Yorozuya Toshihiro, Adachi Naoto, Dote Kentaro, Nakanishi Kazuo, Takasaki Yasushi, Arai Tatsuru
Department of Anesthesiology and Resuscitology, Ehime University School of Medicine, Shitsukawa, Shigenobu-cho, Onsen-gun, Ehime 791-0295, Japan.
Eur J Cardiothorac Surg. 2004 Nov;26(5):981-7. doi: 10.1016/j.ejcts.2004.06.009.
Ischemic preconditioning (IP) has been shown to attenuate intracellular Na+ accumulation and Ca2+ overload during ischemia and reperfusion, both of which are closely related to the outcome of myocardial damage. We compared the effects of single- and four-cycle IP in Na+,K(+)-activated adenosine 5'-triphosphatase (Na+,K(+)-ATPase) and Ca(2+)-activated adenosine 5'-triphosphatase (Ca(2+)-ATPase) activities in in vivo rabbit hearts, correlating these differences to the quality of protection against subsequent ischemia.
The morphological outcome was evaluated in in vivo rabbit hearts subjected to 30 min of coronary occlusion and reperfusion for 180 min by assessing the ratio of infarct volume to risk zone volume. The effects of single- and four-cycle preconditioning ischemia were then examined. Another set of in vivo rabbit hearts was subjected to the measurement of ATPase activities at the conclusion of final preconditioning ischemia and at 60 min after reperfusion following 30 min of ischemia.
The infarct volume was reduced by single-cycle IP to 38% of that in the control group. The four-cycle IP further reduced the infarct volume, which was 11% of that in the control group. Na+,K(+)-ATPase activity at 60 min after reperfusion in the four-cycle group was increased to 172% of that in the control group (10.8 micromol ADP/h/mg protein), whereas no difference was found in the single-cycle group. On the other hand, Ca(2+)-ATPase activity at the conclusion of IP was increased by single-cycle IP, the value being 255% of that in the control group (4.9 micromol ADP/h/mg protein). The four-cycle IP further increased the activity, and the value was 158% of that in the single-cycle group.
Since increases in Na+,K(+)-ATPase and Ca(2+)-ATPase activities contribute to the decrease in intracellular Ca2+ concentration, the enhancement of these activities by four-cycle IP may be involved in the additional protection.
缺血预处理（IP）已被证明可减轻缺血和再灌注期间细胞内钠离子蓄积和钙离子超载，这两者均与心肌损伤的结果密切相关。我们比较了单次和四次循环IP对体内兔心脏中钠钾激活的三磷酸腺苷酶（Na +，K（+）-ATP酶）和钙激活的三磷酸腺苷酶（Ca（2 +）-ATP酶）活性的影响，并将这些差异与对随后缺血的保护质量相关联。
通过评估梗死体积与危险区体积之比，对经历30分钟冠状动脉闭塞和180分钟再灌注的体内兔心脏的形态学结果进行评估。然后检查单次和四次循环预处理缺血的效果。另一组体内兔心脏在最终预处理缺血结束时以及缺血30分钟后再灌注60分钟时进行ATP酶活性测量。
单次循环IP使梗死体积减少至对照组的38％。四次循环IP进一步减少了梗死体积，为对照组的11％。四次循环组再灌注60分钟时的Na +，K（+）-ATP酶活性增加至对照组的172％（10.8微摩尔ADP /小时/毫克蛋白质），而单次循环组未发现差异。另一方面，单次循环IP使IP结束时的Ca（2 +）-ATP酶活性增加，该值为对照组的255％（4.9微摩尔ADP /小时/毫克蛋白质）。四次循环IP进一步增加了活性，该值为单次循环组的158％。
由于Na +，K（+）-ATP酶和Ca（2 +）-ATP酶活性的增加有助于细胞内钙离子浓度的降低，四次循环IP对这些活性的增强可能参与了额外的保护作用。
