T Iwamoto1, X J Bai, H F Downey. 1. Department of Physiology, University of North Texas Health Science Center at Fort Worth 76107-2699.
Abstract
OBJECTIVE: The aim was to examine whether an absolute reduction in energy supply is required for preconditioning against myocardial infarction, and whether an episode of increased adrenergic activity with or without supply-demand imbalance is capable of triggering cardioprotection. METHODS: 41 anaesthetised dogs were subjected to 60 min left circumflex artery occlusion followed by 5 h reperfusion (control group, n = 8). The left stellate cardiac nerve was stimulated for 5 min starting 10 min before coronary occlusion in the stimulation group (STIM group, n = 8). The left circumflex artery flow increase that normally accompanies adrenergic stimulation was prevented by a pneumatic occluder in another group (STIM-R group, n = 8). Infarct size and area at risk were determined by triphenyl tetrazolium chloride staining and Evans blue dye, respectively. Regional myocardial blood flow during ischaemia and during stimulation (STIM-R group) was measured with radioactive microspheres. RESULTS: In the STIM group, adrenergic stimulation increased the coronary blood flow by approximately twofold from baseline. In the STIM-R group, transmural myocardial blood flow in the flow restricted left circumflex artery region was 64% of the flow to the non-flow-restricted left anterior descending coronary artery region. Haemodynamic variables were not different among the experimental groups except during adrenergic stimulation. Collateral blood flow and area at risk were comparable among the three groups. Infarct size as a percentage of area at risk (%IS/AAR) was significantly smaller in the STIM-R group [7.6(3.2)%] than in the control group [27.9(7.3)%], whereas %IS/AAR in the STIM group [21.7(4.1)%] was not. Furthermore, the regression line between collateral blood flow and %IS/AAR was significantly shifted downward in the STIM-R group, but not in the STIM group. CONCLUSIONS: (1) Transient energy supply-demand imbalance triggers infarct size limitation; an absolute reduction in energy supply is not required for preconditioning. (2) Increased adrenergic activity without supply-demand imbalance seems unable to trigger appreciable cardioprotection.
OBJECTIVE: The aim was to examine whether an absolute reduction in energy supply is required for preconditioning against myocardial infarction, and whether an episode of increased adrenergic activity with or without supply-demand imbalance is capable of triggering cardioprotection. METHODS: 41 anaesthetised dogs were subjected to 60 min left circumflex artery occlusion followed by 5 h reperfusion (control group, n = 8). The left stellate cardiac nerve was stimulated for 5 min starting 10 min before coronary occlusion in the stimulation group (STIM group, n = 8). The left circumflex artery flow increase that normally accompanies adrenergic stimulation was prevented by a pneumatic occluder in another group (STIM-R group, n = 8). Infarct size and area at risk were determined by triphenyl tetrazolium chloride staining and Evans blue dye, respectively. Regional myocardial blood flow during ischaemia and during stimulation (STIM-R group) was measured with radioactive microspheres. RESULTS: In the STIM group, adrenergic stimulation increased the coronary blood flow by approximately twofold from baseline. In the STIM-R group, transmural myocardial blood flow in the flow restricted left circumflex artery region was 64% of the flow to the non-flow-restricted left anterior descending coronary artery region. Haemodynamic variables were not different among the experimental groups except during adrenergic stimulation. Collateral blood flow and area at risk were comparable among the three groups. Infarct size as a percentage of area at risk (%IS/AAR) was significantly smaller in the STIM-R group [7.6(3.2)%] than in the control group [27.9(7.3)%], whereas %IS/AAR in the STIM group [21.7(4.1)%] was not. Furthermore, the regression line between collateral blood flow and %IS/AAR was significantly shifted downward in the STIM-R group, but not in the STIM group. CONCLUSIONS: (1) Transient energy supply-demand imbalance triggers infarct size limitation; an absolute reduction in energy supply is not required for preconditioning. (2) Increased adrenergic activity without supply-demand imbalance seems unable to trigger appreciable cardioprotection.