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采用在家兔全麻、开胸、自主呼吸和自主心律的条件下,结扎冠脉左室支造成急性心肌缺血模型,进而松开结扎结形成再灌注损伤模型。对心肌缺血和再灌注损伤的组织脂质过氧化物含量和局部血流量变化进行测定,同时辅以心电图监护;以丹参注射液为保护剂观察其作用效果。结果表明,随着缺血时间的延续,心肌脂质过氧化物含量逐渐增加;当缺血60分钟后再灌注30分钟,脂质过氧化物含量仍继续上升,明显高于缺血60分钟组,但与缺血90分钟组比较则无显著差异;其缺血区局部组织血流量再灌注后仅恢复53.2%。给予丹参保护的再灌注组,其缺血区组织脂质过氧化物含量较再灌注损伤组下降56.0%(P<0.005),而局部组织血流量恢复则提高32.0%(P<0.001)。
Under the conditions of general anesthesia, thoracotomy, spontaneous respiration and spontaneous heart rhythm in rabbits, ligating the left ventricular branches of the coronary arteries to create acute myocardial ischemia model, and then loosen the ligation knot to form a reperfusion injury model. Myocardial ischemia and reperfusion injury tissue lipid peroxidation and local blood flow changes were measured, supplemented by ECG monitoring; Danshen injection as a protective agent to observe the effect. The results showed that myocardial lipid peroxides gradually increased with the prolongation of ischemic time. When the animals were reperfused for 30 minutes after 60 minutes of ischemia, the content of lipid peroxides continued to increase, which was significantly higher than that of 60 minutes of ischemia , But there was no significant difference compared with the 90-minute ischemia group. Only 53.2% of the ischemic areas were re-infused with local blood flow. Compared with reperfusion group, the content of lipid peroxidation in ischemia reperfusion group was decreased by 56.0% (P <0.005), while the local tissue blood flow recovery was increased by 32.0% (P <0.001).