Why the study?
Does intracoronary gadolinium attenuate ischemic ST-segment elevation in a canine model of regional transmural ischemia?
Does intracoronary gadolinium attenuate ischemic ST-segment elevation in a canine model of regional transmural ischemia?
Blockade of stretch-activated ion channels with gadolinium attenuates ischemic ST-segment elevation in a canine model, suggesting that mechanical stretch alters transmembrane potential during ischemia.
Gadolinium attenuates ischemic ST elevation in canines via stretch-activated channels; leaves open translation to human ischemia mechanisms or therapy.
Regional transmural ischemia causes both ST-segment elevation and systolic elongation (bulging) of the myocardium. Mechanical stretch might alter the transmembrane potential via stretch-activated ion channels (SAC); however, the role of SAC on ischemic ST-segment elevation has not yet fully studied. The present study investigated the role of SAC in the genesis of ischemic ST-segment elevation in the in-vivo canine heart. In 6 anesthetized dogs, an extracorporeal conduit connected to the left anterior descending coronary artery was occluded for 5 min before and after the intracoronary infusion of gadolinium (Gd, 500 micromol/min). To eliminate the effect of ischemic preconditioning, the bypass was occluded for 5 min before the experiment. Percent systolic shortening (%SS) and percent systolic elongation (%bulging) were measured using a pair of ultrasonic dimension crystals. A unipolar epicardial ECG was monitored at the center of the ischemic area for the measurement of the ST-segment level. At the end of coronary occlusion, there was no difference in the reduction of %SS or the increase of %bulging between before and after infusion of Gd. ST-segment elevation, however, was significantly attenuated by the infusion of Gd. These data demonstrated that the activation of SAC is one cause of ischemic ST-segment elevation.
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Shimada et al. (1999) studied this question.
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