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Biomedical subjects

F Berti

Publications and source records attributed to F Berti.

188 records · Page 11Linked to original sources
PubMedDate not supplied

Flunoxaprofen, a new non-steroidal anti-inflammatory drug, does not interfere with prostaglandin synthesis in rat gastric mucosa.

The anti-inflammatory activity and the eicosanoid generation in rat gastric mucosa after a single oral dose of S-(+)-2(4-fluorophenyl)-alpha-methyl-5-benzoxazolacetic acid (flunoxaprofen, 10 mg/kg) or indomethacin (5 mg/kg) were compared. The two compounds, at the dose used, show a similar degree of anti-inflammatory activity (50% inhibition of carrageenan-induced oedema in rat paw). Moreover flunoxaprofen does not modify the formation of 6-keto-PGF1 alpha by rat gastric mucosa in vitro while indomethacin causes 50% inhibition of gastric cyclooxygenase activity. This biochemical change induced by indomethacin is associated with gastric lesions. Chronic treatment of rats with flunoxaprofen (5 or 50 mg/kg p.o. for 15 days) shows an anti-inflammatory activity in the range of 60-70% inhibition in the rat paw oedema test without gastric mucosa damages and prostaglandin synthesis inhibition.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Pharmacological activity of bamifylline on lung anaphylaxis: in vitro studies.

Bamifylline, a 7-8 disubstituted theophylline derivative, reduces in a dose dependent way (1 x 10(-5) M, 1 x 10(-4) M and 1 x 10(-3) M) the release of histamine, TXB2 (measured also as TXA2-like material) and SRS-A (as LTD4-like material) during the immunological challenge of actively sensitized guinea-pig lungs perfused in vitro. Theophylline was significantly less potent than bamifylline and particularly, at the higher concentrations used (1 x 10(-3) M), bamifylline was 2.7 times more potent than theophylline in reducing the immunological release of histamine and 1.6 and 1.5 times more potent in inhibiting the production of TXB2 and SRS-A, respectively. These data suggest that the ability of the two xanthine derivatives to control the immunological release of histamine represents an important point in understanding the mechanism of their anti-anaphylactic activity.

Anaphylaxis↗
PubMedDate not supplied

Immunization of rabbits with secific components of postsynaptic membrane. Acetylcholinesterase and cholinergic receptor.

Rabbits were immunized versus either an acetylcholinesterase- or a cholinergic receptor-rich fraction isolated from the electric organ of Torpedo marmorata. In both groups of animals we obtained a production of specific antibodies detected by immunodiffusion without cross reaction for the two antigens. Only rabbits immunized with the receptor-rich fraction developed a progressive flaccid paralysis, which affected first the leg muscles, progressively the neck muscles and eventually the respiratory muscles. The paralysis lasted in several animals up to 20 days. Eserine reversed the paralysis only in the first days but was ineffective in the "chronic" stage of the disease. In these animals high frequency stimulation of sciatic nerve induced a rapid failure of the responses of the anterior tibialis muscle while the muscle responded normally to a direct stimulation. A period of rest allowed a complete recovery of the muscle from fatigue. Tetani did not evoke the post-tetanic potentiation. Abnormalities, such as lymphocytic infiltration, fibers atrophy and necrosis, smearing and widening of Z line were sometimes present in muscles of Cho-R-immunized rabbits. In ACh-E immunized animals the neuromuscular transmission and the muscle morphology were similar to that of normal animals. Glycogen, ATP, cytochrome C oxidase, phosphorylases and acetylcholinesterase did not change significantly in the muscles of the immunized animals, while a large increase of cholineacetyltransferase activity was present. Red blood cell acetylcholinesterase showed a particularly high activity in ACh-E-immunized animals. The autoimmune paralysis induced in Cho-R-immunized rabbits may be a useful experimental model for further studies on human myasthenia gravis.

Acetylcholinesterase↗
PubMedDate not supplied

Subsensitivity of cardiac beta-adrenoceptors in renal hypertensive rats.

beta-Adrenoceptors were labeled with the selective beta-antagonist (-)[3H]dihydroalprenolol ([3H]DHA). Cardiac membranes isolated from renal hypertensive rats had the same density of adrenoceptors as normotensive rats (28 fmoles/mg of protein in both groups) but showed a significant elevation of the dissociation constant for [3H]DHA (Kd = 1.86 nM versus 1.04 nM for controls), indicating a reduced affinity of cardiac adrenoceptors for the radioligant. The lowered sensitivity to catecholamine is probably due to chronic exposure of beta-receptors to a high concentration of noradrenaline, whose turnover in cardiac nerves of renal hypertensive rats was significantly accelerated (turnover time 10.5 hr for hypertensive versus 17.2 for normotensive).

