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F Berti

Publications and source records attributed to F Berti.

At least 73 records · Page 4Linked to original sources
PubMed1995

Carbamazepine exerts anti-inflammatory effects in the rat.

In a first set of experiments, we evaluated the effects of different doses (5.0, 10, 20 and 40 mg/kg p.o.) of carbamazepine on nociceptive thresholds to thermal and mechanical stimuli, and on paw inflammatory hyperalgesia induced by the injection of brewer's yeast. Moreover, we studied the effect of carbamazepine on paw inflammatory edema by plethysmometry. Carbamazepine did not modify nociceptive latencies, but dose dependently reduced the hyperalgesia and the edema induced by the brewer's yeast injection in the rat hindpaw. In a second set of experiments, we studied the effects induced by the same doses of the drug on subcutaneous carrageenin-induced inflammation. Carbamazepine dose dependently reduced the inflammatory exudate, the prostaglandin E2-like activity in the exudate, and the substance P concentrations in the exudate. Our results demonstrate that carbamazepine is able to inhibit the development of different types of inflammation in the rat.

Animals↗
PubMed1995

Oligotide, a new single-stranded oligodeoxyribonucleotide, preserves postsynaptic beta-adrenergic and cholinergic receptor functions in rabbit hearts after acute infarction.

Acute myocardial infarction was induced in New Zealand male albino rabbits. 3 days after surgery, the mortality rate and plasma CPK activity were reduced by 64% and 66% respectively by intravenous infusion of Oligotide (32 mg/kg/h for 6h), a single-stranded oligodeoxyribonucleotide of mammalian origin. Perfused hearts, obtained from Oligotide-treated rabbits 3 days after surgery, showed a strength of contraction in the range of that of hearts of sham-operated animals and an ameliorated postsynaptic beta-adrenergic and cholinergic receptor function. In addition, in these hearts, "ex vivo" treatment with Oligotide resulted in almost complete preservation of both adrenergic and cholinergic responses to their specific agonists. These data suggest that Oligotide by protecting the hearts from the ischemic damage and possibly by restricting left ventricular tissue necrosis may have normalized the biological responses of this organ to isoproterenol and preserved the integrity of coronary endothelial-dependent relaxant function.

Acetylcholine↗
PubMed1995

Effects of chlomipramine and fluoxetine on subcutaneous carrageenin-induced inflammation in the rat.

We have previously shown that, after acute administration, antidepressant drugs exert anti-inflammatory actions in rats. In this study we evaluated the effects of 3 different doses of chlomipramine (10, 20, and 40 mg/kg i.p), and fluoxetine (5.0, 10, and 20 mg/kg i.p.) on subcutaneous carrageenin-induced inflammation. Both drugs dose-dependently reduced the inflammatory exudate, as well as the PGE2-like bio- and immunoactivity in the exudate. Chlomipramine dose-dependently reduced substance P concentrations in the exudate, whereas fluoxetine was effective only at the highest dose. Our results confirm that antidepressant drugs are able to reduce the development of inflammation in the rat and suggest that the inhibition of substance P production might play a role in mediating the anti-inflammatory effects of chlomipramine.

Animals↗
PubMed1995

Protective effect of furosemide combined with non-steroidal anti-inflammatory drugs administered by inhalation route on guinea-pigs anaphylaxis model.

