Key result
Intracoronary infusion of vasoactive intestinal peptide progressively diminished arterial-coronary sinus O2 content difference (from 118 to 61 ml O2/L) and myocardial O2 extraction.
Why the study?
The direct effect of vasoactive intestinal peptide on coronary hemodynamics and blood flow was not well characterized in humans.
Does intracoronary infusion of vasoactive intestinal peptide alter coronary hemodynamics and myocardial oxygen extraction in patients with chest pain and non-obstructive coronary arteries?
Does intracoronary infusion of vasoactive intestinal peptide alter coronary hemodynamics and myocardial oxygen extraction in patients with chest pain and non-obstructive coronary arteries?
Intracoronary infusion of vasoactive intestinal peptide induces direct coronary vasodilation, as evidenced by decreased myocardial oxygen extraction without significant changes in major systemic hemodynamics at lower doses.
Answers are grounded in this paper and cite their sources.
May support direct coronary vasodilation by VIP in non-obstructive disease; leaves open therapeutic role pending controlled trials.
Vasoactive intestinal peptide (VIP) is a neurotransmitter that has been identified in epicardial coronary arteries. To evaluate the direct effect of VIP on coronary hemodynamics and blood flow, graded doses of VIP (0.01, 0.03, 0.10, and 0.30 micrograms/min) were infused into the left coronary artery of 7 patients at the time of diagnostic cardiac catheterization for chest pain syndromes. None of the patients had coronary stenoses greater than 50% during subsequent angiography. Coronary sinus VIP concentrations increased during each infusion (22 +/- 28 pg/ml at baseline to 109 +/- 22 pg/ml at 0.30 micrograms/min; p less than 0.05), but arterial VIP was elevated (39 +/- 29 pg/ml) only at the maximal dose of 0.30 micrograms/min. During all dosages of VIP, heart rate, right atrial and left ventricular end-diastolic pressure, and the heart rate x blood pressure product did not change. Moreover, neither mean aortic pressure nor left ventricular peak + dP/dt changed significantly at doses less than 0.30 micrograms/min; at 0.30 micrograms/min, mean aortic pressure decreased (97 +/- 15 to 90 +/- 15 mm Hg; p less than 0.05) and LV peak + dP/dt increased (1,621 +/- 230 to 1,801 +/- 226 mm Hg/s; p less than 0.05). Compared to baseline, the arterial-coronary sinus O2 content difference and myocardial O2 extraction diminished progressively at the 0.03, 0.10, and 0.30 micrograms/min doses of VIP (118 +/- 12 ml O2/L vs. 94 +/- 15, 70 +/- 9, and 61 +/- 26 ml O2/L, respectively, and 0.64 +/- 0.05 vs. 0.53 +/- 0.10, 0.38 +/- 0.06, and 0.34 +/- 0.15, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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Popma et al. (1990) studied Chest pain syndromes (n=7). Vasoactive intestinal peptide (VIP) vs. Baseline was evaluated on Arterial-coronary sinus O2 content difference and myocardial O2 extraction. Intracoronary infusion of vasoactive intestinal peptide progressively diminished arterial-coronary sinus O2 content difference (from 118 to 61 ml O2/L) and myocardial O2 extraction.
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