Septic shock and chemotherapy-induced cytopenia: effects on microcirculation

Septic shock and chemotherapy-induced cytopenia: effects on microcirculation
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DOI:
10.1007/s00134-012-2582-4
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发表时间:
2012-08-01
影响因子:
38.9
通讯作者:
Matejovic, Martin
Matejovic, Martin
中科院分区:
医学1区
文献类型:
--
作者:
Karvunidis, Thomas;Chvojka, Jiri;Matejovic, Martin

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中性粒细胞和血小板活化及其与内皮细胞的相互作用被认为是脓毒症诱导的微循环改变的中心特征。然而,没有研究评估化疗诱导的严重血细胞减少的感染性休克患者的微血管模式。在四组受试者中收集人口统计学和血液动力学变量以及舌下微循环记录[侧流暗场技术(OPS-SDF)视频显微镜增强的正交偏振光谱成像]:脓毒性休克(SS,N = 9)、血细胞减少患者中的脓毒性休克(NSS,N = 8)、无感染的血细胞减少(NEUTR,N = 7)和健康对照(CTRL,N = 13)。除对照组外,在感染性休克和/或中性粒细胞减少症完全消退后重复所有测量。使用适当的软件工具处理视频文件,并半定量评价[总血管密度(TVD,mm/mm(2)),灌注血管密度(PVD,mm/mm(2))、灌注血管比例(PPV,%)、平均血流指数(MFI)和血流异质性指数(FHI)]。与对照组相比,所有受试患者组均存在统计学显著的微循环改变(TVD:SS = 8.8,NSS = 8.8,NEUTR = 9.1对比CTRL = 12.6,p < 0.001; PVD:SS = 6.3,NSS = 6.1,NEUTR = 6.9对比CTRL = 12.5,p < 0.001; PPV:SS = 71.6,NSS = 68.9,NEUTR = 73.3对比CTRL = 98.7,p < 0.001; MFI:SS = 2.1,NSS = 1.9,NEUTR = 2.1对比CTRL = 3.0,p < 0.05; FHI:SS = 1.0,NSS = 0.9,NEUTR = 0.6对比CTRL = 0.0,p < 0.001)。在基线时,SS、NSS和NEUTR组之间未检测到显著差异。在脓毒性休克和/或中性粒细胞减少症消退后,观察到微循环灌注的不完全恢复,与SS患者相比,NSS患者的MFI和FHI变量有更好恢复的趋势。我们的数据可能表明,严重的中性粒细胞减少症和血小板减少症不会使微循环对脓毒症引起的微血管改变更具抵抗力。与化疗诱导的血细胞减少相关的微血管改变的作用和机制需要进一步研究。
Neutrophil and platelet activation and their interactions with endothelial cells are considered central features of sepsis-induced microcirculatory alterations. However, no study has evaluated the microvascular pattern of septic shock patients with chemotherapy-induced severe cytopenia.Demographic and hemodynamic variables together with sublingual microcirculation recording [orthogonal polarization spectral imaging enhanced by sidestream dark-field technology (OPS-SDF) videomicroscopy] were collected in four groups of subjects: septic shock (SS, N = 9), septic shock in cytopenic patients (NSS, N = 8), cytopenia without infection (NEUTR, N = 7), and healthy controls (CTRL, N = 13). Except for controls, all measurements were repeated after complete resolution of septic shock and/or neutropenia. Video files were processed using appropriate software tool and semiquantitatively evaluated [total vascular density (TVD, mm/mm(2)), perfused vessel density (PVD, mm/mm(2)), proportion of perfused vessels (PPV, %), mean flow index (MFI), and flow heterogeneity index (FHI)].Compared with controls, there were statistically significant microcirculatory alterations within all tested groups of patients (TVD: SS = 8.8, NSS = 8.8, NEUTR = 9.1 versus CTRL = 12.6, p < 0.001; PVD: SS = 6.3, NSS = 6.1, NEUTR = 6.9 versus CTRL = 12.5, p < 0.001; PPV: SS = 71.6, NSS = 68.9, NEUTR = 73.3 versus CTRL = 98.7, p < 0.001; MFI: SS = 2.1, NSS = 1.9, NEUTR = 2.1 versus CTRL = 3.0, p < 0.05; FHI: SS = 1.0, NSS = 0.9, NEUTR = 0.6 versus CTRL = 0.0, p < 0.001). No significant differences were detected between SS, NSS, and NEUTR groups at baseline. Incomplete restoration of microcirculatory perfusion was observed after septic shock and/or neutropenia resolution with a trend towards better recovery in MFI and FHI variables in NSS as compared with SS patients.Microvascular derangements in septic shock did not differ between noncytopenic and cytopenic patients. Our data might suggest that profound neutropenia and thrombocytopenia do not render microcirculation more resistant to sepsis-induced microvascular alterations. The role and mechanisms of microvascular alterations associated with chemotherapy-induced cytopenia warrant further investigation.