The exposure of ovalbumin sensitized guinea-pig to an areosol of the specific antigen causes a respiratory crisis in approximately 100 s (dispnoea time) associated with a substantial increase in blood concentration of both histamine (from 27.5 +/- 1.8 ng/ml to 1570 +/- 26 ng/ml; n = 8) and thromboxane B2 (TXB2, from 0.52 +/- 0.03 ng/ml to 18.1 +/- 0.6 ng/ml; n = 8). The aerosol treatment of the animals (20 min) with furosemide (CAS 54-31-9, frusemide, FRU), nimesulide (CAS 51803-78-2, NIM), acetylsalicylic acid (CAS 50-78-2, ASA) and indometacin (CAS 53-86-1, INDO) at the concentrations of 1-3-10 and 30 mg/ml, before ovalbumin challenge, brought about an attenuation of anaphylactic response. The rank order of potency for the prolongation of dyspnoea time was FRU > NIM > ASA > INDO. In these experiments blood evaluation performed at the peak of the dyspnoea time for histamine concentration in the treated animals indicated that whereas FRU (ED25 = 2.14 mg/ml (1.97-2.38) and NIM (ED25 = 2.74 mg/ml (2.37-3.19)) were equiactive in reducing the release of histamine, ASA and INDO were devoid of this activity. On the contrary, the results obtained with ASA and INDO indicated a greater intrinsic activity in antagonizing TXB2 formation than that shown by the log-dose response curves of NIM and FRU. In another series of experiments the interaction of FRU with the other anti-inflammatory drugs in protecting guinea-pig from immune bronchoconstriction has been evaluated using the combination of two equiactive doses. The mixture considered were FRU+NIM, FRU+INDO and FRU+ASA. The results obtained indicated that FRU interacts positively with the three non-steroidal anti-inflammatory drugs in delaying the onset of the dyspnoeic crisis in guinea-pig. However, when FRU was combined with NIM the gain obtained (209%) appeared superior to that reached when FRU was combined with ASA (180%) or INDO (126%). Taken together these results suggest that non-steroidal anti-inflammatory compounds given by aerosol may represent a valid pharmacological intervention in protecting guinea-pig from anaphylactic bronchoconstriction.

Administration, Inhalation↗
PubMed1995

[Analysis of recurrences following conservative treatment of breast carcinoma].

In the conservative treatment of early breast cancer, great attention must be paid to define the prognostic factors correlated with the local recurrence rate. The goal is to customize surgery, radiotherapy and chemotherapy to the risk predicted in every single patient. To investigate the impact of some prognostic factors in a group of patients treated with homogeneous treatment schedules, 251 women with UICC stage I or II breast cancer were examined in the Padua Radiotherapy Department from 1988 to 1990. All patients underwent conservative surgery consisting in quadrantectomy, axillary node dissection and radiotherapy. During a median follow-up period of 49.2 months, 12 patients presented a breast relapse (4.8%). In 4 patients the relapse occurred in the same quandrant as the primary lesion, whereas a different quadrant was involved in the other 8 patients. The relapse rate in women under 60 was 5% and 4.7% in older patients, with p = 0.73. In pT1 patients, the relapse rate was 4.5% and in pT2 patients it was 7.9% (p = 0.37). No significant difference was observed between pN- and pN+ patients (4.5% vs. 6.25%, p = 0.37). In our series, none of the studied factors significantly influenced breast relapse rates. The number of patients may be too little relative to the low rate of relapses. However, an unfavorable trend was observed in the patients under 60, in pT2 or pN+ patients, or in the patients with positive or unknown surgical margins.

Adult↗
PubMed1995

Protective effects of ITF 296 in the isolated rabbit heart subjected to global ischemia.

The anti-ischemic action of ITF 296 was evaluated in isovolumic, electrically driven rabbit heart preparations subjected to temporary ischemia and reperfusion. Reduction of perfusion rate from 20 to 0.2 ml/min produced a sharp decrease of peak systolic pressure, left ventricular (LV)-developed pressure, and LV dP/dt, which culminated in complete ventricular arrest within 3-4 min. Thereafter, LV end-diastolic pressure (LVEDP) progressively increased, suggesting a severe ischemic episode. Reperfusion with 20 ml Krebs solution/min after 40 min of low-flow perfusion produced only minimal recovery from the rhythm disturbances associated with cardiac mechanical activity. During reperfusion, loss of myocardial elasticity was associated with a significant increase in coronary vascular resistance, as indicated by the augmentation of coronary perfusion pressure. Injection of ITF 296 (0.3-10 microM) into the perfusion system dose-dependently inhibited the increase in LVEDP that took place during ischemia and progressively improved the recovery of a regular rhythm in the isolated heart. Isosorbide dinitrate (ISDN) at a concentration of 10 microM exerted a protective action on the myocardium similar to that obtained with ITF 296 (3 microM). Treatment with ITF 296 (1 and 10 microM) resulted in a dose-dependent increase in the rate of 6-keto-PGF1 alpha biosynthesis during both the ischemia and the reperfusion period (+157% over basal values). Similar results were obtained when hearts were pretreated with ISDN (10 microM). Infusion of a buffer containing NG-monomethyl-L-arginine (L-NMMA; NO synthase inhibitor at 10 microM) just before reduction of flow, markedly exacerbated the effects of ischemia and reperfusion on the myocardium and increased coronary perfusion pressure. The effects of L-NMMA were clearly antagonized by ITF 296 (10 microM) or L-arginine (100 microM). Mechanical activity and sinus rhythm during reperfusion were rapidly and completely restored, and coronary resistance values were close to the preischemic values. As with ISDN, ITF 296 significantly increased the rate of synthesis of 6-keto-PGF1 alpha both under basal conditions and during reperfusion.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

