包括由于血液堵塞引起短暂缺氧而受损的心脏组织。
This would include cases where heart tissue becomes damaged after being deprived temporarily of oxygen due to a blockage in the blood supply.
心脏遭受短暂缺血或高温处理后均产生早期和延迟保护效应。
Preconditioning of the heart induced by a brief ischemia or hyperthermia is exerted in two phases, early and delayed protection.
短暂缺氧血清剥夺再灌注后，存在低能量状态，且可完全恢复。
There existed a lower energy status after transient anoxia-serum deprivation and reperfusion and the lower energy status can resume the normal level.
探讨大鼠在体心肌短暂缺血不同时间后出现再灌注心律失常的变化。
To investigate the effects of different duration of myocardial ischemia on the severity of reperfusion-induced arrhythmias in rat hearts in vivo.
某些时候我会反复往返，不过Esu会在我短暂缺席期间处理问题。
I have at certain times been back and forth but Esu has been holding the forth during my brief absences.
短暂缺血后心肌功能明显减退，再灌注后逐渐恢复，但仍未达到假结扎组水平。
The myocardial contractile function after transient ischemia significantly impaired and gradually recovered after reperfusion, but not to the level of sham-occlusion group.
肢体缺血预适应是指肢体短暂缺血后使肢体本身骨骼肌或远隔组织能耐受较长时间的缺血损伤。
Ischemic preconditioning in limb renders skeletal muscle itself or remote tissue or organ being able to resistant a subsequent more sustained ischemic insult.
目的研究山奈酚对正常和急性短暂缺氧时大鼠海马CA_1锥体神经元电压依赖性钾通道的作用。
OBJECTIVE To investigate the effects of kaempferol on voltage-gated potassium currents in CA_1 pyramidal neurons of rat hippocampus in both normal state and acutely transient hypoxia.
缺血预适应是指心脏遭受短暂缺血后能耐受随后较长时间缺血损伤，是近年发现的一种预防心肌缺血损伤的有效措施。
Ischemic preconditioning has been defined as a tolerance of the myocardium to subsequent sustained ischemic damage after the heart was insulted one or more brief periods of ischemic stress.
结论肝素参与短暂缺血-再灌注顿抑心肌功能的保护，机制可能是通过药物性预适应，增强内皮源性NO的产生，从而减轻心肌缺血-再灌注损伤。
Conclusions: These results suggest that heparin preserve the function of myocardium after brief IR injury, the mechanism in part by promoting the production of NO, preserving the endothelium function.
结论肝素参与短暂缺血-再灌注顿抑心肌功能的保护，机制可能是通过药物性预适应，增强内皮源性NO的产生，从而减轻心肌缺血-再灌注损伤。
Conclusions: These results suggest that heparin preserve the function of myocardium after brief IR injury, the mechanism in part by promoting the production of NO, preserving the endothelium function.
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