MICROVASCULAR FUNCTION AND RHEOLOGICAL CHANGES IN HYPERDYNAMIC SEPSIS
MICROVASCULAR FUNCTION AND RHEOLOGICAL CHANGES IN HYPERDYNAMIC SEPSIS
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DOI：
10.1097/00003246-199502000-00011
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发表时间：
1995-02-01
影响因子：
8.8
通讯作者：
RACKOW, EC
中科院分区：
文献类型：
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作者：
ASTIZ, ME;DEGENT, GE;RACKOW, EC
目的：调查流变学变化和循环异常设计：前瞻性对照试验。地点：大学附属医院的内科和外科重症监护病房。患者：符合研究进入标准的九名正常对照者和八名患有严重脓毒症的成人患者，干预措施：通过空气体积描记法测量静息和反应性充血期间的前臂血流量，同时进行血流动力学测量和用于神学测量的血液样本。测量和主要结果：红细胞使用简单的过滤程序确定变形指数，使用白细胞测试检测人全血中的白细胞聚集，使用单克隆抗体和流式细胞术测量中性粒细胞粘附分子CD11b/CD18的表达，在符合进入研究标准的患者24小时内获取Ah数据，心输出量、氧输送和耗氧量测量结果与严重脓毒症的高动力期一致，前臂血流量显着（p < .05) 脓毒症患者 (21 +/- 3 mL/min) 高于对照组 (12 +/- 2 mL/min)。对照组反应性充血期间的前臂血流量增加了三倍，从 12 +/- 2 到 36 +/- 5 mL/min (p < .05)，而在脓毒症患者中，反应性充血期间的前臂血流量从 21 +/- 3 增加到 32 +/- 4 mL/min。对照组中反应性充血期间的前臂血流量与休息时的前臂血流量之比为 3.2 +/- 0.1脓毒症患者为 1.6 +/- 0.1 (p < .01)，与对照组相比，脓毒症患者全血中的红细胞变形指数显着降低 (p < .01)（0.41 +/- 0.07 vs 0.98 +/- 0.08 mL/min）。当血细胞比容调整至 45% 时，这种差异仍然存在（0.82 +/- 0.06 与 1.04 +/- 0.06 mL/min；p < .05），与对照受试者（233 +/- 26 对数荧光单位）相比，在脓毒症患者中观察到中性粒细胞粘附分子 CD11b/CD18 的表达增加（349 +/- 46 对数荧光单位）； p < .05), 与对照受试者 (8.9 +/- 1.6%) 相比，脓毒症患者的白细胞计数也显着 (p < .05) 增加 (17.7 +/- 3.8%)，对照组和脓毒症患者的白细胞计数与中性粒细胞粘附分子 CD11b/CD18 的表达之间观察到显着相关性 (r(2) = .62；p < .01)，白细胞计数为也与全血红细胞变形指数呈负相关（r(2) = .28；p < .05）。 结论：脓毒症患者前臂反应性充血明显减少，表明微血管血流受损。流变学变化，包括红细胞变形能力受损、白细胞聚集和内皮粘附增加，可能通过损害有效毛细血管横截面积而导致这种异常。
Objective: To investigate the theologic changes and circulatory abnormalitiesDesign: Prospective, controlled trial.Setting: Medical and surgical intensive care units of a university-affiliate hospital.Patients: Nine normal controls and eight adult patients with severe sepsis who met the study entrance criteria,Interventions: Forearm blood flow was measured at rest and during reactive hyperemia by air plethysmography, Simultaneous hemodynamic measurements and blood samples for theologic measurements were taken.Measurements and Main Results: Red blood cell deformability index was determined using a simple filtration procedure, Leukocyte aggregation in whole human blood was detected by using a leukergy test, Expression of the neutrophil adhesion molecule CD11b/CD18 was measured using a monoclonal antibody and flow cytometry, Ah data were taken within 24 hrs of the patient meeting criteria for entrance into the study,Cardiac output, oxygen delivery, and oxygen consumption measurements were consistent with the hyperdynamic phase of severe sepsis, Forearm blood flow was significantly (p < .05) greater in septic patients (21 +/- 3 mL/min) than in controls (12 +/- 2 mL/min). Forearm blood flow during reactive hyperemia increased three-fold in the controls from 12 +/- 2 to 36 +/- 5 mL/min (p < .05), while in the septic patients, forearm blood flow during reactive hyperemia increased from 21 +/- 3 to 32 +/- 4 mL/min, The ratio of forearm blood flow during reactive hyperemia to forearm blood flow at rest was 3.2 +/- 0.1 in the controls and 1.6 +/- 0.1 in the septic patients (p < .01), The red blood cell deformability index in whole blood was significantly (p < .01) decreased in the septic patients compared with the control subjects (0.41 +/- 0.07 vs, 0.98 +/- 0.08 mL/min). This difference remained true when the hematocrit was adjusted to 45% (0.82 +/- 0.06 vs. 1.04 +/- 0.06 mL/min; p < .05), Increased expression of the neutrophil adhesion molecule CD11b/CD18 was observed in septic patients (349 +/- 46 logarithmic fluorescence units) as compared with control subjects (233 +/- 26 logarithmic fluorescence units; p < .05), Leukergy was also significantly (p < .05) increased in septic patients (17.7 +/- 3.8%) as compared with control subjects (8.9 +/- 1.6%), A significant correlation was observed between leukergy and the expression of the neutrophil adhesion molecule CD11b/CD18 in controls and septic patients (r(2) = .62; p < .01), Leukergy was also inversely correlated with whole blood red blood cell deformability index (r(2) = .28; p < .05).Conclusions: Reactive hyperemia in the forearm is significantly diminished in patients with sepsis, suggesting impaired microvascular blood flow, Rheologic changes, including impaired red blood cell deformability, increased leukocyte aggregation and endothelial adherence, may contribute to this abnormality by compromising effective capillary cross-sectional area.