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Biomedical subjects

M Vacca

Publications and source records attributed to M Vacca.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Arrhythmia recurrence in patients with an old myocardial infarct treated by implantable defibrillator: an analysis according to the initial clinical presentation].

INTRODUCTION AND OBJECTIVES: The importance of the clinical presentation in the frequency and type of recurrences of ventricular arrhythmias in patients that received an automatic implantable defibrillator is not well known. The purpose of this study was to analyze the frequency and type of recurrences in patients with an old myocardial infarction that received an automatic implantable defibrillator with electrogram recording. METHODS AND RESULTS: We analyzed 100 patients classified in 3 groups according to their clinical presentation: Sustained Monomorphic Ventricular Tachycardia (VT Group n = 65), Cardiac Arrest (CA Group = 19), and Syncope (Syncope Group n = 16). There were no significant differences in the clinical variables among the different groups, nor in the inducibility of arrhythmia at the electrophysiologic study. In a follow-up 27 +/- 14 months, 54% of patients presented at last one episode of sustained ventricular arrhythmia. All recurrences except one were as sustained monomorphic ventricular tachycardia (776 episodes). 81% of episodes of sustained monomorphic ventricular tachycardia (630) were treated with antitachycardia pacing with an effectiveness of 89%. There were no differences in the probability of arrhythmic recurrence among groups but death probability was higher in the ventricular fibrillation group at 36 follow-up months (38% vs 7% and 12% in the sustained monomorphic ventricular tachycardia and syncope groups respectively, p = 0.0113). CONCLUSIONS: In the patients with an old myocardial infarction and malignant ventricular arrhythmias, most of recurrences are due to sustained monomorphic ventricular tachycardia independently of the clinical presentation. The antitachycardia pacing is not only effective in patients with documented sustained monomorphic ventricular tachycardia but also in those that are presented as cardiac arrest or syncope.

Aged↗
PubMed1998

Postoperative adhesion prevention with low-dose aspirin: effect through the selective inhibition of thromboxane production.

The aim of the present study was to evaluate the efficacy of low-dose versus high-dose aspirin in the prevention of postoperative adhesion formation. Forty New Zealand White rabbits were randomized into three groups: low-dose aspirin (1.7 mg/kg per day for 5 days starting on the day of surgery), high-dose aspirin (28.0 mg/kg per day), and controls. The rabbits underwent a standardized surgical injury on the ovary, uterine horn and abdominal wall on one side at laparotomy. On postoperative day 21, a second-look laparotomy was performed for the evaluation of postoperative adhesions. In five animals in each group, peritoneal fluid samples were collected at initial surgery, then through an additional 2 cm incision performed on postoperative day 3, and at second-look laparotomy. The peritoneal concentrations of thromboxane B2 and 6-keto-prostaglandin F1alpha (the stable hydrolysis product of prostacyclin) were measured by radioimmunoassay. At second-look laparotomy, the adhesion formation rate was 46% in the low-dose aspirin group, 77% in the high-dose group, and 100% in the control group. The adhesion score in the low-dose group was significantly lower (P < 0.01) than in the high-dose and control groups. Peritoneal thromboxane decreased significantly during treatment in both low-dose and high-dose aspirin groups, whereas prostacyclin decreased only in the high-dose group. Postoperative adhesion reduction observed in this study with low-dose aspirin treatment could be due to the selective inhibition of thromboxane over prostacyclin production.

Abdominal Muscles↗
PubMed1996

Interleukin-1 beta specifically stimulates nitric oxide production in the hypothalamus.

In previous experiments we have shown the role of nitric oxide (NO) in basal and interleukin-1 beta (IL-1 beta)-induced CRH and ACTH release in vitro. Now, we have studied the possible production of NO from hypothalamic cell cultures, particularly after IL-1 beta stimulation or L-NOArg inhibition, by high performance liquid chromatographic (HPLC) assay of L-citrulline production, adding further evidence for a role of NO in IL-1 beta activity in the hypothalamus.

Animals↗
PubMed1996

Low-Dose Aspirin to Prevent Postoperative Adhesion Formation in the Rabbit Model

Among the various agents used to prevent postoperative adhesion formation, nonsteroidal antiinflammatory drugs (NSAIDs) have recently gained wide attention because of the relative lack of side effects compared with traditional antiinflammatory agents, namely, corticosteroids. The inconsistency of data published in the literature for the adhesion prophylactic effect of NSAIDs could be related to the different compounds and dosage regimens. We evaluated the efficacy of intramuscular acetylsalycilic acid (ASA) administered perioperatively for 5 days in two regimens: low-dose (L-ASA) 1.7 mg/kg/day, and high-dose (H-ASA) 28.0 mg/kg/day, versus no perioperative treatment (controls) in 24 New Zealand white female rabbits undergoing conservative pelvic surgery in a randomized trial. At second look, the adhesion score was significantly lower in the L-ASA animals than in the H-ASA and control groups. The adhesion score in the H-ASA group was lower, although not significantly, than in the control group. We conclude that the inhibition of postoperative adhesion formation observed with L-ASA could be due to the selective inhibition of thromboxane A2 over prostacyclin.

