ABSTRACT
AIM: Acute myocardial infarction causes neurohumoral activation characterized by increased sympathetic activity. CgA is a protein released during sympathoadrenal stress from neuroendocrine tissue. Recently, increased CgA concentrations in circulation have been reported and suggested to be an independent predictor of mortality after acute myocardial infarction. MATERIALS & METHODS: Eighteen pigs underwent 1 h of regional myocardial ischemia followed by 3 h of reperfusion. Blood samples were collected every hour and plasma CgA was measured with two radioimmunoassays. RESULTS: We found a 30% increase in plasma N-terminal CgA 1 h after re-establishment of coronary blood supply. On the other hand, plasma pancreastatin did not change in response to ischemia or reperfusion but decreased during the entire experiment. CONCLUSION: Our results suggest a differentiated CgA response in myocardial reperfusion after local cardiac anoxia that may reflect tissue-specific post-translational processing and release.
