 2-adrenoceptor blocking properties of idazoxan stereoisomers: stereoselectivity for presynaptic alpha 2-adrenoceptors.
The alpha 2-adrenoceptor blocking properties of idazoxan enantiomers were evaluated at pre- and postsynaptic level. The antagonism of the two idazoxan stereoisomers was assessed, at presynaptic level, by their ability to antagonize clonidine at the alpha 2-adrenoceptors regulating noradrenaline release. The antagonist (+)-idazoxan showed an affinity towards the alpha 2-autoreceptors 40 times higher than that showed by (-)-idazoxan. Binding studies revealed (+)-idazoxan to be 7-8 times more potent than (-)-idazoxan in inhibiting the p-[3H]aminoclonidine binding. These results indicate a different affinity of alpha 2-adrenoceptors for the two idazoxan stereoisomers, thus suggesting that the alpha 2-adrenoceptors located pre- and postsynaptically may be of two stereochemically different subtypes.
Adrenocortical suppression and other endocrine effects of etomidate.
(+/-) Etomidate is a short-acting general anaesthetic given by the intravenous route. It has strong adrenal suppression capability initially shown in the rat and then observed in man. At present, the drug seems the most effective adrenocortical inhibitor on a molar basis in vitro. 11 beta-hydroxylase is the most sensitive target enzyme; 16 alpha-, 17 alpha-hydroxylase and cholesterol side-chain cleavage are inhibited by higher concentrations. (+) Etomidate was more active than the (+/-) and far more than the (-) stereoisomer. Etomidate blood concentrations greatly exceed those needed to block adrenal steroidogenesis both when used inappropriately by infusion for long-term sedation (such previously unrecognized drug-induced adrenal suppression has often proved fatal in severely-injured patients) and also when given in very low doses as an induction anaesthetic. Reactive ACTH increase is currently observed. Etomidate, in vivo, does not appear to affect testicular steroidogenesis although it shares an imidazole moiety with fungicide phenylimidazoles endowed with such an action. However, testosterone production may be reduced by high concentrations in vitro. Other gonadal hormones seem unchanged. Both basal and stress-induced blood prolactin levels are lowered by etomidate in the rat but probably not in man arguably through interference at brain level where the GABA-benzodiazepine receptor complex could be directly involved. Hence, endocrine and neuroendocrine interferences are unique non-anaesthetic effects of etomidate.
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.
Adrenal steroid-induced changes in serotonin receptors in rat hippocampus and hypothalamus.
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