Why the study?
Do prostaglandins A1, E1, and F2α alter coronary and systemic haemodynamics in unanaesthetized dogs?
Do prostaglandins A1, E1, and F2α alter coronary and systemic haemodynamics in unanaesthetized dogs?
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PGA1 and PGE1 significantly increase coronary blood flow and cardiac output while decreasing aortic pressure and peripheral resistance in unanaesthetized dogs, suggesting potential utility in myocardial ischemia.
Since prostaglandins appear to be important mediators of blood flow in the coronary and systemic vascular beds, we studied coronary and systemic haemodynamic effects of prostaglandins A1 (PGA1), E1 (PGE1), and F2α (PGF2α administered by intravenous, intra-atrial, and intracoronary routes in 14 intact, unanaesthetized dogs. PGF2α, (0·01-1·0 (μg/kg intravenously) did not alter coronary or systemic haemodynamics. Intra-atrial doses of PGA1 and PGE1 (0·01-1·0 (xg/kg) increased coronary blood flow, heart rate, and cardiac output by 35—62%, 22—57%, and 8—14%, respectively, while it decreased mean aortic pressure and peripheral vascular resistance by 8—14% and 26—36% respectively. PGA1 and PGA1 injected directly into the circumflex branch of the left coronary artery, increased coronary blood flow by 53% before any change in heart rate, mean aortic pressure, cardiac output, or myocardial oxygen usage. Since PGA1, unlike many other prostaglandins, is not inactivated by transit through the pulmonary circulation, it may be of value in increasing coronary blood flow and in augmenting cardiac output in the setting of myocardial ischaemia.
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Bloor et al. (1973) studied this question.
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