Microvascular dysfunction in sepsis

被引:117
作者
Lush, CW
Kvietys, PR
机构
[1] London Hlth Sci Ctr, Vasc Biol Program, London, ON N6A 4G5, Canada
[2] Univ Western Ontario, Dept Physiol, London, ON N6A 4G5, Canada
关键词
vasoreactivity; tissue oxygenation; nitric oxide; adhesion molecules; leukocyte recruitment; vascular permeability;
D O I
10.1038/sj.mn.7300096
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The micorvascular dysfucntion which occurs in sepsis involves all three elements of the microcirculation:arterioles, capillaries, and venules. In sepsis, the arterioles are hyporesponsive to vasoconstrictors and vasodilators. Sepsis also reduces the number of perfused capillaries, therapy impacting on oxygen diffusion to mitochondria. In the venules of some tissues (e.g., mesentery) there is an inflammatory response characterized by neutrophil infiltration and protein leakage. In addition, PMN-endothelial adhesive interactions occur in precapillary microvessels and capillaries in organs, such as, the lung and heart. Thus, all these elements of the microcirculation are involved in the sepsis-induced inflammation. In this review we address emerging views on the mechanisms involved in the microvascular dysfunction induced by sepsis within the framework of these three basic elements of the microcirculatory.
引用
收藏
页码:83 / 101
页数:19
相关论文
共 200 条
  • [1] Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation
    Abraham, E
    Kaneko, DJ
    Shenkar, R
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1999, 276 (01) : L1 - L8
  • [2] Endothelial-dependent mechanisms regulate leukocyte transmigration: A process involving the proteasome and disruption of the vascular endothelial-cadherin complex at endothelial cell-to-cell junctions
    Allport, JR
    Ding, H
    Collins, T
    Gerritsen, ME
    Luscinskas, FW
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (04) : 517 - 527
  • [3] ROLE OF NITRIC-OXIDE IN PORCINE LIVER CIRCULATION UNDER NORMAL AND ENDOTOXEMIC CONDITIONS
    AYUSE, T
    BRIENZA, N
    REVELLY, JP
    BOITNOTT, JK
    ROBOTHAM, JL
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1995, 78 (04) : 1319 - 1329
  • [4] ARTERIOLAR ENDOTHELIUM-DEPENDENT VASODILATION OCCURS DURING ENDOTOXIN-SHOCK
    BAKER, CH
    SUTTON, ET
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (04): : H1118 - H1123
  • [5] The NF-kappa B and I kappa B proteins: New discoveries and insights
    Baldwin, AS
    [J]. ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 : 649 - 683
  • [6] POLYMORPHONUCLEAR NEUTROPHIL CONTRIBUTION TO INDUCED TOLERANCE TO BACTERIAL LIPOPOLYSACCHARIDE
    BARROSOARANDA, J
    SCHMIDSCHONBEIN, GW
    ZWEIFACH, BW
    MATHISON, JC
    [J]. CIRCULATION RESEARCH, 1991, 69 (05) : 1196 - 1206
  • [7] DOSE-RELATED PATTERN OF SINUSOIDAL LEUKOCYTE ADHESION IN SUBLOBULAR REGIONS OF THE LIVER AFTER SYSTEMIC ENDOTOXIN CHALLENGE IN THE RAT
    BAUER, M
    MARZI, I
    THUMA, B
    BACH, F
    BUHREN, V
    LARSEN, R
    [J]. SHOCK, 1994, 1 (02): : 135 - 140
  • [8] BAUER P, 1999, AM J PHYSIOL, V276, pC479
  • [9] iNOS expression in human intestinal microvascular endothelial cells inhibits leukocyte adhesion
    Binion, DG
    Fu, SD
    Ramanujam, KS
    Chai, YC
    Dweik, RA
    Drazba, JA
    Wade, JG
    Ziats, NP
    Erzurum, SC
    Wilson, KT
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1998, 275 (03): : G592 - G603
  • [10] Blackwell TS, 1996, J IMMUNOL, V157, P1630