omega-Conotoxin GVIA binds to and blocks rat neuromuscular junction.

The effect of omega-conotoxin GVIA, a specific blocker of N-type calcium channels, on the synaptic transmission at the mammalian neuromuscular junction is controversial. We have found that 125I-omega-conotoxin binds to rat tibialis muscle end-plate; that omega-conotoxin blocks the neuromuscular transmission both in vivo, in the sciatic nerve-tibialis anterior muscle, and in vitro in the isolated phrenic nerve-diaphragm preparation; and does not affect muscle nicotinic receptors. We conclude that in rat neuromuscular junctions N-type calcium channels are important for neurotransmitter secretion.

Animals↗
PubMed1994

Prostacyclin production by different human grafts employed in coronary operations.

Segments of human saphenous vein, internal mammary artery, right gastroepiploic artery, and inferior epigastric artery were incubated in vitro in Krebs-Henseleit solution and compared in terms of their capacity to generate and release into the medium 6-keto-prostaglandin F1 alpha (PGF1 alpha), the stable metabolite of prostacyclin. The four vascular conduits were also challenged with endothelin-1 (40 ng/mL), and accumulation of the lipidic material in the bathing fluid was also studied. The results obtained show clearly that under both normal and endothelin-1-stimulated conditions, the four vascular segments generate a substantial amount of 6-keto-PGF1 alpha. Multiple-comparisons analysis of the results indicates that the rank order in producing 6-keto-PGF1 alpha is as follows: inferior epigastric artery > internal mammary artery > right gastroepiploic artery > saphenous vein (p < 0.01). A similar order of potency was obtained in vascular conduits stimulated with endothelin-1. The rate of formation of immunoreactive 6-keto-PGF1 alpha under both normal and stimulated conditions by the inferior epigastric artery (normal, 301 +/- 8 pg/mg of tissue; stimulated, 519 +/- 15 pg/mg of tissue) was at 10 minutes more than 2 times (p < 0.01) that of the saphenous vein and about 1.5 times (p < 0.01) that of the right gastroepiploic artery.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Influence of theophylline on both bronchoconstriction and plasma extravasation induced by acetaldehyde in guinea-pigs.

Acetaldehyde administered intravenously at various doses (20, 40 and 80 mg/kg) elicits a dose-dependent increase in intratracheal pressure (ITP) and a proportional rise in histamine blood concentration in anaesthetized guinea-pigs. Similar effects were observed in ovalbumin-sensitized guinea-pigs upon aerosol of acetaldehyde (20 mg/ml) which has been administered at the flow rate of 0.1 ml/min for 2 min. Theophylline (CAS 58-55-9) antagonized both the increase of ITP values and the rise of histamine in the blood caused by acetaldehyde given intravenously (ED50 = 5.8 mg/kg i.v.) or by aerosol (ED50 = 4.9 mg/kg i.v.). Furthermore, in animals where combined treatment with pyrilamine (2 mg/kg i.v.) and captopril (2 mg/kg i.v.) resulted in a remarkable potentiation of the bronchoconstrictor response to acetaldehyde (20 mg/kg i.v.), the administration of theophylline (5 mg/kg i.v.) or of the substance P (SP) receptor antagonist, [D-Pro4, D-Trp7.9] SP 4-11 (10 mg/kg i.v.) reduced the augmented action of acetaldehyde on respiratory airways induced by captopril by more than 50%. Moreover, the bronchoconstriction induced by acetaldehyde (40 mg/kg i.v.) was also associated with a significant increase of extravasation of Evans blue in tracheal tissue. Both these effects of acetaldehyde were inhibited by theophylline (10 mg/kg i.v.), whereas a NK1-TK (neurokinin 1-tachykinin) receptor antagonist (412 micrograms/kg i.v.) reduced (81%; p < 0.001) only the vascular permeability changes caused by acetaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1994

Influence of acetaldehyde on airway resistance and plasma exudation in the guinea-pig.

