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Biomedical subjects

F Berti

Publications and source records attributed to F Berti.

At least 127 records · Page 7Linked to original sources
PubMed1986

Beneficial effects of defibrotide against myocardial ischemia and decline of beta-adrenoceptor function in the rabbit.

Defibrotide is a polydeoxyribonucleotide of mammalian origin which possesses profibrinolytic effect and PGI2-releasing capacity. Because of these properties, defibrotide has antithrombotic effects which are demonstrated in various experimental models of venous and arterial thrombosis. The present study indicates that defibrotide clearly protects against myocardial damage in the rabbit 3 days after total coronary artery occlusion. Furthermore, defibrotide prevents the decline of beta-adrenergic receptor function, a phenomenon related to excessive circulating catecholamines that occurs during the myocardial infarct. Defibrotide prevents the dramatic fall of creatine phosphokinase activity in the ischemic ventricle: metabolic changes which reflect changes in the cells affected by prolonged ischemia. Assumptions about the mode of action of defibrotide are given particularly in consideration of the interaction between the fibrinolytic activity and the PGI2-releasing capacity of this substance.

Animals↗
PubMed1986

Cardioprotective effects of defibrotide in acute lethal and nonlethal myocardial ischemia in the cat.

We evaluated the effects of defibrotide (D), a natural profibrinolytic and antithrombotic agent with endogenous PGI2-stimulating properties, on acute lethal and nonlethal myocardial ischemia (L-AMI and NL-AMI) in the cat. The coronary artery was occluded at 12-14 mm from its origin. In L-AMI, 12 of 15 control cats developed ventricular fibrillation and died; D (32 mg kg-1, bolus intravenously plus infusion) provided total protection against death and showed protective effects on plasma and myocardial creatine phosphokinase (CPK), hemodynamics and ECG. In NL-AMI, pretreatment of cats with D at the same dosage (intravenous infusion) reduced AMI-ST segment increases and AMI changes in hemodynamics. AMI-induced changes in lactate adenosine triphosphate and CPK in ischemic tissues were prevented by D. The beneficial effects of D in NL-AMI could be partly attributed to its stimulatory effect on vascular PGI2 release; the mechanism of the impressive protection by D observed in L-AMI has still to be elucidated.

Adenosine Triphosphate↗
PubMed1986

Non-steroidal antiinflammatory drug therapy: advantages and disadvantages of long half-life drugs versus slow-release formulations.

A single daily administration of non-steroidal antiinflammatory drugs is widely recognized as the best dose regimen in chronic diseases such as degenerative osteoarthropathy, in inflammatory affections of the skeletal muscles, etc. Biomedical research has therefore developed drugs characterized either by a long half-life or available in a slow-release formulation. Isoxicam, piroxicam and benoxaprofen, which possess long half-lives, were compared with diclofenac sodium, indomethacin and ketoprofen, in their slow-release formulations, in terms of pharmacodynamics, pharmacokinetics and toxicity. Isoxicam, piroxicam and diclofenac showed excellent long lasting antiinflammatory properties: however the evidence showed that in cases of mild or severe renal pathology, drugs in their slow-release formulations are to be preferred.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1986

Androstane derivative devoid of anabolic-virilizing effects and endowed with an antiglucocorticoid activity.

2-Carbodecyloxy-17 alpha-methylandrosta-1,4-dien-11 beta,17 beta-dihydroxy-3-one (decylroxibolone, BR 917) is a new androstane derivative, esterified with decyl alcohol, carrying a methyl group in the 17 position, a hydroxyl group in the 11 beta position and a carboxyl group in position 2. Unlike norandrostenolone decanoate, decylroxibolone did not cause any weight increase of the levator ani muscle and of the seminal vesicles in castrated rats, nevertheless exerting a marked antiglucocorticoid activity. This new steroid agent can consequently act positively on the nitrogen metabolism, being concurrently devoid of undesired virilizing anabolic effect.

