Coronary prostaglandin synthesis is accelerated by moderate hypoxia but suppressed by extreme oxygen deprivation, mediating corresponding changes in vessel tone.
Answers are grounded in this paper and cite their sources.
Hypoxia-modulated prostaglandin effects on vessel tone remain hypothesis-generating in animal models; human studies needed before any clinical consideration.
The relationship between bath Po2, intramural prostaglandin synthesis, and vessel tone in isolated coronary arteries of cattle was studied. The basal output of prostaglandin under 95% O2-5% CO2 (580 mmHg) was elevated markedly when the Po2 was decreased to 47 mmHg but extreme hypoxia (9 mmHg) sharply curtailed output. The coronary vessels responded to 47 mmHg with relaxation but they contracted when the Po2 was decreased further to 9 mmHg. Known inhibitors of prostaglandin synthesis attenuated both the hypoxia-induced relaxations and contractions. Analysis of the effects of extreme hypoxia and of inhibitors of prostaglandin synthesis on tone indicated that both suppress prostaglandin production. It is concluded that coronary prostaglandin synthesis is accelerated by hypoxia unless the oxygen deprivation is so severe as to limit the availability of oxygen for synthesis.
No takes yet. Share an insight, caveat, or question.
Stanley Kalsner (1977) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: