title: Nitric oxide, leukocytes and microvascular permeability: causality or bystanders?
abstract: Increased microvascular permeability resulting in tissue edema is a hallmark of sepsis-related microcirculatory failure, and leukocyte-endothelium interaction is thought to assume major importance in this context. However, the role of nitric oxide (NO) in the interplay of inflammation, leukocyte-endothelium interaction and increased microcirculatory permeability is still a matter of debate. Hollenberg et al. now report, in the previous issue of Critical Care, that neither genetic deletion nor pharmacologic blockade of the inducible isoform of the NO synthase (iNOS) affected the sepsis-related aggravation of leukocyte rolling and adhesion, whereas iNOS inhibition attenuated microvascular permeability. The authors conclude that excess NO resulting from iNOS activation is important in modulating vascular permeability during sepsis, but that this effect is independent of its action on leukocytes.
authors.forename: Balázs
authors.initials: B
authors.lastname: Hauser
authors.forename: Martin
authors.initials: M
authors.lastname: Matejovic
authors.forename: Peter
authors.initials: P
authors.lastname: Radermacher
mesh_terms: D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects* / Q000502:physiology; D004487:Edema / Q000209:etiology*; D006801:Humans; D007962:Leukocytes / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors*; D018805:Sepsis / Q000150:complications*
chemical_list: D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II