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MAF 17μM,50μM增加离体豚鼠心脏冠脉流量,分别为12.9％及20.4％,同时,均伴有负性心力及频率作用。MAF 50mg/kg,ip使小鼠心脏营养性血流量增加13％,当MAF(50mg/kg,ip)与so(2.5mg/kg,sc)合用时,有一定程度的加强后者增加血流量的作用(增加14.3％),而当其与CaCl_2(300 mg/kg,ip)联用时,又明显减弱CaCl_2增加心肌营养性血流量的作用(减少14.9％)。在离体冠脉螺旋条,MAF还可明显抑制高K~+去极化所致收缩反应,CaCl_2又可逆转此抑制效应,以上结果提示其扩张冠脉、负性心力及负性频率作用,可能与阻钙内流有一定关系。 此外,MAF 30μM抑制去甲肾上腺素及苯福林所致冠脉条的依剂量性收缩,这可能是由于阻止了激动α受体引起收缩反应时所需CaCl_2内流所致。
MAF 17μM and 50μM increased the coronary flow in isolated guinea pig hearts, which were 12.9% and 20.4%, respectively. Meanwhile, they all had negative cardiac and frequency effects. MAF 50 mg / kg, ip increased cardiac trophic blood flow in mice by 13%. When MAF (50 mg / kg, ip) was administered in combination with so (2.5 mg / kg, sc), the latter increased to some extent (14.3% increase). When combined with CaCl 2 (300 mg / kg, ip), the effect of CaCl 2 on myocardial nutritional blood flow (14.9%) was significantly attenuated. In isolated coronary spheroids, MAF also significantly inhibited the contractile response induced by high K ~ + depolarization. CaCl 2 reversed this inhibitory effect. These results suggest that the coronary artery may be dilated coronary artery, negative cardiac and negative frequency, May have a certain relationship with calcium influx. In addition, MAF 30 μM dose-dependently inhibited the dose-dependent contractions of norepinephrine and phenylephrine-induced coronary arteries probably due to the blockade of the CaCl 2 influx required to agonize the α receptor for its contractile response.