Redistribution of intestinal microcirculatory oxygenation during acute hemodilution in pigs
Redistribution of intestinal microcirculatory oxygenation during acute hemodilution in pigs
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DOI：
10.1152/japplphysiol.00861.2004
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发表时间：
2005-03-01
影响因子：
3.3
通讯作者：
Ince, C
中科院分区：
文献类型：
--
作者：
Schwarte, LA;Fournell, A;Ince, C
急性等容血液稀释(ANH)损害肠道微循环氧合；然而，其潜在的机制尚不完全清楚。我们假设，在这方面的贡献包括肠道外氧气的重新分配和肠道内氧气的分流。后者可能是由于红细胞在微循环中卸载氧的能力受损，从而导致组织/血浆PO2降低，但微循环血红蛋白氧(HBO(2))饱和度升高。或者，氧分流也可能是由于红细胞变形能力降低，阻碍了红细胞进入毛细血管的能力。麻醉猪行ANH(羟乙基淀粉20、40、60、90ml/kg)，ANH组10只，对照组5只。我们测量了全身和肠系膜的血流灌注。用缓解分光光度法[微循环HBO(2)饱和度(muHbO(2))]和钯-卟啉磷光猝灭[血浆/组织微循环氧分压(muPO(2)]]独立测定微血管肠道氧合。微循环氧分流以粘膜和肠系膜静脉HBO(2)饱和度(HBO(2)-GAP)之间的差值来评估。红细胞变形性以剪切力诱导的细胞伸长率(洛卡折射仪)测量。ANH使血红蛋白浓度从8.1 g/dl降至2.2g/dl。相对肠系膜灌注量减少(肠系膜/全身灌注率降低)。粘膜muHbO(2)(68+/-2至41+/-3%)和MuPO(2)(28+/-1至17+/-1 Torr)也出现平行下降。因此，所提议的指示氧卸载不足的星座(在muPO(2)下降时持续的muHbO(2))没有发展。HBO(2)-GAP的两倍增加表明肠道微循环氧分流增加。ANH期间，红细胞变形能力明显受损。我们的结论是，ANH期间肠道氧合减少，除了肠道外的氧气输送重新分配外，还与肠道内的氧气分流有关。这种分流似乎主要不是由氧卸载不足引起的，而是由氧/红细胞绕过毛细血管引起的，其中一个潜在的贡献者是红细胞变形能力受损。
Acute normovolemic hemodilution (ANH) compromizes intestinal microcirculatory oxygenation; however, the underlying mechanisms are incompletely understood. We hypothesized that contributors herein include redistribution of oxygen away from the intestines and shunting of oxygen within the intestines. The latter may be due to the impaired ability of erythrocytes to off-load oxygen within the microcirculation, thus yielding low tissue/plasma PO2 but elevated microcirculatory hemoglobin oxygen (HbO(2)) saturations. Alternatively, oxygen shunting may also be due to reduced erythrocyte deformability, hindering the ability of erythrocytes to enter capillaries. Anesthetized pigs underwent ANH ( 20, 40, 60, and 90 ml/kg hydroxyethyl starch; ANH group: n = 10; controls: n = 5). We measured systemic and mesenteric perfusion. Microvascular intestinal oxygenation was measured independently by remission spectrophotometry [ microcirculatory HbO(2) saturation (muHbO(2))] and palladium-porphyrin phosphorescence quenching [ microcirculatory oxygen pressure in plasma/tissue (muPO(2))]. Microcirculatory oxygen shunting was assessed as the disparity between mucosal and mesenteric venous HbO(2) saturation (HbO(2)-gap). Erythrocyte deformability was measured as shear stress-induced cell elongation (LORCA difractometer). ANH reduced hemoglobin concentration from 8.1 to 2.2 g/dl. Relative mesenteric perfusion decreased ( decreased mesenteric/systemic perfusion fraction). A paralleled reduction occurred in mucosal muHbO(2) (68 +/- 2 to 41 +/- 3%) and muPO(2) (28 +/- 1 to 17 +/- 1 Torr). Thus the proposed constellation indicative for oxygen off-load deficits ( sustained muHbO(2) at decreased muPO(2)) did not develop. A twofold increase in the HbO(2)-gap indicated increasing intestinal microcirculatory oxygen shunting. Significant impairment in erythrocyte deformability developed during ANH. We conclude that reduced intestinal oxygenation during ANH is, in addition to redistribution of oxygen delivery away from the intestines, associated with oxygen shunting within the intestines. This shunting appears to be not primarily caused by oxygen off-load deficit but rather by oxygen/erythrocytes bypassing capillaries, wherein a potential contributor is impaired erythrocyte deformability.