Fatty acid and prostaglandin composition of left ventricular myocardium from dexamethasone-treated dogs with severe low output syndrome (LOS).
The effects of dexamethasone (DEX) administration on the left ventricular myocardial content of fatty acids and prostaglandins E1, E2 and F2alpha were studied. Following a complete right and left cardiac catheterization, either DEX (8 mg/kg) or an equivalent volume of its vehicle was given intravenously 30 minutes prior to low output syndrome (LOS induction, and supplemental doses of DEX (4 mg/kg) or vehicle administered at 15 and 75 minutes post-LOS induction. Low output syndrome was induced by intravenous administration of a myocardial depressor protein (MDP) which has been isolated from the venom of the Western diamondback rattlesnake, Crotalus atrox. Neither DEX nor its vehicle had a significant effect during the entire experiment, that is, in the normal or low cardiac output state in most of the hemodynamic parameters investigated. The three hour mortality rate for the DEX-treated animals was 22% (n=10) while that of the control group was 41% (n=26) indicating that the beneficial effects of this corticosteroid are not really apparent from hemodynamic evaluation alone. Since DEX only had a significant post-LOS induction effect in maintaining a lower left ventricular end-diastolic and pulmonary capillary wedge pressures, a higher arterio-venous oxygen saturation difference, and a more efficient contractile state of myocardial fibers (Vmax), an indirect correlation to coronary arterial blood flow at the subcellular level was sought. To this effect, prostaglandins and specific lipid classes of left ventricular myocardium (LVM) from control and LOS animals receiving either vehicle or DEX were analyzed. Low output state induction alone raised myocardial PG levels above those of sham-catheterized animals; on the other hand, dexamethasone induced a significant decrease in the three prostaglandins studied when administered to control (no LOS) animals. In the presence of LOS, however, dexamethasone overrode in part the increase in PGE1 and PGE2 brought about by LOS while in the case of PGF2alpha the LOS effect was totally prevented and its concentration was not significantly higher than in control animals receiving dexamathasone. LOS induction led to an increase in myristic and arachidonic acids and a decrease in palmitic and linolenic acids. Dexamethasone administration to control animals increased the concentration of stearic acid above all the other groups but decreased the concentration of linolenic acid when compared to DEX-treated animals with LOS or sham-catheterized animals. There were no significant differences in the total myocardial lipid among the four groups of animals studied. It is suggested that the potentially beneficial effects of corticosteroid administration to animals with low output syndrome are related to their effects on fatty acid and prostaglandin content of myocardium.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D006328:Cardiac Catheterization; D002302:Cardiac Output / Q000187:drug effects; D003907:Dexamethasone / Q000627:therapeutic use*; D004285:Dogs; D005227:Fatty Acids / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism*; D011460:Prostaglandins F / Q000378:metabolism*; D012770:Shock, Cardiogenic / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism
D005227:Fatty Acids; D011458:Prostaglandins E; D011460:Prostaglandins F; D003907:Dexamethasone