Adrenal Glands↗
PubMed1986

Androstane derivatives--roxibolone and decylroxibolone--devoid of any affinity for the androgenic prostate and muscle receptors.

Unlike testosterone propionate and norandrostenolone decanoate, some new androstane derivatives did not cause any weight increase of the levator ani muscle and of the seminal vesicles in castrated rats. Actually, these new androsterone derivatives, characterized by the presence of a carboxyl group in the position 2 and a hydroxyl group in the 11 alpha or beta position, have entirely lost their affinity for the androgenic receptors of the prostate and of the skeletal muscles.

Administration, Oral↗
PubMed1985

Positive interaction between leukotriene C4 and histamine and other mediators on vascular tissues.

The interaction of leukotriene C4 (LTC4) with the contractile activity of histamine (H), serotonin (5HT) and norepinephrine (NE) has been investigated in isolated vascular preparations. Threshold concentration of LTC4 (5 X 10(-9) M) significantly potentiated the vasoconstricting effect of these compounds on guinea-pig pulmonary artery (GPPA). This phenomenon was long-lasting for H since it was still present 40 min after LTC4 had been washed. FPL-55712 (10(-5) M) counteracted the increased H response on GPPA induced by LTC4. Potentiation of H activity due to LTC4 was also observed on guinea-pig thoracic aorta (GPTA) indicating that LTC4-induced hyperreactivity is not a phenomenon restricted to the pulmonary vascular bed. In the experiments carried out in presence of indomethacin (3 X 10(-6) M), LTC4 still potentiated H-induced vasoconstriction on GPPA, however the time course of the phenomenon was significantly shorter than that observed in absence of the cyclooxygenase inhibitor. The contractile activity of H and NE on guinea-pig portal vein (GPPV) was not potentiated by LTC4. These results demonstrate that LTC4 induces hyperreactivity of the arterial vascular tissue to vasoactive compounds and suggest that cysteinyl-leukotrienes may have pathological significance in the hemodynamic changes occurring during anaphylactic reactions. Preliminary experiments carried out on human intralobar pulmonary artery strongly support this hypothesis.

Anaphylaxis↗
PubMed1985

Isolation of a polypeptide from the venom of Bungarus multicinctus that binds to ganglia and blocks the ganglionic transmission in mammals.

A 15,000 dalton polypeptide purified from Bungarus multicinctus venom (which normally copurifies with alpha-bungarotoxin) was characterized biochemically and its biological effects were studied. This polypeptide, P15, had an aminoacid composition and molecular weight different from those of both alpha- and beta-bungarotoxin. It inhibited the ganglionic transmission in the guinea-pig hypogastric nerve-vas deferens preparation and did not block, even at very high concentrations, the neuromuscular transmission in the rat phrenic nerve-diaphragm preparation. In the same preparations alpha-bungarotoxin was unable to block the response at the ganglionic synapse while it was fully active in blocking the neuromuscular transmission. However, a pretreatment of the vas deferens preparation with alpha-bungarotoxin prevented the inhibitory effect of P15. 125I-Labeled P15 showed a specific and saturable binding to rat superior cervical ganglia homogenate and to a Torpedo postsynaptic membrane fraction. The binding of P15 to ganglia was inhibited by curare. The binding was Ca2+ dependent. The density of binding sites was of 300 fmol/mg of protein in the ganglion and 500 fmol/mg of protein in Torpedo membranes. The amount of P15-binding sites in ganglia was not modified by denervation, indicating that P15 binds to postsynaptic receptors. The binding of 125I-labeled P15, both in ganglia and Torpedo membranes, was inhibited by alpha-bungarotoxin. P15 had a Ca2+-dependent phospholipase A2 activity. Lowering Ca2+ concentration in incubation media affected the phospholipase A2 activity more than binding properties and inhibition of phospholipase activity with p-bromophenacyl bromide did not affect the activity of P15 on vas deferens preparation, suggesting that the phospholipase activity is not necessary for the activity of P15 on nicotinic receptors. Our results suggest that P15 toxin may be a specific and valuable probe for studying the ganglionic nicotinic receptor.

