An animal and clinical study on the change of neuropeptide Y release evoked by electrical stimulation and myocardial ischemia

OBJECTIVE: To investigate the change characteristics of neuropeptide Y (NPY) release during acute myocardial ischemia period. METHODS: The animal test was carried out in in situ perfused guinea pig hearts with intact sympathetic innervation. Electrical stimulation-evoked exocytotic release of NPY during ischemia and reperfusion was tested by radioimmunoassay (RIA). The plasma NPY concentrations were measured in patients with acute myocardial infarction (AMI) and angina pectoris (AP) in different times. RESULTS: Electric stimulation of the left ganglion in guinea pig heart evoked an exocytic release of neuropeptide Y. Stimulation after 20 minutes of global ischemia (S2), compared with control period stimulation (S1) produced the inhibition of NPY to a certain extent (S2/S1: 0.72, P < 0.05), whereas the inhibition of NPY release disappeared after 5 minutes reperfusion (with S2/S1 of 1.01, P > 0.05). Ischemia alone, without the electric stimulation, did not apparently induce NPY release. The clinical test found that the plasma NPY level was increased significantly during the acute ischemia attack period of coronary heart disease (CHD). The plasma NPY level reached peak (136.3 +/- 66.5 pg/ml) in patients during the first day after AMI. It began to decrease from the third day and came to normal level in the end of the first week. The plasma NPY level was 159.3 +/- 98.5 pg/ml in AP patients during angina attack. After two weeks treatment, the plasma NPY level was decreased to 118.9 +/- 54.3 pg/ml (P < 0.05). CONCLUSIONS: The NPY release of global ischemia have some relation with sympathetic nerve activity. At the early stage of ischemia, NPY release is inhibited to some degree and the inhibition factors will fade away on reperfusion. NPY interferes with the pathogenesis and the pathophysiolgy.