The microcirculation is the motor of sepsis

被引:598
作者
Ince, C [1 ]
机构
[1] Univ Amsterdam, Acad Med Ctr, Dept Physiol, NL-1105 AZ Amsterdam, Netherlands
来源
CRITICAL CARE | 2005年 / 9卷 / Suppl 4期
关键词
D O I
10.1186/cc3753
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Regional tissue distress caused by microcirculatory dysfunction and mitochondrial depression underlies the condition in sepsis and shock where, despite correction of systemic oxygen delivery variables, regional hypoxia and oxygen extraction deficit persist. We have termed this condition microcirculatory and mitochondrial distress syndrome (MIMIDS). Orthogonal polarization spectral imaging allowed the first clinical observation of the microcirculation in human internal organs, and has identified the pivotal role of microcirculatory abnormalities in defining the severity of sepsis, a condition not revealed by systemic hemodynamic or oxygen-derived variables. Recently, sublingual sidestream dark-field (SDF) imaging has been introduced, allowing observation of the microcirculation in even greater detail. Microcirculatory recruitment is needed to ensure adequate microcirculatory perfusion and the oxygenation of tissue cells that follows. In sepsis, where inflammation-induced autoregulatory dysfunction persists and oxygen need is not matched by supply, the microcirculation can be recruited by reducing pathological shunting, promoting microcirculatory perfusion, supporting pump function, and controlling hemorheology and coagulation. Resuscitation following MMDS must include focused recruitment of hypoxic-shunted microcirculatory units and/or resuscitation of the mitochondria. A combination of agents is required for successful rescue of the microcirculation. Single compounds such as activated protein C, which acts on multiple pathways, can be expected to be beneficial in rescuing the microcirculation in sepsis.
引用
收藏
页码:S13 / S19
页数:7
相关论文
共 73 条
  • [1] Systemic and renal macro- and microcirculatory responses to arginine vasopressin in endotoxic rabbits
    Albert, M
    Losser, MR
    Hayon, D
    Faivre, V
    Payen, D
    [J]. CRITICAL CARE MEDICINE, 2004, 32 (09) : 1891 - 1898
  • [2] Fluids reverse the early lipopolysaccharide-induced albumin leakage in rodent mesenteric venules
    Anning, PB
    Finney, SJ
    Singh, S
    Winlove, CP
    Evans, TW
    [J]. INTENSIVE CARE MEDICINE, 2004, 30 (10) : 1944 - 1949
  • [3] ATASEVER B, 2005, CRIT CARE S1, V8, pP73
  • [4] Nitric oxide causes dysfunction of coronary autoregulation in endotoxemic rats
    Avontuur, JAM
    Bruining, HA
    Ince, C
    [J]. CARDIOVASCULAR RESEARCH, 1997, 35 (02) : 368 - 376
  • [5] INHIBITION OF NITRIC-OXIDE SYNTHESIS CAUSES MYOCARDIAL-ISCHEMIA IN ENDOTOXEMIC RATS
    AVONTUUR, JAM
    BRUINING, HA
    INCE, C
    [J]. CIRCULATION RESEARCH, 1995, 76 (03) : 418 - 425
  • [6] BAKER CH, 1984, CIRC SHOCK, V12, P165
  • [7] Red blood cell aggregation in experimental sepsis
    Baskurt, OK
    Temiz, A
    Meiselman, HJ
    [J]. JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1997, 130 (02): : 183 - 190
  • [8] Bench-to-bedside review: Microvascular dysfunction in sepsis - hemodynamics, oxygen transport, and nitric oxide
    Bateman, RM
    Sharpe, MD
    Ellis, CG
    [J]. CRITICAL CARE, 2003, 7 (05): : 359 - 373
  • [9] Efficacy and safety of recombinant human activated protein C for severe sepsis.
    Bernard, GR
    Vincent, JL
    Laterre, P
    LaRosa, SP
    Dhainaut, JF
    Lopez-Rodriguez, A
    Steingrub, JS
    Garber, GE
    Helterbrand, JD
    Ely, EW
    Fisher, CJ
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (10) : 699 - 709
  • [10] BOERMA EC, 2005, ACTA ANAESTYH SCAND