Lasley R D, Anderson G M, Mentzer R M
Department of Surgery, University of Wisconsin, Madison 53792-0001.
Cardiovasc Res. 1993 Apr;27(4):565-70. doi: 10.1093/cvr/27.4.565.
The aims were (1) to determine whether ischaemic and hypoxic preconditioning enhance recovery of left ventricular function after global ischaemia in the rat, and (2) to evaluate the effects of selective adenosine A1 receptor antagonists on ischaemic and hypoxic preconditioning.
Isolated rat hearts, perfused at constant pressure, were subjected to 30 min ischaemia and 30 min reperfusion. Control hearts were compared to hearts preconditioned with 5 min ischaemia in the presence or absence of the adenosine A1 antagonist A1433U (10 microM), and hearts preconditioned with 5 min hypoxia in the presence or absence of the adenosine A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 5 microM). Recovery of left ventricular function was assessed by percent recovery of preischaemic rate-pressure product.
Control hearts recovered 64(SEM 4)% of preischaemic rate-pressure product after 30 min reperfusion, whereas ischaemic and hypoxic preconditioned hearts recovered 86(3)% and 94(5)%, respectively (p < 0.05 v control). Despite enhanced recovery of postischaemic ventricular function, ischaemic and hypoxic preconditioning reduced the time to onset of ischaemic contracture from a control value of 12.6(0.6) min to 9.3(0.7) and 9.0(0.6) min, respectively (p < 0.05). Neither adenosine receptor antagonist blocked preconditioning. Ischaemic preconditioned hearts recovered 80(5)% of preischaemic function in the presence of A1433U, and hypoxic preconditioned hearts in the presence of DPCPX recovered 85(4)%.
Ischaemic and hypoxic preconditioning enhance recovery of function following global ischaemia in the rat. The observations that adenosine receptor antagonists do not block the salutary effects of ischaemic or hypoxic preconditioning suggest that adenosine is not the sole mediator of preconditioning.
本研究旨在（1）确定缺血预处理和缺氧预处理是否能增强大鼠全心缺血后左心室功能的恢复，以及（2）评估选择性腺苷A1受体拮抗剂对缺血预处理和缺氧预处理的影响。
采用恒压灌注的离体大鼠心脏，进行30分钟缺血和30分钟再灌注。将对照心脏与在存在或不存在腺苷A1拮抗剂A1433U（10微摩尔）的情况下经5分钟缺血预处理的心脏，以及在存在或不存在腺苷A1拮抗剂8-环戊基-1,3-二丙基黄嘌呤（DPCPX，5微摩尔）的情况下经5分钟缺氧预处理的心脏进行比较。通过缺血前速率-压力乘积的恢复百分比来评估左心室功能的恢复情况。
对照心脏在30分钟再灌注后恢复了缺血前速率-压力乘积的64（标准误4）%，而缺血预处理和缺氧预处理的心脏分别恢复了86（3）%和94（5）%（与对照相比，p<0.05）。尽管缺血后心室功能恢复增强，但缺血预处理和缺氧预处理将缺血性挛缩开始的时间从对照值12.6（0.6）分钟分别缩短至9.3（0.7）分钟和9.0（0.6）分钟（p<0.05）。两种腺苷受体拮抗剂均未阻断预处理。在A1433U存在的情况下，缺血预处理的心脏恢复了缺血前功能的80（5）%，在DPCPX存在的情况下，缺氧预处理的心脏恢复了85（4）%。
缺血预处理和缺氧预处理可增强大鼠全心缺血后功能的恢复。腺苷受体拮抗剂未阻断缺血或缺氧预处理的有益作用，这表明腺苷不是预处理的唯一介质。