Journal Article↗
PubMed1996

Production of Prostaglandin F2alpha by the Different Forms of Endometriosis

It has been suggested that atypical, nonpigmented endometriotic lesions have an increased capacity to synthesize prostaglandin (PG)F2alpha compared with typical endometriosis, and could therefore represent the more active forms of the disease. We took biopsy specimens of various endometriotic lesions and of normal endometrium and peritoneum during operative laparoscopy in 12 infertile women. The specimens were transferred in flasks containing Krebs solution and placed in a shaking incubator for 1 hour at 37&deg; C. The incubation solution was changed every 20 minutes and assayed by radioimmunoassay procedures for the concentration of PGF2alpha. Biopsy specimens from normal peritoneum and normal endometrium were also taken from five control patients with no evidence of endometriosis. The PGF2alpha concentration/milligram of tissue was not significantly less different between typical and atypical implants, and among the different atypical forms. Endometriotic cyst wall produced significantly less PGF2alpha than both typical and atypical peritoneal implants, and significantly more than normal peritoneum. There was no difference in production for normal tissue (endometrium or peritoneum) between patients with endometriosis and controls. We did not confirm evidence from the literature of a higher production of PGF2alpha in atypical versus typical endometriotic lesions. Our data do not support selective ablation of atypical forms, since typical endometriotic lesions could be similarly active in prostaglandin production.

Journal Article↗
PubMed1995

A possible role for nitric oxide but not for prostaglandin E2 in basal and interleukin-1-beta-induced PRL release in vitro.

In previous experiments we have shown that nitric oxide (NO) was able to modulate CRH and ACTH release from cultured rat hypothalamic and anterior pituitary cells, in vitro. Now, we show experimental evidence of an involvement of NO in basal and interleukin-1 beta-induced prolactin (PRL) release. L-NG-nitro-arginine, an inhibitor of nitric oxide synthetase, and hemoglobin, a NO scavenger, impaired basal and interleukin-1-beta-induced PRL release, while molsidomine, a NO donor, was able to release PRL and to amplify interleukin-1-beta-induced PRL release, confirming a modulatory role for nitric oxide in pituitary hormone secretion. On the other hand, no evidence regarding a possible role of prostaglandin E2 (PGE2) in IL-1beta-induced PRL release came out from our experiments.

Animals↗
PubMed1995

Effects of vindesine on hypothalamic-pituitary-adrenal axis.

Vindesine, a cell-cycle-specific agent currently employed in the treatment of some neoplasias, was able to produce a remarkable dose-dependent adrenocortical activation, but it was unable to increase plasma corticosterone in hypophysectomized rats in vivo. In addition, vindesine was able to increase ACTH release in vitro when tested on isolated pituitary cells in culture suggesting a direct involvement of the pituitary gland in the increase of adrenal secretion in vivo.

Adrenocorticotropic Hormone↗
PubMed1994

Effects of lipopolysaccharide on hypothalamic-pituitary-adrenal axis in vitro.

The possible involvement of lipopolysaccharide (LPS) and interleukin-1 beta (IL-1 beta) and their eventual interplay in CRH and ACTH release from cultured hypothalamic and pituitary cells respectively, have been studied. IL-1 beta was able to activate the hypothalamo-pituitary-adrenal axis at both hypothalamic and pituitary sites; LPS showed no direct action at hypothalamic level but it was able to inhibit basal and IL-1 beta-induced ACTH release: this could be responsible for a blunting of the adrenal cortex response that normally occurs in septic shock syndrome.

Adrenocorticotropic Hormone↗
PubMed1990

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.

Adrenal Glands↗
PubMed1989

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)

Adrenergic alpha-Antagonists↗
PubMed1988

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.

Adrenal Cortex↗
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

Granular cell myoblastoma of the parapharyngeal space.

A granular cell myoblastoma of the parapharyngeal space is presented. Although uncommon, this neoplasm of controversial origin must be considered in the differential diagnosis of all nonenhancing parapharyngeal space masses.

Adolescent↗
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↗