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Biomedical subjects

R Gryglewski

Publications and source records attributed to R Gryglewski.

At least 37 records · Page 2Linked to original sources
PubMed1976

An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation.

Microsomes prepared from rabbit or pig aortas transformed endoperoxides (PGG2 or PGH2) to an unstable substance (PGX) that inhibited human platelet aggregation. PGX was 30 times more potent in this respect than prostaglandin E1. PGX contracted some gastrointestinal smooth muscle and relaxed certain isolated blood vessels. Prostaglandin endoperoxides cause platelet aggregation possibly through the generation by platelets of thromboxane A2. Generation of PGX by vessel walls could be the biochemical mechanism underlying their unique ability to resist platelet adhesion. A balance between formation of anti- and pro-aggregatory substances by enzymes could also contribute to the maintenance of the integrity of vascular endothelium and explain the mechanism of formation of intra-arterial thrombi in certain physiopathological conditions.

Animals↗
PubMed1976

Arterial walls generate from prostaglandin endoperoxides a substance (prostaglandin X) which relaxes strips of mesenteric and coeliac ateries and inhibits platelet aggregation.

Fresh arterial tissue generates an unstable substance (prostablandin X) which relaxes vascular smooth muscle and potently inhibits platelet aggregation. The release of prostaglandin (PG) X can be stimulated by incubation with arachidonic acid or prostaglandin endoperoxides PGG2 or PGH2. The basal release of PGX or the release stimulated with arachidonic acid can be inhibited by previous treatment with indomethacin or by washing the tissue with a solution containing indomethacin. The formation of PGX from prostaglandin endoperoxides PGG2 or PGH2 is not inhibited by indomethacin. 15-hydroperoxy arachidonic acid (15-HPAA) inhibits the basal release of PGX as well as the release stimulated by arachidonic acid or prostaglandin endoperoxides (PGG2 or PGH2). Fresh arterial tissue obtained from control or indomethacin treated rabbits, when incubated with platelet rich plasma (PRP) generates PGX. This generation is inhibited by treating the tissue with 15-HPAA. A biochemical interaction between platelets and vessel wall is postulated by which platelets feed the vessel wall with prostaglandin endoperoxides which are utilized to form PGX. Formation of PGX could be the underlying mechanism which actively prevents, under normal conditions, the accumulation of platelets on the vessel wall.

Animals↗
PubMed1972

The generation from arachidonic acid of rabbit aorta contracting substance (RCS) by a microsomal enzyme preparation which also generates prostaglandins.

1. Sodium arachidonate was incubated with a crude prostaglandin synthetase preparation made from dog spleen. The incubation was made in a dynamic system so that the products could be delivered to strips of rabbit aorta and rat stomach.2. A rabbit aorta contracting substance (RCS) and a prostaglandin-like substance were formed. The RCS had similar properties to that released in anaphylaxis. It was unstable and as the RCS activity declined, so the prostaglandin-like activity increased. Its formation was prevented by prostaglandin synthetase inhibitors such as indomethacin.3. A different rabbit aorta contracting substance was formed by incubation of arachidonate with lipoxygenase, which generates peroxides. This substance was stable and did not lead to prostaglandin production.4. We conclude that RCS may be an intermediate in prostaglandin production, such as the postulated cyclic endoperoxide.

Animals↗
PubMed1972

The release of prostaglandins and rabbit aorta contracting substance (RCS) from rabbit spleen and its antagonism by anti-inflammatory drugs.

1. Slices of rabbit spleen generate rabbit aorta contracting substance (RCS) and a prostaglandin of the E series when they are vibrated or stirred.2. The release of both substances is increased by arachidonic acid and inhibited by aspirin-like drugs.3. When the spleen effluent containing RCS and prostaglandin E is incubated for a further 3 min, the prostaglandin concentration increases and the RCS concentration declines.4. RCS may therefore be an unstable intermediate in the biosynthesis of prostaglandins.

Animals↗