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 intac...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 exoc ytotic release of NPY during ischemia and reperfusion was tested by radioimmunoa ssay (RIA). The plasma NPY concentrations were measured in patients with acute m yocardial infarction (AMI) and angina pectoris (AP) in different times.Results Electric stimulation of the left ganglion in guinea pig heart e voke d an exocytic release of neuropeptide Y. Stimulation after 20 minutes of global ische mia (S 2), compared with control period stimulation (S 1) produced the inhibit ion of NPY to a certain extent (S 2/S 1: 0.72, P<0.05), whereas th e inhibition of NPY release disappeared after 5 minutes reperfusion (with S 2/S 1 o f 1.01, P>0.05). Ischemia alone, without the electric stimulation, d id not apparently induce NPY release. The clinical test found that the plasma NPY level was increased significantly du ring the acute ischemia attack period of coronary heart disease (CHD). The plasm a NPY level reached peak (136.3±66.5 pg/ml) in patients during the first day af ter AMI. It began to decrease from the third day and came to normal level in th e e nd 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 decre ased 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 inhib ited to some degree and the inhibition factors will fade away on reperfusion. NP Y interferes with the pathogenesis and the pathophysiolgy.展开更多
文摘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 exoc ytotic release of NPY during ischemia and reperfusion was tested by radioimmunoa ssay (RIA). The plasma NPY concentrations were measured in patients with acute m yocardial infarction (AMI) and angina pectoris (AP) in different times.Results Electric stimulation of the left ganglion in guinea pig heart e voke d an exocytic release of neuropeptide Y. Stimulation after 20 minutes of global ische mia (S 2), compared with control period stimulation (S 1) produced the inhibit ion of NPY to a certain extent (S 2/S 1: 0.72, P<0.05), whereas th e inhibition of NPY release disappeared after 5 minutes reperfusion (with S 2/S 1 o f 1.01, P>0.05). Ischemia alone, without the electric stimulation, d id not apparently induce NPY release. The clinical test found that the plasma NPY level was increased significantly du ring the acute ischemia attack period of coronary heart disease (CHD). The plasm a NPY level reached peak (136.3±66.5 pg/ml) in patients during the first day af ter AMI. It began to decrease from the third day and came to normal level in th e e nd 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 decre ased 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 inhib ited to some degree and the inhibition factors will fade away on reperfusion. NP Y interferes with the pathogenesis and the pathophysiolgy.
