Endothelium-dependent vasodilation in the skin microcirculation of patients with septic shock
Endothelium-dependent vasodilation in the skin microcirculation of patients with septic shock
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DOI：
10.1097/00024382-200303000-00013
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发表时间：
2003-03-01
期刊：
影响因子：
3.1
通讯作者：
Feihl, F
中科院分区：
文献类型：
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作者：
Kubli, S;Boëgli, Y;Feihl, F
脓毒症时内皮细胞功能障碍的证据大多局限于动物模型。我们研究了8名在重症监护病房(ICU)因感染性休克住院的患者皮肤微循环中的内皮功能。所有患者都需要肾上腺素支持。未接受任何血管活性药物治疗的12例血流动力学稳定的无脓毒症患者作为对照。两组的年龄和性别比例相似。作为额外的参考，16名年龄和性别与前两组匹配的健康、不吸烟的受试者也被研究。内皮功能的评估是基于比较离子导入应用乙酰胆碱(Ach)和硝普钠(SNP)的皮肤血流反应。用激光多普勒成像技术测量前臂掌侧皮肤血流量。在应用Ach或SNP之前，所有受试者的平均基线皮肤血流量都在100个灌流单位(PU)以下，并且不同组之间没有差异。与ICU对照组(Ach：291+/-135PU，P<；0.05；SNP：261+/-121PU，P<；0.01)和健康非吸烟组(Ach：336+/-98PU，P<；0.01；SNP：304+/-81PU，P<；0.01)相比，脓毒症患者两种药物引起的最大血流增量(Ach：167+/-63PU；SNP：138+/-34PU，Mean+/-SID)显著低于ICU对照组(Ach：336+/-98PU，P<；0.01；SNP：304+/-81PU，P<；0.01)。两组对Ach和SNP的反应率差异无统计学意义(脓毒症：1.22+/-0.40；ICU对照组：1.18+/-0.46；健康非吸烟组：1.12+/-0.24，P=0.86)。因此，脓毒症与内皮依赖性反应的选择性抑制无关。这些结果表明，感染性休克患者的皮肤微循环中，内皮细胞产生血管松弛信号的能力保持不变。
The evidence for endothelial dysfunction in sepsis is mostly restricted to animal models. We investigated endothelial function in the skin microcirculation of eight patients hospitalized for septic shock in an intensive care unit (ICU). All patients required adrenergic support. Twelve hemodynamically stable ICU patients without sepsis who did not receive any vasoactive medication were used as controls. The two groups were of similar age and sex ratio. For additional reference, 16 healthy, nonsmoking subjects matched for age and sex to the first two groups were also studied. The evaluation of endothelial function was based on the comparison of skin blood flow responses to iontophoretically applied acetylcholine (Ach, an endothelium-dependent vasoclilator) and sodium nitroprusside (SNP, an endothelium-independent vasodilator). Skin blood flow was measured on the volar face of the forearm using laser Doppler imaging. Before application of Ach or SNP, the mean baseline skin blood flow was below 100 perfusion units (PU) in all subjects and did not differ between groups. The maximal increase in blood flow elicited by both agents was significantly depressed in the patients with sepsis (Ach: 167 +/- 63 PU; SNP: 138 +/- 34 PU, mean +/- SID) compared with the ICU control patients (Ach: 291 +/- 135 PU, P < 0.05; SNP: 261 +/- 121 PU, P < 0.01) and the healthy, nonsmoking groups (Ach: 336 +/- 98 PU, P < 0.01; SNP: 304 +/- 81 PU, P < 0.01). The ratio of responses to Ach and SNP did not significantly differ between groups (septic: 1.22 +/- 0.40; ICU control 1.18 +/- 0.46, healthy, nonsmoking 1.12 +/- 0.24, P = 0.86). Thus, sepsis was not associated with a selective depression of the endothelium-dependent response. These results suggest that the capacity of the endothelium to produce signals for vasorelaxation remains intact in the skin microcirculation of patients with septic shock.