Increased mechanical tension in the ischemic region during acute coronary occlusion might favor the occurrence of phase Ib ventricular arrhythmias. We aimed to investigate whether intracoronary administration of Gd³⁺, a stretch-activated channel blocker, into the ischemic zone reduces the incidence of these arrhythmias. In thiopental-anesthetized, open-chest pigs, the left anterior descending coronary artery (LAD) was ligated for 45 or 48 min. Phosphate-free, HEPES-buffered saline bubbled with 100% N₂ was infused into the ischemic region for 4 min, starting 5 min (series A, n = 16) or 20 min (series B, n = 16) after coronary occlusion, at a rate doubling the baseline blood flow. Animals were blindly allocated to receive 40 µM Gd³⁺ or only the buffer during the 2 final minutes of the infusion. There were not differences between groups with respect to hemodynamic variables, plasma K⁺ levels or size of the ischemic region. In none of the series was the number of phase Ib premature ventricular beats reduced by Gd³⁺ (46 ± 20 in untreated vs. 91 ± 37 in Gd³⁺-treated animals in series A and 19 ± 7 vs. 22 ± 13, respectively, in series B, both P = NS). The occurrence of ventricular tachycardia or fibrillation was significantly associated with the magnitude of early ischemic expansion of the LAD region, as measured by ultrasonic crystals, but was also not prevented by Gd³⁺. These results argue against a major role of stretch-activated channels inside the area at risk in the genesis of phase Ib ischemic ventricular arrhythmias.