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Biomedical subjects

F V DeFeudis

Publications and source records attributed to F V DeFeudis.

At least 37 records · Page 2Linked to original sources
PubMed1985

Mechanism of endothelium-dependent vasorelaxation.

A sequential mechanism for endothelium-dependent vasorelaxation is proposed. The following events appear to be involved: Endothelial cell: activation of a receptor----activation of membrane phospholipases----increase in intracellular free Ca2+----formation of endothelium-derived relaxing factor(s) (EDRF) via a cytochrome P450-dependent epoxygenase or non-enzymatic lipid peroxidation pathway----release of EDRF----diffusion of EDRF to the smooth muscle cell; Smooth muscle cell: activation of guanyl cyclase----activation of protein kinase----protein phosphorylation----dephosphorylation of myosin light chain----relaxation. Relationships between endothelium-dependent and endothelium-independent vasorelaxation are indicated. EDRF-candidates include aldehydes and epoxides.

Animals↗
PubMed1984

Ligand-binding studies on GABA receptors--relation to physiology and behavior.

Some studies that have been conducted with ligand-binding methods support the contention that activation of cerebral GABA-receptors is involved in the control of certain behaviors. Further study of the changes in GABA-receptors that are associated with altered physiology and behavior in experimental animals and in man might lead to the development of new therapies for certain neuropsychiatric, cardiovascular, and endocrinological disorders.

Aging↗
PubMed1984

gamma-Aminobutyric acid-ergic analgesia: implications for gamma-aminobutyric acid-ergic therapy for drug addictions.

Recent in vivo and in vitro studies regarding the involvement of gamma-aminobutyric acid (GABA)-ergic systems in analgesia and in opiate dependence have been reviewed and analyzed. It seems evident that GABA-ergic systems play a role in mediating the effects of opiates and that some interplay might exist between endogenous opioid systems and GABA-ergic systems. Systemic administration of GABA-agonists, GABA uptake blockers and inhibitors of GABA-alpha-oxoglutarate transaminase (GABA-T) can produce potent analgesic actions in experimental animals and in man. Further study of such agents might lead to the development of new analgesics and/or new drugs for treating certain types of drug addiction.

Animals↗
PubMed1984

Endothelium-dependent relaxations of rabbit isolated aorta produced by carbachol and by Ginkgo biloba extract.

Spirally-cut strips of rabbit aorta were used to examine the relaxations produced by carbachol and extract of Ginkgo biloba (Gb) under isometric conditions. After precontracting the strips with phenylephrine (10(-7) M), carbachol produced a dose-related relaxation (PD2 congruent to 6.2 +/- 0.1) and this effect was antagonized competitively by atropine (PA2 congruent to 9.4 +/- 0.1). Gb (0.2 or 0.3 mg/ml) also relaxed the strips. Removal of the endothelium or a 30-min pre-treatment of the strips with a substance that has lipoxygenase-inhibitor activity (nordihydroguaiaretic acid, NDGA, 10(-5) M) abolished the relaxant effect of carbachol and partially blocked the relaxant effect of Gb. Thus, at least part of the relaxant effect of Gb is mediated by a factor(s) (e.g., EDRF) that is released from endothelial cells.

Animals↗
PubMed1983

gamma-Aminobutyric acid and cardiovascular function.

Evidence supporting the hypothesis that GABA-ergic mechanisms are involved in controlling mammalian cardiovascular function has been reviewed and analyzed. In vivo and in vitro studies with GABA-agonists and GABA-antagonists have revealed that activation of GABA-receptors is involved in the control of blood pressure and heart rate. Further studies conducted with agents that modify central and/or peripheral GABA-ergic systems could lead to the discovery of drugs that might be useful for treating certain cardiovascular disorders in man, such as hypertension and stroke, and should increase our understanding of the pathophysiological bases of such disorders.

Animals↗
PubMed1983

Na+-dependent and Na+-independent binding of GABA in CNS subcellular particles--a search for GABA receptors.

Studies of the Na+-dependent and Na+-independent binding of [3H] gamma-aminobutyric acid ([3H]GABA) and [3H]muscimol to central nervous system (CNS) subcellular preparations have been briefly reviewed and analyzed. Although some of the binding process that have been detected in vitro, in the presence or absence of Na+, appear to represent GABA-receptor interactions, further studies conducted with physiologic media and with highly purified membrane preparations are necessary in order to define the properties of those neuronal membrane receptors that mediate the in vivo actions of GABA.

