Ischemic postconditioning and size of myocardial infarction during inhibition of norepinephrine reuptake

Abstract

We studied the effect of inhibition of norepinephrine reuptake during the reperfusion period on the size of infarction zone after focal myocardial ischemia and under conditions of ischemic postconditioning. In groups 1 and 2, 30-min occlusion of the left coronary artery followed by 120-min reperfusion was performed. In groups 3 and 4, ischemia was followed by ischemic postconditioning (six 10-sec occlusions alternating with 10-sec reperfusions). Ringer solution (1 ml, groups 1 and 3) and desipramine (0.8 mg/kg, groups 2 and 4) were injected intravenously at the beginning of reperfusion. The area of myocardial infarction in group 1 was 32.0±3.1% of the area of the risk zone; in groups 2, 3, and 4 the corresponding value was 46.1±3.4% (p=0.006), 22.2±2.6% (p=0.028), and 50.3±3.1% (p=0.018), respectively. It was shown that inhibition of norepinephrine reuptake in the early reperfusion period after ischemia increased myocardial injury and abolished the protective effect of ischemic postconditioning.

Desvenlafaxine reduces apoptosis in amygdala after myocardial infarction

“…As a matter of fact, the timing of norepinephrine uptake inhibition relative to MI onset is critical for its cardioprotective effect since norepinephrine accumulates in the extracellular space rapidly after ischemia onset (Fujii et al, 2004), which enhances cardiac work (Zhou et al, 2012) and can be harmful to the ischemic myocardium. Indeed, Naumenko et al (2011) observed that desipramine administration at the onset of reperfusion is associated with a significant increase in infarct size. We speculate that DV could have better cardioprotective properties than desipramine, even when treatment is started after the onset of reperfusion.…”