Gilles R J, D'Orio V, Ciancabilla F, Carlier P G
Department of Physiology, University Hospital, Liege, Belgium.
Crit Care Med. 1994 Mar;22(3):499-505. doi: 10.1097/00003246-199403000-00022.
To identify possible alterations in the skeletal muscle high-energy phosphate metabolism at the early phase of endotoxic shock in rats.
A prospective, randomized study of skeletal muscle energetics in endotoxemic and in control rats, by in vivo 31P nuclear magnetic resonance (NMR) spectroscopy at rest, under regional ischemia, and during reperfusion.
Biochemical NMR laboratory equipped for surgery and hemodynamic monitoring.
Wistar rats were randomized to different groups. Eight rats were injected with Escherichia coli endotoxin (15 mg/kg, survival time 19 +/- 4 hrs) intraperitoneally. Seven other rats served as controls. The additional nine rats were studied for the saturation recovery pulse sequence.
In the treatment group, endotoxin was injected 8 hrs before NMR spectroscopy. The right hind limbs were studied under anaesthesia using a surface coil NMR probe. Their high-energy phosphate contents and intracellular pH were determined by 31P NMR spectroscopy. After baseline measurements, an ischemia-reperfusion challenge was imposed on the muscle by transient clamping of the abdominal aorta. Contralateral femoral artery pressure was constantly monitored.
During the baseline period, the endotoxin-treated muscles did not show any difference in the distribution of the high-energy phosphate compounds or in intracellular pH, as compared with the controls. Ischemia resulted in a significantly faster decline of the inorganic phosphate/creatine phosphate ratio in the endotoxin-treated rats (1.35 +/- 0.17 vs. 0.51 +/- 0.06 at the end of the 38-min ischemic period). Skeletal muscle acidosis developed earlier and was deeper in the endotoxemic animals (pH: 6.94 +/- 0.02 vs. 7.02 +/- 0.03 at the end of ischemia). During reperfusion, the calculated time constants of recovery of inorganic phosphate to phosphocreatine ratios were identical between groups.
Resting nonischemic muscles of endotoxin-treated rats show no evidence of alterations in high-energy phosphate metabolism. However, under ischemic conditions, high-energy phosphate metabolism deteriorates faster in the skeletal muscles of treated animals. These data support the hypothesis of a greater mismatch during perfusion at very low pressure between residual oxygen availability and oxygen needs in the endotoxin-treated muscle cell.
确定大鼠内毒素休克早期骨骼肌高能磷酸代谢可能存在的改变。
一项对内毒素血症大鼠和对照大鼠骨骼肌能量学的前瞻性、随机研究，通过在静息状态、局部缺血期间及再灌注期间进行体内31P核磁共振（NMR）光谱分析。
配备手术和血流动力学监测设备的生化NMR实验室。
将Wistar大鼠随机分为不同组。8只大鼠腹腔注射大肠杆菌内毒素（15mg/kg，存活时间19±4小时）。另外7只大鼠作为对照。对另外9只大鼠进行饱和恢复脉冲序列研究。
在治疗组中，在进行NMR光谱分析前8小时注射内毒素。使用表面线圈NMR探头在麻醉状态下研究右后肢。通过31P NMR光谱分析测定其高能磷酸盐含量和细胞内pH值。在基线测量后，通过短暂夹闭腹主动脉对肌肉施加缺血-再灌注刺激。持续监测对侧股动脉压力。
在基线期，与对照组相比，内毒素处理的肌肉在高能磷酸化合物分布或细胞内pH值方面没有显示出任何差异。缺血导致内毒素处理大鼠的无机磷酸盐/磷酸肌酸比值下降明显更快（在38分钟缺血期结束时为1.35±0.17，而对照组为0.51±0.06）。骨骼肌酸中毒在内毒素血症动物中出现更早且更严重（缺血结束时pH值：6.94±0.02，而对照组为7.02±0.03）。在再灌注期间，两组间无机磷酸盐与磷酸肌酸比值恢复的计算时间常数相同。
内毒素处理大鼠的静息非缺血肌肉没有显示出高能磷酸代谢改变的证据。然而，在缺血条件下，处理动物的骨骼肌高能磷酸代谢恶化更快。这些数据支持这样的假设，即在内毒素处理的肌肉细胞中，在非常低的压力下灌注期间，残余氧供应与氧需求之间存在更大的不匹配。
