Korthuis R J, Smith J K, Carden D L
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130-3932.
Am J Physiol. 1989 Jan;256(1 Pt 2):H315-9. doi: 10.1152/ajpheart.1989.256.1.H315.
The results of several recent studies have demonstrated that reactive oxygen metabolites are responsible for a major portion of ischemia/reperfusion (I/R) injury in skeletal muscle. Presumably, the cytotoxic oxidants are produced during reperfusion when molecular oxygen (the source of the reactive oxygen metabolites) is reintroduced to the tissues. The purpose of this study was to test the hypothesis that molecular oxygen must be provided at reperfusion to produce I/R injury in skeletal muscle. Isolated, maximally vasodilated (papaverine) canine gracilis muscles were reperfused, after 4 h of inflow occlusion, from reservoirs containing autologous blood equilibrated with either 95% O2-5% CO2 or 95% N2-5% CO2 gas mixtures. Arterial PO2 fell from approximately 120 mmHg to less than 3-5 mmHg, during the use of nitrogen. The solvent drag reflection coefficient for total plasma proteins (sigma f) and total vascular resistance was determined for the following conditions: control (no ischemia), reperfusion with oxygenated blood after 4 h ischemia; and reperfusion (after 4 h ischemia), first with anoxic blood and then oxygenated blood. Reperfusion with oxygenated blood, after 4 h of ischemia, significantly reduced solvent drag reflexion coefficient (sigma f) from 0.93 +/- 0.02 to 0.63 +/- 0.02, indicating a dramatic increase in vascular permeability. Total vascular resistance increased from 6.1 +/- 1.1 mmHg.ml-1.min.100 g during the preischemic period to 12.9 +/- 3.0 mmHg.ml-1.min.100 g during normoxic reperfusion. In muscles reperfused with anoxic blood, sigma f averaged 0.82 +/- 0.06, whereas vascular resistance increased by 56 +/- 13%.(ABSTRACT TRUNCATED AT 250 WORDS)
最近几项研究的结果表明，活性氧代谢产物是骨骼肌缺血/再灌注（I/R）损伤的主要原因。据推测，细胞毒性氧化剂是在再灌注期间产生的，此时分子氧（活性氧代谢产物的来源）被重新引入组织。本研究的目的是检验以下假设：在再灌注时必须提供分子氧才能在骨骼肌中产生I/R损伤。将分离的、最大程度血管舒张（用罂粟碱）的犬股薄肌在血流阻断4小时后，从含有与95% O₂ - 5% CO₂ 或95% N₂ - 5% CO₂ 气体混合物平衡的自体血的储液器中进行再灌注。在使用氮气期间，动脉血氧分压从约120 mmHg降至低于3 - 5 mmHg。在以下条件下测定了总血浆蛋白的溶剂拖曳反射系数（σf）和总血管阻力：对照（无缺血）、缺血4小时后用含氧血再灌注；以及再灌注（缺血4小时后），先用缺氧血然后用含氧血。缺血4小时后用含氧血再灌注，显著降低了溶剂拖曳反射系数（σf），从0.93 ± 0.02降至0.63 ± 0.02，表明血管通透性急剧增加。总血管阻力在缺血前期从6.1 ± 1.1 mmHg·ml⁻¹·min⁻¹·100 g增加到常氧再灌注期间的12.9 ± 3.0 mmHg·ml⁻¹·min⁻¹·100 g。在用缺氧血再灌注的肌肉中，σf平均为0.82 ± 0.06，而血管阻力增加了56 ± 13%。（摘要截断于250字）