In anaesthetized ventilated guinea-pig, acetaldehyde (CAS 75-07-0) (40-80 mg/kg i.v.) elicits a dose-dependent increase in intratracheal pressure accompanied by an increase in circulating histamine. When acetaldehyde is injected repeatedly at 15 min intervals in capsaicin-desensitized animals, it already loses its activity at the second administration (50% reduction; p < 0.01); this does not happen in control animals. This phenomenon is even more marked when acetaldehyde is given at the dose of 80 mg/kg i.v., since at the third injection both the bronchoconstriction and the increase in blood histamine are almost completely reduced to baseline values. The increase in intratracheal pressure caused by acetaldehyde (20, 40, 80 mg/kg i.v.) is associated with a dose related increase in microvascular permeability and leakage of protein-bound Evans blue in lower tracheal tissue. This event and the bronchoconstrictor response caused by acetaldehyde (40 mg/kg i.v.) are 87% and 35% inhibited, respectively, (p < 0.01) in tachykinin-depleated animals. On the contrary, thiorphan (2 mg/kg i.v.) remarkably potentiates both the rise in intratracheal pressure (110%; p < 0.01) and Evans blue extravasation (215%; p < 0.01) induced by acetaldehyde (20 mg/kg i.v.) in normal guinea-pigs. Furthermore, treatment with CP-96,345, a selective tachykinin NK1-receptor antagonist, only prevents plasma extravasation in lower tracheal tissue (82% inhibition; p < 0.01) without affecting the bronchoconstriction caused by acetaldehyde (40 mg/kg i.v.).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1994

[The immunological aspects of Kikuchi's disease. A clinical case report].

We report a case of histiocytic necrotizing lymphadenitis (NHL) (Kikuchi-Fujimoto disease) in a 23-year-old patient with fever, lymphadenopathy and leukopenia. There were no other significant findings in laboratory data and all bacterial and viral researches were negative. Fever resolved spontaneously after one month, but lymphadenopathy and leukopenia persisted. The immunophenotype of bone marrow and peripheral blood cells showed an increase of B lymphocytes (CD20+, CD21+, CD22+) and activated (CD30+) and NK cells (CD16+, CD56+). This finding persisted after six months. The authors suggest that the clinical feature of NHL is sustained by an immunological substrate.

Adult↗
PubMed1993

Nitric oxide and prostacyclin influence coronary vasomotor tone in perfused rabbit heart and modulate endothelin-1 activity.

Using isolated perfused rabbit heart electrically paced, we assessed the relevance of both nitric oxide (NO) and prostacyclin (PGI2) in regulation of resting coronary perfusion pressure (CPP). In preparations in which NO-synthase was inhibited by NG-monomethyl-L-arginine (L-NMMA, 10 microM), resting CPP increased significantly; this phenomenon was potentiated by indomethacin infusion (3 microM), prevented by L-arginine (100 microM) and significantly reduced by iloprost (55 nM) and defibrotide (200 micrograms/ml). Furthermore, the increase in resting CPP induced by graded doses of endothelin-1 (ET-1 0.6-160 pmol), was further augmented by blocking of prostaglandin biosynthesis with indomethacin (3 microM) and was substantially reduced when the rate of formation of PGI2 was enhanced by defibrotide (200 micrograms/ml). Moreover, the coronary vasoconstriction induced by ET-1 (2, 4, and 8 pmol) was increased in hearts in which NO-synthase was blocked by L-NMMA (10 microM) and this event was abolished in preparations in which PGI2 synthesis was stimulated by defibrotide (200 micrograms/ml). These results further emphasize that rabbit coronary vessels are continuously dilated by NO released from endothelial cells. They also indicate that PGI2 takes part in NO generation in the endothelial-derived relaxing mechanism. Inactivation of this mechanism, owing to decreased formation of NO and PGI2 in rabbit heart, induces hyperreactivity of coronary smooth muscles to ET-1. Finally, an increase in PGI2 production (such as that caused by defibrotide) may counterbalance impaired NO generation and attenuate hyperreactivity of the coronary vasculature.