Animals↗
PubMed1985

Release of leukotrienes, induced by the Ca++ ionophore A23187, from human lung parenchyma in vitro.

When chopped human lung is stimulated with the Ca++ ionophore A23187 (0.25-10 microM) leukotriene (LT) B4, LTD4 and LTE4 are found in the incubation medium according to different patterns. LTD4 is released promptly and its levels increase up to 45 min after the stimulus (A23187, 10 microM) and decline later (120 min); LTE4 formation follows a sigmoidal shape and continues to accumulate even 2 hr after the challenge; LTB4 levels reach a plateau at 45 min. LTC4 was undetectable in most experiments but it was found to accumulate when reduced glutathione (10 mM) was added. Addition of exogenous LTC4 to unstimulated fragments of human lung shows that an effective interconversion to LTD4 and LTE4 takes place: A23187 stimulates formation of LT and cyclo-oxygenase products dose dependently; a statistically significant formation of LT occurs at A23187 concentration of 1 microM whereas thromboxane B2 (TXB2) and 6-K-prostaglandin F1 alpha levels increased significantly only at 2.5 microM A23187. Pretreatment with U-60257 (100 microM) prevented formation of LT without a concomitant increase of TXB2 levels. Indomethacin (1.5 microM) blocked the release of 6-K-prostaglandin F1 alpha and TXB2 without a shift of arachidonic acid towards LT-like activity. Addition of exogenous LTC4 did not trigger synthesis of TXB2 or 6-K-prostaglandin F1 alpha. Our results indicate that reduced glutathione levels and the activity of the enzymes involved in LT biosynthesis and/or metabolism play an important role in controlling the pattern of LT release from human lung.

Arachidonic Acid↗
PubMed1985

Anti-inflammatory activity of S-adenosyl-L-methionine in animal models: possible interference with the eicosanoid system.

In rats, the anti-inflammatory activity of parenteral S-adenosyl-L-methionine (SAMe) in carrageenin- and nystatin-induced oedemas and in carrageenin-induced pleurisy was tested. The capability of the drug to inhibit the production of PG-like material in sponge exudates and by peritoneal leukocytes during bacterial phagocytosis was also evaluated. Two of these experimental models were used to administer the compound by the oral route in order to see whether oral and injected SAMe had similar effects. The results obtained show that SAMe can exert anti-inflammatory activity by inhibiting the oedema and pleurisy in rats and PG-like material production in inflammatory exudates and in the phagocytosis process by leukocytes. The mechanism of action of SAMe is discussed.

Animals↗
PubMed1984

Inhibitory effects of 2-guanidinebenzimidazole and 1-phenylbiguanide on gastric acid secretion in rats.

In this study 2-guanidinebenzimidazole (GBI) and 1-phenylbiguanide (PBG) appear to be capable of decreasing gastric acid secretion, while the compounds dimethylbiguanide and cyanoguanidine do not. Thus, the antisecretory effect is present when the biguanide groups are associated with lipophilic molecules. GBI and PBG depress gastric acid secretion, even when it has been stimulated by carbamoylcholine (carbachol) or betazole. The antihistamine effects of GBI and PBG on betazole-stimulated gastric acid secretion were confirmed by the inhibitory activity of these compounds on the isolated guinea pig auricle stimulated by histamine. The antimuscarine activity of GBI and PBG on carbachol-stimulated gastric acid secretion in rats is also supported by the way in which these same drugs depress the motility of the duodenum and colon of the anaesthetized cat stimulated by prostigmine. The above mentioned effects of these compounds are also associated with myolytic activity, since they decrease the spontaneous and histamine-stimulated motility of the duodenum and colon. GBI and PBG probably depress gastric acid secretion by interfering with both histamine and acetylcholine receptors and with other sites involved in the secretory process.

