Circulation, Vol 70, 297-302, Copyright © 1984 by American Heart Association
DJ Fitzgerald, L Roy, RM Robertson and GA FitzGerald
The results of prior studies indicate that nitroglycerin stimulates
prostacyclin release by cultured endothelium and by the coronary
vasculature in vivo. However, the accuracy of these findings in coronary
vasculature relies on plasma samples obtained from the circulation via
cardiac catheters, a procedure we have shown to stimulate prostacyclin
release, thereby confounding interpretation of drug action. We studied the
effects of short-acting (nitroglycerin) and long-acting (isosorbide
dinitrate) nitrates on a noninvasive index of prostacyclin synthesis,
excretion of urinary 2,3-dinor-6-keto-PGF1 alpha. Nitroglycerin was infused
into six subjects to either a maximum of 480 micrograms/min or until mean
arterial pressure fell by 20 mm Hg. Urine was collected for negative ion
chemical ionization gas chromatographic, mass spectrometric analysis before
and during the nitroglycerin infusion and for two 2 hr periods after
nitroglycerin. The peak nitroglycerin infusion rate was 387 +/- 67
micrograms/min, which caused a fall in supine blood pressure
(systolic/diastolic) of 11 +/- 5/14 +/- 4 mm Hg and a 12 +/- 3 beats/min
increase in heart rate. Excretion of 2,3-dinor-6-keto-PGF1 alpha (pg/mg
creatinine) was unchanged from control infusion values (106 +/- 19.5)
either during (123 +/- 21) or after (134 +/- 14.6; 139 +/- 36)
nitroglycerin infusion. Platelet aggregation to arachidonic acid (0.33 to
1.33 microM) and epinephrine (1 to 10 microM) ex vivo was inhibited in only
one subject in whom excretion of 2,3-dinor-6-keto-PGF1 alpha was unaltered.
Serum thromboxane B2 was not changed by nitroglycerin infusion.(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
The effects of organic nitrates on prostacyclin biosynthesis and platelet function in humans
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