Animals↗
PubMedDate not supplied

Defibrotide, an antithrombotic substance that preserves postsynaptic alpha- and beta-adrenergic function in post acute infarcted rabbit hearts.

Defibrotide, a simple strand polydeoxyribonucleotide of mammalian origin with a molecular weight of 20,000 daltons, given intravenously to the rabbit before and after production of left ventricular infarction, prevents the alteration of the contractile response to postsynaptic adrenergic stimulation tested in isolated perfused heart preparations 3 days after coronary artery occlusion. According to the dose-response curves for isoproterenol and tyramine, left ventricular dP/dtmax was significantly depressed in infarcted hearts, whereas the dose-response curve for the inotropic effect of phenylephrine was markedly enhanced. These alterations were prevented by pretreatment of the rabbits with defibrotide (32 mg/kg/h i.v. for 6 h). In fact the potency ratios, calculated from the dose-response curves related to dP/dtmax of isoproterenol, tyramine, and phenylephrine in infarcted and control hearts excised from defibrotide treated and shamoperated rabbits, are nearly 1. The observed alterations in myocardial contractility in infarcted hearts seem to be specific for postsynaptic alpha and beta-adrenoceptors since the dose-response curve of left ventricular dP/dtmax for histamine is not different from control. The results obtained with defibrotide reflect the ability of this substance to protect the myocardial tissue from ischemic damage: this is also supported by the capacity of defibrotide (8 mg/kg/h i.v. for 6.5 h) to prevent the reduction of CPK-activity in the infarcted ventricle. Finally, we suggest that the observed beneficial effect of defibrotide in rabbit heart may also be explained by the antithrombotic effect of this substance, which is based on its profibrinolytic activity and PGI2-release.

Animals↗
PubMedDate not supplied

Protectant activity of defibrotide in cardioplegia followed by ischemia/reperfusion injury in the isolated rat heart.

BACKGROUND: Previous studies have shown that defibrotide, a polydeoxyribonucleotide obtained by depolymerization of DNA from porcine tissues, has important protective effects on myocardial ischemia, which may be associated with a prostacyclin-related mechanism. The purpose of this study was to investigate the direct effects of defibrotide (given in cardioplegia or after ischemia) on a model of rat heart recovery after cardioplegia followed by ischemia/reperfusion injury. METHODS: Isolated rat hearts, undergoing 5 minutes of warm cardioplegic arrest followed by 20 minutes of global ischemia and 30 minutes of reperfusion, were studied using the modified Langendorff model. The cardioplegia consisted of St. Thomas' Hospital solution augmented with defibrotide (50, 100, and 200 microg/mL) or without defibrotide (controls). Left ventricular mechanical function and the levels of creatine kinase, lactate dehydrogenase, and 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha; the stable metabolite of prostacyclin) were measured during preischemic and reperfusion periods. RESULTS: After global ischemia, hearts receiving defibrotide in the cardioplegic solution (n = 8) manifested in a concentration-dependent fashion lower left ventricular end-diastolic pressure (p < 0.001), higher left ventricular developed pressure (p < 0.01), and lower coronary perfusion pressure (p < 0.001) compared to the control group. After reperfusion, hearts receiving defibrotide in the cardioplegic solution also had, in a dose-dependent way, lower levels of creatine-kinase (p < 0.01), lactate dehydrogenase (p < 0.001), and higher levels of 6-keto-PGF1alpha (p < 0.001) compared to the control group. Furthermore, when defibrotide was given alone to the hearts at the beginning of reperfusion (n = 7), the recovery of postischemic left ventricular function was inferior (p < 0.05) to that obtained when defibrotide was given in cardioplegia. CONCLUSIONS: Defibrotide confers to conventional crystalloid cardioplegia a potent concentration-dependent protective effect on the recovery of isolated rat heart undergoing ischemia/reperfusion injury. The low cost and the absence of contraindications (cardiac toxicity and hemodynamic effects) make defibrotide a promising augmentation to cardioplegia.

Animals↗
PubMedDate not supplied

Defibrotide protects rabbit myocardium from ischemia: relationship with the eicosanoid system.

In the isolated rabbit heart preparation we studied the action of defibrotide--a natural polydesoxyribonucleotide from mammalian lungs--on the ischemic myocardial injury and on concentration of prostaglandin-like material in the perfusate. Defibrotide counteracted the ischemic myocardial contracture and significantly improved the recovery of cardiac contractibility and normalization of the rhythm in the postischemic period. This effect seems to be correlated with the concentration of the prostaglandin-like material in the cardiac perfusate. A simultaneous infusion of indomethacin inhibited both the protective effect of defibrotide and the prostaglandin-like material release from the cardiac muscle.

Animals↗