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Biomedical subjects

A Genovese

Publications and source records attributed to A Genovese.

99 records · Page 6Linked to original sources
PubMedDate not supplied

Inhibition of hypoxia-induced cardiac hypertrophy by verapamil in rats.

Male Sprague-Dawley rats (200-220 g) were employed to study the effect of a calcium antagonistic drug on hypoxia-induced myocardial hypertrophy. The hypoxic condition was obtained by exposure of animals to reduced barometric pressure in a hypobaric chamber. The rats, divided in groups, were exposed to acute or chronic intermittent hypoxia (0.42 atmospheres of air for 24 hrs or 0.42 atm for 12 hrs per day for 10 days, respectively). Verapamil (VRP) was given subcutaneously in a total dose of 200 mg/kg/b.w./rat. In hypoxic rats, the drug significantly reduced the values of dry heart weight calculated on the basis of its relationship to total body weight. This phenomenon is probably due to: (1) reduced activation of the contractile system and a thereby resulting decrease in ATP breakdown as a result of blocking of Ca++ inflow into myocardial cells; (2) the effect of Verapamil on hypoxia-induced pulmonary hypertension and/or (3) a direct effect of the drug on the myocardial cell.

Adenosine Triphosphate↗
PubMedDate not supplied

Functional and biochemical evidence of a specific adenosine A2/Ra receptor on human platelets.

5'-N-ethylcarboxamideadenosine (NECA) greater than 2-chloroadenosine greater than adenosine greater than (-)-N6-(R-phenyl-isopropyl)-adenosine [(-)-R-PIA] greater than (+)-N6-(S-phenyl-isopropyl)-adenosine [(+)-S-PIA] inhibited in vitro human platelet aggregation in a dose-dependent fashion. 6-nitrobenzylthioinosine and dipyridamole, which inhibit adenosine uptake, and erythro-9-(2-hydroxy-3-nonyl)-adenine, which blocks adenosine metabolism, did not impair the inhibition induced by NECA and adenosine. 8-phenyltheophylline and theophylline, two competitive antagonists of adenosine receptors, blocked the inhibition of platelet aggregation caused by NECA and adenosine. NECA greater than 2-chloroadenosine greater than adenosine greater than (-)-R-PIA greater than (+)-S-PIA increased platelet cyclic adenosine monophosphate (cAMP) levels in a dose-dependent fashion. A significant linear correlation (r = 0.70, p less than 0.001) was found between the increase of platelet cAMP and the inhibition of platelet aggregation induced by adenosine and its analogs. 8-phenyltheophylline, which is a competitive antagonist of adenosine in platelets, also blocked the cAMP accumulation caused by NECA. These data suggest that NECA and other adenosine analogs activate a specific cell surface adenylate cyclase-linked adenosine receptor whose properties are similar to those of an adenosine A2/Ra receptor.

Adenosine↗
PubMedDate not supplied

Cardiac hypertrophy in the absence of pressure overload: an experimental and clinical report.

A stimulated altitude of 7000 m was applied in rats chronically exposed to hypoxia in a hypobaric chamber. In these experimental conditions the contralateral ventricle not exposed to pressure overload (that is, the left) showed a significant degree of hypertrophy. The hypoxic stimulus did not affect systemic artery pressure or the heart rate. Chronic adrenergic stimulation performed in the rat treated with low doses of isoprenaline (a direct stimulating adrenergic drug) or with tyramine (primarily a releaser of endogenous catecholamines) induced hypertrophy of the right ventricle, left ventricle, and interventricular septum without modifying the haemodynamic parameters mentioned above. The development of ventricular hypertrophy in the absence of pressure overload is stressed. A role for neurohumoral factors (that is, adrenergic stimulation and catecholamines) in the development of ventricular hypertrophy is suggested.

Animals↗
PubMedDate not supplied

Human heart mast cells in anaphylaxis and cardiovascular disease.

