Chronic Emotional Stress Exposure Increases Infarct Size in Rats: The Role of Oxidative and Nitrosative Damage in Response to Sympathetic Hyperactivity

We investigated the level of sympathetic hyperactivity in response to stress exposure in an acute in myocardial infarction (AMI) model and the contribution of oxidative and nitrosative damage to this phenomenon. Stress was induced by 20-day administration of different emotional stress factors: daylight/darkness exposure, overcrowding, isolation, new hierarchy, tilting the cage and restriction of water or food. AMI was induced surgically, Heart I-ate (HR) and heart rate variability (HRV) measurements were done before and after AMI. Oxidant parameters were measured in heart tissue and cortisol levels were measured in plasma specimens. Compared with the nonstressed group, stress-exposed rats showed sympathetic hyperactivity characterised by increased HR together with decreased HRV. In the stressed group serum corticosterone levels were high both below and after A All. Mean infarct size in the stressed group was significantly larger (44.6 +/- 3.23% and 53.1 +/- 4.52%, respectively; P < 0.05). Increasecl tissue malondialdehyde (MDA) levels (0.63 +/- 0.59 and 1.60 +/- 0.31 nmol/mg protein, respectively: P < 0.05) and decreased superoxide dismutase (SOD) activity and glutathione (GSH) content were seen in stress-exposed rots. Likewise, heart peroxynitrite levels were also high in stress-exposed rats (141.8 +/- 18 nmol/g tissue vs. 164.2 +/- 21 nmol/g tissue). Chronic emotional stress is a deteriorating factor for the induction and prognosis of MI. Exaggerated sympathetic activity may be the major contributing factor. Oxidative and nitrosative damage in response to this sympathetic hyperactivity is the kelp mechanism.