Animals↗
PubMed1983

Effects of calcium-antagonists on passive cutaneous anaphylaxis in the rat.

The actions of four Ca2+-antagonists (nifedipine, verapamil, diltiazem and D 600) were compared with those of four substances that are used clinically in treating asthma (theophylline, isoproterenol, disodium cromoglycate and clemastine), using the passive cutaneous anaphylaxis (PCA) reaction in the rat. Nifedipine, verapamil and diltiazem produced a partial, but dose-related inhibition of the PCA reaction. A slight, but significant inhibitory effect was also observed with D 600. Isoproterenol, theophylline and disodium cromoglycate also produced dose-related inhibition of the PCA reaction, their maximum effects being greater than those of the Ca2+-antagonists. As the histamine H1-antagonist clemastine was about as active as nifedipine, verapamil or diltiazem in inhibiting the PCA reaction, it seems possible that certain Ca2+-antagonists might be of value in treating allergic disorders in man.

Animals↗
PubMed1983

Effects of various substances on two types of inflammatory reaction in animals.

The effects of 16 substances, including non-steroidal anti-inflammatory agents, a corticoid, phenols, immunomodulators and gold salts, were studied using two types of acute inflammatory reaction, a non-specific reaction (carrageenan-induced oedema) and an immune reaction (reversed passive Arthus reaction in the rat or active Arthus reaction in the mouse). Results revealed that the active Arthus model appears to be more selective than the passive reversed Arthus model, which is itself less sensitive than the carrageenan model. The active Arthus reaction might be useful for secondary screening of molecules that act on mechanisms modulating the intervention of complement and the various functions of polymorphonuclear leucocytes, and the passive Arthus reaction appears to be more suitable for preliminary screening. The activities of the different substances studied are discussed in terms of their modes of action and toxicity.

Adrenal Cortex Hormones↗
PubMed1983

Comparison of the analgesic actions of THIP and morphine.

The antinociceptive actions of intraperitoneally-administered 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) and morphine were compared using three strains of mice. With the hot-plate assay, ED50 values for the action of THIP were about 4 mg/kg in OF1, CD1 and NMRI strains, whereas ED50 values for morphine varied among strains, being 6.8 mg/kg for OF1, 16.9 mg/kg for CD1, and about 29 mg/kg for NMRI mice; thus, the genetic control of the analgesic action of THIP appears to differ from that of morphine. The analgesic action of THIP in the hot-plate test was not blocked by naloxone, bicuculline, phentolamine or methysergide, but was partially reversed by a high dose of atropine, indicating that classic opiate-receptors, bicuculline-sensitive GABA-receptors, alpha-adrenoceptors and serotonin-receptors do not appear to mediate the action of THIP but that cholinergic receptors might be indirectly involved. THIP was about equipotent or more potent than morphine in the phenylbenzoquinone writhing test, evasion test, and traction test. Since the ED50 values for THIP in OF1 mice were similar for hot-plate, evasion and traction tests, the analgesic action of THIP might not be readily dissociated from its sedative or myorelaxant action.

Analgesics↗
PubMed1983

Antinociceptive action of sodium valproate in the mouse.

The antinociceptive action of sodium valproate (VPA) was examined using male NMRI mice. Using the hot-plate assay at 60 degrees C, orally-administered VPA (50-400 mg/kg) produced antinociceptive effects; the ED50 was about 160 mg/kg. Oral doses of VPA (6.3-400 mg/kg) decreased the writhing response elicited by intraperitoneally-injected acetic acid. The antinociceptive effect of VPA, as determined with the writhing test, exhibited complex characteristics, the most pronounced effect occurring at doses of 12.5-50 mg/kg. The antinociceptive effect of VPA in the writhing test was not antagonized by bicuculline or by naloxone. VPA, like other agents which enhance central GABA-ergic mechanisms, might possess analgesic activity.

Acetates↗
PubMed1982

Inhibition of food intake in the rat by cyproheptadine.

In a model of conditioned feeding behavior, oral administration of cyproheptadine (1-100 mg/kg), 30 min before presentation of food, produced a dose-dependent reduction of food intake in the rat (ED50 congruent to 17 mg/kg during the 1st h of testing). This anorexic effect persisted for at least 24 h. These results provide further evidence that under certain conditions cyproheptadine, which is used as an orectic agent in man, can produce anorexia.

Animals↗