The vasoactive effect of serotonin on canine coronary arteries after ischemia and reperfusion

Reperfusion of the ischemic myocardium is a cornerstone of current therapy for acute coronary syndromes. Experiments show that reperfusion is associated with injury to the coronary artery. Such injury may manifest as augmented vasospasm or impaired vasodilation, and in this study we assessed whether such coronary responses to serotonin do occur.

Left anterior descending arteries (LAD) were occluded in 12 open-chested dogs for 1 h, then reperfused for 1 h. Vasoreactivity to serotonin was measured in isolated rings from the LAD and circumflex arteries (Cx), both at basal resting tension and after preconstriction with U-46619. Endothelium was removed in half of the rings.

In the basal state, LAD rings displayed increased initial constriction and decreased dilation in response to serotonin (maximum dilation: LAD, -4.5 +/- 1.7% versus Cx, -7.6 +/- 1.4%, P < 0.05). With endothelium removed, peak constrictions of the LAD and Cx were significantly augmented, and LAD dilations remained slightly impaired compared with the Cx. After U-46619, dilation in response to serotonin was impaired in the LAD compared with Cx rings (maximum dilation: LAD, -18.3 +/- 11.4% versus Cx, -44.0 +/- 8.4 LAD, P < 0.05). Endothelium removal diminished, but did not abolish, this relationship. De-endothelialized Cx, but not LAD, rings displayed slightly impaired dilations in response to serotonin compared with their respective controls.

After ischemia-reperfusion, coronary arteries respond to serotonin with enhanced constriction and impaired dilation. Changes in both the endothelium and the smooth muscle may determine these responses to serotonin.