Animals↗
PubMed1993

Formation of sulphidopeptide-leukotrienes by cell-cell interaction causes coronary vasoconstriction in isolated, cell-perfused heart of rabbit.

1. We have studied the transcellular biosynthesis of bioactive leukotrienes (LTs), generated upon blood cell-vascular wall interactions and their functional consequences, in the spontaneously beating, cell-perfused, heart of the rabbit. Rabbit isolated hearts were perfused under recirculating conditions (50 ml) with 5 x 10(6) cells of unpurified (buffy coat) or purified human neutrophils (PMNL), and challenged with 0.5 microM A23187 for 30 min. Coronary perfusion pressure (CPP), heart rate (HR), left ventricular end-diastolic pressure (LVEDP) and left ventricular pressure (LVP) were monitored continuously. Leukotriene formation was measured by specific enzyme-immunoassay and confirmed by reversed phase h.p.l.c. and u.v. spectral analysis. 2. Basal CPP values averaged 44 +/- 1.4 mmHg; A23187 triggered a marked increase in CPP both in the presence of buffy coat cells (+100% above basal) and PMNL (+270% above basal); the latter change in CPP was accompanied by a rise in LVEDP (+138% above basal). 3. The increase in CPP was preceded by a statistically significant rise in iLTC4-D4 concentration in the circulating buffer. Pretreatment with two structurally unrelated LTD4 receptor antagonists, LY171883 and SKF104353 (10 microM), fully prevented the increase in CPP and LVEDP. A similar protection was also observed when the rabbit heart was perfused with PMNL that had been pretreated with MK886 (1 microM), a potent inhibitor of leukotriene biosynthesis. 4. The increased coronary tone was accompanied by a marked release of lactate dehydrogenase (LDH), a marker of ischaemic damage; pretreatment of the heart with the LTD4 receptor antagonists as well as of the PMNL with MK886 resulted in a complete suppression of LDH activity release. 5. Positive identification of LTC4-D4 in the perfusates was obtained and a significant correlation observed between the CPP values and iLTC4-D4 concentrations.6. This study suggests that challenge of PMNL present within the coronary vasculature, causes a LTD4-dependent coronary vasoconstriction, favoured by an efficient uptake of PMNL-derived LTA4 by endothelial cells. The activation of the 5-lipoxygenase pathway in the context of tight interactions between blood cells and coronary vasculature, is suggested to have an important outcome in the alterations of coronary flow and cardiac contractility.

Animals↗
PubMed1993

New data concerning the antianaphylactic and antihistaminic activity of nimesulide.

The time to respiratory crisis in ovalbumin-sensitised guinea-pigs following exposure to aerosol administered antigen was dose dependently delayed by inhalation of nimesulide (0.1% to 1%), whereas indomethacin had no effect. At the same time, nimesulide significantly reduced blood histamine concentrations, in contrast to the slight increase observed with indomethacin. In human bronchial muscle preparations, nimesulide, but not indomethacin, antagonised H1-histamine-receptor activation by histamine and was without effect on acetylcholine-induced responses. Bronchoconstriction was also elicited in anaesthetised guinea-pigs by intravenous acetaldehyde (5% in saline, 1 ml/kg). This effect, which is paralleled by a rise in blood histamine concentrations, was significantly attenuated by inhaled nimesulide (0.1% to 1%), but not by indomethacin (1%). These data, which further support the antihistaminic and antiallergic activity of nimesulide, may have therapeutic relevance in patients who are affected by inflammation of the respiratory tract and who also have a history of allergic bronchoconstriction.

Anaphylaxis↗
PubMed1993

Agonistic activity and charge driven interaction potentiality of PAF derivatives.

Taking into account the contribution of the C2 substituent to the interaction ability of PAF derivatives, an investigation has been undertaken on: i) the role of the presence of two unitary charges of opposite sign in the molecule; ii) the role of the spacing of the same charged moieties. For this purpose, the theoretical analysis of model compounds for newly synthesized and already known compounds has been performed by means of computer-aided modelling, molecular mechanics and semiempirical quantum chemical computational methods. The combination of the results with the available pharmacological data allows a discussion about the stereoelectronic features required for agonist interaction at the PAF receptor.

Animals↗