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Biomedical subjects

S Moncada

Publications and source records attributed to S Moncada.

At least 469 records · Page 26Linked to original sources
PubMed1978

Effect of prostacyclin on myogenic activity and adrenergic neuroeffector interaction in canine isolated veins.

In isolated strips of canine mesenteric vein prostacyclin (PGI2) causes a dose-dependent depression of the amplitude of the spontaneous rhythmic contractions without influencing their frequency. This suggests that prostacyclin affects the events leading from the depolarization of the smooth muscle cells to their contractions, rather than the induction of the myogenic activity itself. Furthermore, prostacyclin reduces the noradrenaline-induced contraction of the canine saphenous vein without affecting the electrically induced responses, suggesting a possible dual effect of the drug: at the smooth muscle it causes depression of the responsiveness to noradrenaline whereas at the adrenergic nerve endings it enhances the evoked release of the adrenergic transmitter.

Animals↗
PubMed1978

Effect of prostacyclin (PGI2) on platelet adhesion to rabbit arterial subendothelium.

The effect of prostacyclin on platelet aggregation and adhesion was investigated in everted pieces of rabbit abdominal aorta, from which the endothelium had previously been removed. Citrated human blood, to which different, concentrations of prostacyclin (0.1-100 ng/ml) were added, was perfused through the vessels, after which sections were examined and evaluated by light microscopy. Prostacyclin inhibited thrombus formation at concentrations greater than 0.1 ng/ml, whereas 20 ng/ml were required to reduce the amount of adhesion to the subendothelial surface. Thus prostacyclin prevents thrombus formation at much lower concentrations than are needed to inhibit platelet-vessel wall interaction.

Animals↗
PubMed1978

Comparison of the effects of prostacyclin (PGI2), prostaglandin E1 and D2 on platelet aggregation in different species.

The activity of prostacyclin (PGI2), PGE1 or PGD2 as inhibitors of platelet aggregation in plasma from human, dog, rabbit, rat, sheep and horse was investigated. Prostacyclin was the most potent inhibitor in all species. PGD2 was a weak inhibitor in dog, rabbit and rat plasma whereas PGE1 and prostacyclin were highly active. Theophylline or dipyridamole potentiated the inhibition of human platelet aggregation by prostacyclin, PGE1 or PGD2. Compound N-0164 abolished the inhibition by PGD2 of human platelet aggregation but did not inhibit the effects of PGE1 or prostacyclin. The results suggest that prostacyclin and PGE1 act on similar sites on platelets which are distinct from those for PGD2.

Animals↗
PubMed1978

Implications of prostacyclin generation for modulation of vascular tone.

1. The biotransformation of arachidonic acid and prostacyclin in the circulation was studied in anaesthetized dogs, using the blood-bathed organ technique. 2. In passage through the lungs, arachidonate (50-800 microgram kg-1 min-1) was transformed into prostacyclin. No thromboxane A2 or prostaglandin E2 could be detected in arterial blood. 3. In dogs treated with indomethacin (5 mg/kg), intravenous infusions of arachidonate had no cardiovascular effects and no prostacyclin was produced. Therefore, the vasodilator effects of arachidonate in vivo may be attributable to prostacyclin formation. 4. Prostacyclin, unlike prostaglandin E2, is not inactivated by passage across the lungs, and only about 50% disappears in one passage through peripheral vascular beds. 5. Thus prostacyclin released from the lungs could function as a circulating vasodilator and contribute to the regulation of blood vessel tone and blood pressure.

Animals↗
PubMed1978

Comparison of the vasodepressor effects of prostacyclin and 6-oxo-prostaglandin F1alpha with those of prostaglandin E2 in rats and rabbits.

1 Vasodepressor effects of prostacyclin (5z-5,6-didehydro-9-deoxy-6,9alpha-epoxyprostaglandin F1) and its decomposition product 6-oxo-prostaglandin F1alpha (6-oxo-PGF1alpha) have been compared with those of prostaglandin E2 (PGE2) in anaesthetized rats and rabbits. 2 In rats intravenous prostacyclin produced hypotension and was 4--8 times more potent than PGE2 and about 128 times more potent than 6-oxo-PGF1alpha. 3 In rabbits also, intravenous prostacyclin (less than 2 microgram/kg) produced hypotension and was twice as active as PGE2 and approximately 250 times more active than 6-oxo-PGF1alpha. 4 In rats and rabbits vasodepressor responses induced by prostacyclin were similar in magnitude after either intravenous or intra-aortic administration. 5 Thus, in both species prostacyclin resembles PGE2 in producing vasodepression but does not lose activity on passage through the lungs. The results emphasize the need to consider prostacyclin in addition to PGE2 as a major determinant influencing blood pressure.

Animals↗
PubMed1978

Prostacyclin (PGI2) inhibits the formation of platelet thrombi in arterioles and venules of the hamster cheek pouch.

1 Isolated rings of hamster aorta produced an unstable substance which inhibited platelet aggregation in vitro and had the same characteristics as prostacyclin. 2 Prostacyclin inhibited adenosine diphosphate (ADP)-induced aggregation of hamster platelets in vitro. 3 The effects of prostacyclin on ADP-induced platelet thrombi in the microcirculation of the hamster cheek pouch were studied with a television microscope. 4 Prostacyclin caused a dose-dependent increase in the time of iontophoretic application of ADP which was required to induce platelet thrombi formation and embolization in venules (30 to 40 micron diameter). 5 Prostacyclin caused a dose-dependent reduction in the total time during which ADP-induced thrombi were observed following local electrical damage to arterioles (40 to 80 micron diameter). 6 Thrombus formation in venules and arterioles was abolished by 500 ng/ml prostacyclin in the Krebs solution superfusing the hamster cheek pouch. 7 Prostacyclin was approximately twenty times more potent than prostaglandin E1 in preventing thrombus formation in the microcirculation.

Animals↗
PubMed1978

Recirculation of prostacyclin (PGI2) in the dog.

1 The inactivation of prostacyclin (PGI2) in the circulation of anaesthetized dogs has been studied by the blood-bathed organ bioassay technique. 2 Spiral strips of bovine coronary and rabbit coeliac or mesenteric artery detected concentrations of PGI2 of 2 to 5 ng/ml. These tissues were insensitive to concentrations at least 200 fold higher of 15-oxo-PGI2 and 6-oxo-PGF1alpha. 3 PGI2 assayed on bovine coronary artery, rabbit coeliac artery or rat stomach strip, had a half life in blood of 3.0 +/- 0.3 min, indicating non-enzymatic degradation. 4 No disappearance could be detected by bovine coronary artery when PGI2 was infused across the lungs (0.1 to 0.5 microgram kg-1 min-1). However, PGI2 was partially inactivated in passage through vascular beds of hindquarters and liver. 5 Of PGI2 infused into the aorta 35 to 65% escaped inactivation in one complete circulation. Therefore, endogenous PGI2 released from the lungs may function as a circulating hormone.

Animals↗
PubMed1978

Some actions of prostacyclin (PGI2) on the cardiovascular system and the gastric microcirculation.

Prostacyclin, generated by the vascular wall, is a potent vasodilator, reducing systemic blood pressure, increasing coronary blood flow and relaxing isolated vascular strips. Its vasoactive properties are little changed by passage through the lung. Prostacyclin, which is also formed by the gastric mucosa, increases gastric mucosal blood flow and inhibits gastric acid secretion and indomethacin-induced erosions. It is the most potent inhibitor of platelet aggregation in all species tested. It is suggested that prostacyclin and PGE1 act on similar sites on platelets distinct from those for PGD2.

Animals↗