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首页> 外文期刊>Artificial Organs >Liposome-Encapsulated Hemoglobin Improves Energy Metabolism in Skeletal Muscle Ischemia and Reperfusion in the Rat
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Liposome-Encapsulated Hemoglobin Improves Energy Metabolism in Skeletal Muscle Ischemia and Reperfusion in the Rat

机译：脂质体包裹的血红蛋白改善大鼠骨骼肌缺血和再灌注中的能量代谢

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The effect of liposome-encapsulated hemoglobin (LEH) was tested in a rodent model of limb ischemia and reperfusion—causing local reperfusion injury and a cascade of systemic responses. Intracellular pH (pHi) and phosphocreatine (PCr)/inorganic phosphate (Pi) ratio were serially monitored using 31P-nuclear magnetic resonance spectroscopy with a 2-cm solenoid coil on a rodent hind limb. After baseline measurements, the right hind limb underwent ischemia for 70?min, followed 10?min later by intravenous administration of LEH (10?mL/kg, n?=?6), homologous red blood cells (RBCs, n?=?6), saline (n?=?6), or no treatment (n?=?6). Reperfusion was then observed for an additional 60?min. While pHi decreased precipitously after the onset of ischemia and even following reperfusion, LEH-treated rats had significantly milder intracellular acidosis compared with all other groups during ischemia, and after reperfusion as well throughout the observation with the saline-treated rats. In contrast, the PCr/Pi ratio decreased regardless of treatment after ischemia until reperfusion, when the ratio returned toward normal or the energy status improved only in the LEH-treated rats, while the ratio remained depressed in the control animals receiving RBC, saline, or no treatment. Morphological studies 7?days later revealed a tendency toward suppressed mononuclear cell infiltration with preservation of muscular mass and structure in the LEH-treated rats. LEH treatment after early limb ischemia appeared to improve intracellular energy metabolism and eventually preserve skeletal muscle in a rodent model of limb ischemia and reperfusion.
机译：在肢体缺血和再灌注的啮齿动物模型中测试了脂质体包裹的血红蛋白（LEH）的作用-引起局部再灌注损伤和一系列全身反应。用 31 P-核磁共振波谱对啮齿类动物后肢上的2 cm螺线管线圈进行连续监测细胞内pH（pHi）和磷酸肌酸（PCr）/无机磷酸（Pi）的比率。基线测量后，右后肢缺血70分钟，然后10分钟后静脉内注射LEH（10 mL / kg，n = 6），同源红细胞（RBCs，n = 6）。 6），盐水（n≥6）或不进行任何处理（n≥6）。然后观察再灌注60分钟。尽管在缺血发作后甚至再灌注后pHi急剧下降，但在缺血期间以及在整个盐水治疗大鼠的观察中，与所有其他组相比，LEH治疗的大鼠的细胞内酸中毒明显轻于所有其他组。相比之下，缺血再灌注后无论治疗如何，PCr / Pi比率均下降，当比率恢复正常或仅在LEH治疗的大鼠中能量状态改善时，而在接受RBC，盐水，或不治疗。 7天后的形态学研究显示，在LEH治疗的大鼠中，单核细胞浸润趋于抑制，同时保留了肌肉质量和结构。在肢体缺血和再灌注的啮齿动物模型中，早期肢体缺血后的LEH治疗似乎可以改善细胞内能量代谢，并最终保留骨骼肌。

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