|
Background and Purpose: limb ischemia-reperfusion injury is very common in clinical, peripheral vascular surgery, limb trauma, limb replantation surgery, thrombosis, abdominal aortic aneurysm surgery, crush syndrome can cause limb ischemia reperfusion injury. Recent studies have found that limb ischemia-reperfusion injury affects not only the ischemic tissue survival and function, and can also cause systemic inflammatory response syndrome, involving the heart, liver, lung, kidney, small intestine, brain and other distant organs, leading to multiple impaired organ function, in which the most important cardiovascular system damage. Currently limb ischemia-induced lung, brain, liver, intestinal injury mechanism more research on skeletal muscle ischemia-reperfusion myocardial injury induced pathophysiological mechanisms, has not yet been fully elucidated, numerous studies show that: Serious limb ischemia-reperfusion injury can lead to stress-induced hypertension, arrhythmia stress, stress myocardial ischemia, heart failure, etc., heme oxygenase -1 (heme oxygenase-1, HO-1) is found by a maximum factor-induced stress proteins. These stimuli have in common is can cause oxidative stress. HO-1 have anti-inflammatory, anti-apoptotic, anti-proliferative, anti-oxidation properties, as well as other aspects of the immune response has an important role, and in recent years become a research hotspot. The experimental application of a tourniquet to build limb ischemia-reperfusion model in rats was observed after limb ischemia-reperfusion myocardial pathological changes, oxidative stress mechanisms and inducible heme oxygenase (HO-1) to illustrate the expression of myocardial injury and self-protection mechanism. The experiment was divided into two parts: First, observe limb ischemia-reperfusion injury after myocardial changes, and learn of oxidative stress in limb ischemia secondary to myocardial reperfusion injury in rats. Second, the observation of endogenous HO-1 in limb ischemia-reperfusion myocardial expression changes in the law and its significance. Methods: This study applied a tourniquet to construct limbs tied rat limb ischemia-reperfusion model, the experimental rats were randomly divided into seven groups. Namely: the normal group, ischemia-reperfusion 2 hours 4 hours group, reperfusion group 4 hours, 6 hours reperfusion group, reperfusion group of eight hours, 16 hours reperfusion group, reperfusion 24 hours group. The first part of the experiment: light microscopy myocardial pathological changes; were measured in serum and myocardial tissue malondialdehyde (MDA) content, total superoxide dismutase (T-SOD) activity and myeloperoxidase (MPO ) activity. The second part of the experiment: reverse transcription - polymerase chain reaction (RT-PCR) detection of myocardial HO-1mRNA expression variation. Results: 4,6 hours ischemia-reperfusion, myocardial cells was swelling, muscle gap widened significantly smaller vascular congestion, muscle gap seen in the large number of red blood cells leak gap nucleated muscle cells increased, reperfusion 24 hours mitigate these changes. Compared with normal group, plasma MDA and myocardial MDA: ischemia-reperfusion in each group were significantly higher (P <0.01), peaked at 4h reperfusion; plasma SOD: ischemia-reperfusion in each group were significantly decreased (P <0.01) reperfusion, 4 hours and reached the lowest value, myocardial SOD: reperfusion in each group were significantly decreased (P <0.01), reperfusion eight hours and reached the lowest value; plasma and myocardial MPO: ischemia-reperfusion 2h ~ 8h appeared significantly higher ( P <0.01), peak plasma MPO 4h, myocardial MPO 6h peaked, 16,24 h decline. Limb ischemia can induce HO-1mRNA upregulated in the myocardium, compared with the normal group, reperfusion 2h, HO-1mRNA expression did not change significantly (P> 0.05); reperfusion 4h, 6h, 8h, 16h, 24h after HO 1 expression significantly increased (P <0.01), and reached the peak at 16h. Conclusion: limbs can cause myocardial ischemia-reperfusion injury, reperfusion myocardial injury heaviest 4-6 hours, systemic and myocardial inflammatory cell aggregates activation, activation of inflammatory cytokines and excessive oxidative stress and antioxidant imbalance is oxidized limb ischemia-reperfusion induced myocardial injury mechanisms, the body's own protective mechanisms exist, reactive oxygen species and inflammatory factors can increase the expression of HO-1, against oxidative stress, which play a protective role in myocardial cells.
|