Catecholamines and preconditioning: studies of contraction and function inisolated rat hearts

The aims of this study were to determine whether 1) like ischemic precondit ioning, transient exposure to norepinephrine before ischemia exacerbates co ntracture during ischemia and 2) protection afforded by norepinephrine is s tereospecific (receptor mediated). Isolated perfused rat hearts were random ized into five groups (n = 6/group): 1) ischemic preconditioning (3 min of ischemia +3 min of reperfusion +5 min of ischemia +5 min of reperfusion), 2 ) untreated control, 3) vehicle control (ascorbic acid), 4) substitution of preconditioning ischemia by perfusion with d-norepinephrine, and 5) substi tution of preconditioning ischemia by perfusion with l-norepinephrine. This was followed by 40 min of zero-flow ischemia and 50 min of reperfusion. Is chemic preconditioning and l-norepinephrine exacerbated contracture (time t o 50% contracture = 9.2 +/- 1.1 and 9.0 +/- 1.1 vs. 13.3 +/- 0.3, 12.4 +/- 0.5, and 13.2 +/- 0.4 min for untreated control, vehicle control, and d-nor epinephrine, respectively, P < 0.05). Postischemic left ventricular develop ed pressure was poor in untreated control (23.0 +/- 2.2%), vehicle control (26.9 +/- 2.3%), and d-norepinephrine (19.8 +/- 2.8%) groups but good in pr econditioned (52.4 +/- 5.1%) and l-norepinephrine (52.5 +/- 1.1%) groups (P < 0.05). Thus norepinephrine preconditioning, like ischemic preconditionin g, causes a paradoxical exacerbation of contracture coupled with enhanced p ostischemic recovery; both effects are stereospecific.