Protective effects of adenosine on acute myocardial ischemia

成年杂种犬用戊巴比妥钠和安氟醚吸入麻醉。在左前降支上加一个液压套，造成严重狭窄。降压期给予腺苷100微克/公斤/分。血压明显降低，体循环血管阻力(SVR)明显降低。心输出量增加，Emax无变化。在心肌缺血时给予腺苷，与对照组相比，腺苷处理组犬的心输出量、Emax维持得更好。在60min的缺血期结束后，取出心脏，在缺血区和非缺血区切除心脏。用高效液相色谱法测定心肌细胞内腺苷、二磷酸腺苷、三磷酸腺苷的浓度，用H3-二氢丙烯醇(DHA)结合法测定细胞内β受体密度。腺苷处理组心肌高能磷酸盐浓度和β受体密度与对照组无显著差异，提示腺苷在急性缺血心脏后负荷减少的情况下，保留了心肌泵功能。在这种犬模型中，细胞内高能磷酸盐和β受体密度的保存可能不会对维持心脏收缩功能起到重要作用。

Adult mongrel dogs were anesthetized with pentobarbital and enflurane in air. A hydraulic snare was applied over the left anterior descending artery to make a critical stenosis. In the hypotensive period, adenosine 100 mcg/kg/min was infused. Blood pressure was significantly decreased with a significant decrease in systemic vascular resistance (SVR). Cardiac output was increased with no change in Emax. When adenosine was given during myocardial ischemia, cardiac output, Emax were better maintained in adenosine-treated dogs than in the control group. After completion of the 60 min of ischemic period, the heart was excised and resected in ischemic and non-ischemic areas. The intracellular concentrations of adenosine, adenosine diphosphate, adenosine triphosphate, and beta-receptor density on the myocytes were measured using HPLC and H3-dihydroalprenol (DHA) binding assay respectively. There were no significant differences in high-energy phosphates concentrations and beta-receptor density between adenosine-treated myocardium and the control myocardium.The results suggested that adenosine preserved the myocardial pump function secondary to the decreased afterload in acute ischemic heart. Preservation of the intracellular high-energy phosphates and beta-receptor density probably did not play an important role to maintain cardiac systolic function in this canine model.