All sections of human heart tissue demonstrate tryptase- and chymase-containing mast cells (HHMCs) which have for the first time been isolated, partially purified and studied in vitro. HHMCs contain similar histamine levels as lung and skin mast cells, but tryptase levels are lower than in skin and higher than in lung mast cells. Complement C5a causes rapid dose-dependent release of histamine from HHMCs, but they are refractory to substance P and fMLP. Cross-linking IgE receptors on HHMCs leads to arachidonic acid metabolism through both the cyclooxygenase and 5-lipoxygenase pathways. HHMCs and their vasoactive mediators may be involved in anaphylactic/anaphylactoid reactions in humans and in the pathogenesis of some cardiovascular diseases.

Anaphylaxis↗
PubMedDate not supplied

Eosinophil granule proteins are selective activators of human heart mast cells.

Eosinophilia in humans is associated with eosinophil infiltration and cardiac localization of eosinophil granule proteins. Eosinophil cationic proteins are responsible for cardiac disease in some patients with eosinophilia. We have investigated the in vitro effect of four eosinophil granule proteins: eosinophil cationic protein (ECP), major basic protein (MBP), eosinophil-derived neurotoxin (EDN) and eosinophil peroxidase (EPO), on mast cells isolated from human cardiac tissue (HHMC). ECP and, to a lesser extent MBP (0.3-3 microM), but not EDN and EPO, stimulated the release of histamine and tryptase from HHMC. This release reaction induced by ECP and MBP was Ca(2+)- and temperature-dependent and was abolished by preincubation with anti-ECP and anti-MBP, respectively. The activation of HHMC by ECP and MBP was abolished by preincubation with 2-deoxy-D-glucose and antimycin A. These data demonstrate that some eosinophil cationic proteins, ECP and MBP, are selective activators of HHMC, thus contributing to the cardiac lesions in patients with eosinophilia.

Blood Proteins↗
PubMedDate not supplied

[A case of strangulated trans-omentum hernia].

After a review of the Literature, the Authors report a case of intestinal obstruction caused by trans-omentum hernia. This unusual disease is due to a defect of the greater omentum with herniation and secondary strangulation of small bowel. The clinical presentation was that of an intestinal obstruction with rare possibility of preoperative diagnosis. Therefore, a correct knowledge of this pathology and immediate surgery are necessary for the prognosis.

Aged↗
PubMedDate not supplied

[Surgical treatment of pancreatic carcinoma. Our experience].

BACKGROUND: Currently, pancreatic exocrine carcinoma presents high mortality, poor survival after curative surgery and poor resectability rates at the time of diagnosis. The factors which mostly influence prognosis and therapeutic management (curative surgery or palliative treatments) of the patient affected by pancreatic carcinoma, particularly the peroperative stage, are analyzed and discussed in this article. METHODS: From 1969 to 1997, 142 patients with pancreatic ductal carcinoma were admitted to our Department: at the time of diagnosis only 32 patients (22.5%) were considered resectable, and 30 pancreaticoduodenectomies (PD), 1 distal pancreatectomy (DP) and 1 total pancreatectomy (TP) were performed. RESULTS: Postoperative morbidity and mortality was 53.1% and 12.5% respectively; the survival at 1, 3 and 5 years was 45.5%, 36.4% and 17.6% respectively. The worst prognosis was seen in N+ and T4 patients, with a mean survival of 9 and 10 months. CONCLUSIONS: On the basis of these results and of the literature, the indications for curative surgery, the operative strategy and the lymphoadenectomy extension are discussed: these problems are still open and not resolved definitively. The authors conclude by indicating the need for curative surgery for T1/2 N0 M0 tumors: for T3/4 and/or N+ tumors a careful evaluation of single case is necessary, because of high risk/benefit rate. Pancreatic resections (PD, DP) and standard lymphoadenectomy (D1) are performed by the authors, rather than total pancreatectomy and radical lymphadenectomy (D2-3).

Adult↗