The effects of bolus injections of the prostaglandin precursor, arachidonic acid, and PGD 2, PGF 2α, PGE 2, and the PGH 2 analog ((15S)-hydroxyl-9α,11α(epoxymethano)-prosta-5Z-dienoic acid) were compared on the pulmonary circulation in the intact spontaneously breathing pentobarbital-anesthetized dog. Arachidonic acid increased pulmonary arterial pressure, decreased aortic pressure, and increased cardiac output when injected into the superior vena cava or right atrium. PGE 2 like arachidonic acid, increased pulmonary arterial pressure and cardiac output and decreased aortic pressure whereas PGF 1, and PGD 2 increased pulmonary arterial pressure but did not affect cardiac output or aortic pressure when injected into the superior vena cava or right atrium. The PGH 2 analog increased pulmonary arterial pressure and to a lesser extent, aortic pressure, without affecting cardiac output. None of these substances changed left atrial or right atrial pressure. The cardiopulmonary effects of arachidonic acid were blocked by indomethcin whereas the rise in pulmonary arterial pressure in response to the bisenoic prostaglandins and the analog were enhanced by the cyclooxygenase inhibitor. These data suggest that the increase in pulmonary vascular resistance in response to arachidonic acid may be due to conversion of the precursor into vasoactive intermediates and products such as bisenoic prostaglandins whereas the decrease in systemic vascular resistance is probably due to the formation of PGE 2 and other peripheral vasodilator substances.
|Original language||English (US)|
|Number of pages||9|
|Journal||Canadian Journal of Physiology and Pharmacology|
|Publication status||Published - 1977|
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