Animals↗
PubMed1984

Bronchodilating activity of mequitazine.

The bronchodilating activity of mequitazine (MQ) (10-[3- quinuclidynilmethyl ]-phenothiazine) has been investigated in the guinea-pig using various spasmogens such as acetylcholine, histamine and leukotriene-C4 (LTC4). Mequitazine showed a potent protecting activity versus bronchoconstriction induced by the above agonists and was also able to prevent their capacity to trigger activation of arachidonic acid metabolism and preferential formation of TXA2. The results obtained with the "in vivo" experiments correlate well with those obtained "in vitro" using guinea-pig perfused lungs, where LTC4 and histamine stimulate TXA2 formation and release in the pulmonary effluent. MQ demonstrated its efficacy in protecting passively sensitized guinea-pigs from antigen challenge; this protection is accompanied by a substantial reduction of circulating TXA2. The bronchodilating and antiallergic activity of MQ is likely due to a direct control of histamine and muscarinic receptors and to a diminished bioamplification via eicosanoid activation. In addition, the capacity of MQ to counteract the "in vitro" and "in vivo" effects of LTC4 adds interest to its therapeutic potential.

Acetylcholine↗
PubMed1983

New pharmacological aspects of the bronchodilating activity of procaterol.

The selectivity of procaterol for beta 2-adrenoceptors vs beta 1-adrenoceptors in animals has been already described. In these studies the ability of procaterol to protect guinea-pig against bronchoconstriction induced by various spasmogens such as histamine, LTC4 and acetylcholine is demonstrated. The results obtained both in anaesthetized animals and in perfused lungs clearly show that procaterol antagonizes not only the direct effect of the bronchoconstrictors quoted above but also their ability to activate arachidonic acid metabolism and to augment the generation of TXA2. Procaterol (0, 3-3 micrograms/Kg i.v.) is more potent than salbutamol in protecting passively sensitized guinea-pig from massive bronchoconstriction following antigen challenge: a phenomenon which is paralleled by an increment of the circulating TXA2. The possibility that the adenylate-cyclase-stimulating properties of procaterol may explain its antiasthmatic activity is discussed.

Animals↗
PubMed1983

Anti-inflammatory activity of S-adenosyl-L-methionine: interference with the eicosanoid system.

S-adenosyl-L-methionine (SAMe) displays anti-inflammatory as well as antalgic activity without damaging the gastrointestinal mucosa in experimental animals. In fact, carrageenin-induced edema in rats and writhings provoked in mice by phenylquinone and acetic acid are controlled by SAMe in a dose dependent manner. Since PG-like substance concentration in the inflammatory exudate decreased in SAMe-treated animals the mode of action of this compound is also discussed, in view of SAMe ability to interfere with the eicosanoid system.

Animals↗
PubMed1983

Sulglycotide displays cytoprotective activity in rat gastric mucosa.

Sulglycotide, a well known antisecretory and antiulcer compound, has been further investigated for its ability to protect rat gastric mucosa against extensive necrosis induced by absolute ethanol, NaOH (0.2N) and NaCl (30%). Sulglycotide, which has been compared with cimetidine, displays a dose-dependent cytoprotective activity against the above necrotizing agents. The results obtained indicate that Sulglycotide requires a normal prostaglandin biosynthetic process in order to manifest its antiulcer activity. In fact gastric mucosa from animals treated with Sulglycotide releases in vitro a greater amount of PGl2-like activity; and furthermore no protection was observed against gastric lesions induced by indomethacin. As far as the mode of action of Sulglycotide is concerned it is tempting to speculate that the compound may interfere with prostaglandin degradation or it may trigger an adaptive cytoprotection which is important in maintaining the cellular integrity of rat gastric mucosa.

Animals↗