Intermittent hypoxic training protects canine myocardium from infarction
Intermittent hypoxic training protects canine myocardium from infarction
复制标题
DOI：
10.1177/153537020422900813
复制
发表时间：
2004-09-01
影响因子：
3.2
通讯作者：
Downey, HF
中科院分区：
文献类型：
--
作者：
Zong, P;Setty, S;Downey, HF
本研究旨在探讨常压间歇低氧训练对心脏的保护作用。6只犬在常压舱内进行连续20天的间歇性低氧训练，间歇性通入N-2，使吸入氧分数（F-IO_2）降至9.5%~ 10%。低氧期，最初为5分钟，增加到10分钟，随后为4分钟的常氧期。重复该低氧-常氧方案，最初5次，增加至8次。狗在间歇性低氧训练期间没有表现出不适。低氧训练20天后，在急性实验中评估心室肌对梗死的抵抗力。结扎冠状动脉左前降支（LAD）60 min，再灌注5 h。在LAD闭塞30分钟时，通过左心房导管注射放射性微球以评估进入缺血区域的冠状动脉侧支血流。再灌注5小时后，对心脏进行染色以描绘梗死危险区（AAR），并用氯化三苯基四唑染色以鉴定梗死心肌。左前降支阻断及再灌注期间，全身血流动力学和整体左室功能稳定。4例未检出梗死，2例占AAR的1.6%。相比之下，6只在压缩空气通气室中进行假训练的狗和5只接受相同LAD闭塞/再灌注方案的未经训练的狗的梗死分别为AAR的36.8% +/- 5.8%和35.2% +/- 9.5%。6只低氧训练犬中有4只的梗死面积减少不能用增强的AAR侧支血流来解释。低氧训练的狗没有室性心动过速或室颤。三个假训练的狗有室性心动过速和两个心室颤动。3只未经训练的犬出现室颤。总之，间歇性低氧训练可以保护犬心肌在冠状动脉闭塞和再灌注过程中免于梗死和危及生命的心律失常。这种有效的心脏保护机制值得进一步研究。
This investigation examined cardiac protective effects of normobaric intermittent hypoxia training. Six dogs underwent intermittent hypoxic training for 20 consecutive days in a normobaric chamber ventilated intermittently with N-2 to reduce fraction of inspired oxygen (F-IO2) to 9.5%-10%. Hypoxic periods, initially 5 mins and increasing to 10 mins, were followed by 4-min normoxic periods. This hypoxia-normoxia protocol was repeated, initially 5 times and increasing to 8 times. The dogs showed no discomfort during intermittent hypoxic training. After 20 days of hypoxic training, the resistance of ventricular myocardium to infarction was assessed in an acute experiment. The left anterior descending (LAD) coronary artery was occluded for 60 mins and then reperfused for 5 hrs. At 30 mins of LAD occlusion, radioactive microspheres were injected through a left atrial catheter to assess coronary collateral blood flow into the ischemic region. After 5 hrs reperfusion, the heart was dyed to delineate the area at risk (AAR) of infarction and stained with triphenyl tetrazolium chloride to identify infarcted myocardium. During LAD occlusion and reperfusion, systemic hemodynamics and global left ventricular function were stable. Infarction was not detected in 4 hearts and was 1.6% of AAR in the other 2 hearts. In contrast, 6 dogs sham-trained in a chamber ventilated with compressed air and 5 untrained dogs subjected to the same LAD occlusion/reperfusion protocol had infarcts of 36.8% +/- 5.8% and 35.2% +/- 9.5% of the AAR, respectively. The reduction in infarct size of four of the six hypoxia-trained dogs could not be explained by enhanced collateral blood flow to the AAR. Hypoxia-trained dogs had no ventricular tachycardia or ventricular fibrillation. Three sham-trained dogs had ventricular tachycardia and two had ventricular fibrillation. Three untrained dogs had ventricular fibrillation. In conclusion, intermittent hypoxic training protects canine myocardium from infarction and life-threatening arrhythmias during coronary artery occlusion and reperfusion. The mechanism responsible for this potent cardioprotection merits further study.