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为了解腺苷Ａ１受体激动剂ＲＰＩＡ对血一氧化氮（ＮＯ）水平及急性心肌梗塞范围的影响，２０只新西兰兔随机分为四组：Ⅰ，前降支缺血６０ｍｉｎ，再灌注９０ｍｉｎ；Ⅱ，缺血前１５ｍｉｎ给予ＲＰＩＡ（０．３ｍｇ／ｋｇ）ｉｖ，余同Ⅰ组；Ⅲ，两次缺血１０ｍｉｎ，间隔１０ｍｉｎ然后缺血６０ｍｉｎ，再灌注９０ｍｉｎ；Ⅳ，缺血前１５ｍｉｎ给予选择性腺苷Ａ１受体拮抗剂ＤＰＣＰＸ（１．０ｍｇ／ｋｇ）ｉｖ余同Ⅲ组。分别测定缺血再灌注期血ＮＯ水平、心率、平均血压及ｄｐ／ｄｔ，实验结束经ＴＴＣ染色测定心肌梗塞范围。结果显示，ＲＰＩＡｉｖ后血ＮＯ水平迅速上升达基础值二倍，并在整个缺血期持续高于对照组，同时伴有心率（２６．３％）和平均血压（１７．３％）的下降，ｄｐ／ｄｔ测值各组无明显差异。心肌梗塞范围，Ⅰ．２３．１±９．４％，Ⅱ．１２．１±２．２％，Ⅲ．１１．４±３．０％，Ⅳ．２１．４±７．８％。结论：缺血预适应（ＩＰＣ）减少急性心肌梗塞范围，腺苷Ａ１受体激动剂可以达到ＩＰＣ效果，而该受体阻滞可以取消ＩＰＣ效果；血ＮＯ水平的升高有可能是ＲＰＩＡ引起ＩＰＣ效应的原因之一。
To understand the influence of adenosine A1 receptor agonist RPIA on the level of blood nitric oxide (NO) and acute myocardial infarction, twenty New Zealand rabbits were randomly divided into four groups: Ⅰ, ischemia of anterior descending artery for 60 min, reperfusion 90min; Ⅱ, R-PIA (0.3mg / kg) iv given for 15min before ischemia, the rest were in group Ⅰ; Ⅲ, two times of ischemia 10min, interval 10min and then ischemia 60min, reperfusion 90min; Ⅳ, 15min given selective adenosine A1 receptor antagonist DPCPX (1.0mg / kg) iv Yu Tong Ⅲ group. The levels of blood glucose, heart rate, mean blood pressure and dp / dt during ischemia / reperfusion were measured. The extent of myocardial infarction was determined by TTC staining at the end of the experiment. The results showed that R-PIAiv blood NO levels increased rapidly to the basal value of two times, and continued throughout the ischemic period was higher than the control group, accompanied by heart rate (26.3%) and mean blood pressure (17.3%) Decline, dp / dt measured no significant difference between each group. Myocardial infarct size, Ⅰ. 23.1 ± 9.4%, Ⅱ. 12.1 ± 2.2%, Ⅲ. 11.4 ± 3.0%, Ⅳ. 21.4 ± 7.8%. Conclusions: Ischemic preconditioning (IPC) reduces the range of acute myocardial infarction, and adenosine A1 receptor agonist can achieve IPC effect, and this receptor blockade can cancel IPC effect; the increase of blood NO level may be RPIA One of the causes of the IPC effect.