Biomedical subjects
Publications and source records attributed to J Damas.
Three organo-selenium compounds have been synthetized : methyl seleno-2 benzoic acid, acetylseleno-2 benzoic acid and diselenosalicylic acid. These compounds induce convulsive seizures in the rat, the most active of them being methyl seleno 2 benzoic acid. Convulsions are stopped after anaesthesia with pentobarbitone.
In the rat, diethylcarbamazine, imidazole and L 8027 do not modify the hypotensive activity of PGE2 and arachidonic acid. The formation of SRS-A from arachidonic acid does not compete with the synthesis of PG in the cardiovascular system of the rat. The thromboxane A2 does not participate in the hypotensive activity of arachidonic acid in the rat.
The hypotensive activity of arachidonic acid is more important by intraaortic than by intravenous injection, in the rat. The evisceration of the animal abolishes this difference and reduces the activity of arachidonic acid. This action is not accompanied by thrombopenia and is only observed with high doses of arachidonic acid in this species. The hypotensive activity is inhibited by indomethacin but not by tranylcypromine.
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In normal rat, anaesthetized with pentobarbital, 5-HT, injected or perfused by intravenous route, provokes different types of cardiovascular responses. These variations are due to the activation of three classes of receptors. The first ones explain the fall of the arterial blood pressure: they are located on arterioles which are dilatated. The second one are para- or perivascular nervous receptors: when stimulated, they induce vago-vagal reflexes (Bezold-Jarisch reflexes) suppressed by vagotomy. The third ones are vasoconstrictor and located on arterioles.
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Intravenous injection of arachidonic acid induces cardiovascular and respiratory effects due to its transformation into prostaglandins, This activation could take place not only in the platelets but also in the vacular wall. Platelet aggregation induced by arachidonic acid is not the main factor responsible of its cardiovascular actions.
In the rat, silybine and Z 12007, a derivative of rutoside, increase the vasodepressive activities of arachidonic acid, a prostaglandin precursor. They reduce the activity of PGE2. Quercetine also increases the hypotensive action of arachidonic acid. These three flavonoids are supposed to increase the prostaglandin biosynthesis.
In the rat, hydrocortisone, dexamethasone and chloroquine do not inhibit the hypotensive activity of arachidonic acid, which is due to endogenous prostaglandin synthesis. They reduce or suppress the secondary hypotensive phase induced by bradykinin. These substances inhibit the prostaglandin releasing activity of bradykinin but do not interfere with prostaglandin synthesis.
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In the rat, carrageenan injected intravenously lowers the systemic blood pressure. This activity depends on kininogen-kinin system activation, on prostaglandin release by these kinins and on mechanic pulmonary vascular blockade. Neither histamine nor 5-hydroxytryptamine releases are observed.
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In normal rats, prostaglandin F2alpha is a potent vasoconstrictor. The corresponding systemic hypertension is progressively attenuated by tachyphylaxis, revealing a longlasting fall of blood pressure. Tachyphylaxis is accelerated by previous injection of arachidonic acid and bradyskinin. The vasodepressive activity of PGF2alpha is inhibited by indomethacin.
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Bradykinin induces a release of unsaturated fatty acids and of prostaglandins from the perfused rat lung. This release is inhibited by chloroquine, a phospholipase A inhibitor. Histamine has no stimulating effect on fatty acids production. It is suggested that prostaglandins release induced by bradykinin might depend on a phospholipase activation.
Conjugated noradrenaline (NA) has been identified as a constituant of the walls of a Vespid wasp: Vespula germanica Linne. Concentrations range between 1,8 mug/g (external wall) and 18 mug/g (internal structure). Probably NA originates from the saliva of the Hymenoptera.