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观察兔心肌缺血-再灌注损伤结扎前、缺血后20min和再灌注30min 3个不同时期冠状动脉血中氧分压(PcaO_2)、二氧化碳分压(PcaCO_2)、pH值、血氧饱和度(SaO_2)、氧含量(CaO_2)、实际碳酸氢盐(AB)、标准碳酸氢盐(SB)和剩余碱(BE)8项参数的变化规律,结果显示,除PcaCO_2和BE在灌注30min与结扎前无明显变化外,其余参数在缺血后20min和灌注30min均明显低于结扎前(P<0.01),且灌注后30min冠状动脉血中的pH、PcaO_2、SaO_2、CaO_24项参数也较缺血后20min显著降低(<0.01或P<0.05)。作者认为,低氧血症既是冠状动脉缺血造成的直接恶果,又是引起代谢性酸中毒的直接原因。低氧血症和代谢性酸中毒是加重心肌进一步损伤的两大主要因素。
The changes of PcaO_2, PcaCO_2, pH and oxygen saturation (P <0.05) before and after myocardial ischemia / reperfusion injury were observed in 20 min after ischemia and 30 min after reperfusion. (CaO 2), actual bicarbonate (AB), standard bicarbonate (SB) and remaining alkaloid (BE). The results showed that except PcaCO 2 and BE, The other parameters were significantly lower than those before ischemia (P <0.01) at 20 min after ischemia and 30 min after perfusion, and the parameters of pH, PcaO_2, SaO_2 and CaO_24 in coronary artery blood were also significantly lower than those before ischemia 20min significantly reduced (<0.01 or P <0.05). The author believes that hypoxemia is not only a direct result of coronary ischemia, but also a direct cause of metabolic acidosis. Hypoxemia and metabolic acidosis are two major contributors to further myocardial damage.