title: Role of neutrophils in ischemia-reperfusion-induced microvascular injury.
abstract: Recent studies indicate that polymorphonuclear neutrophils (PMNs) infiltrate the intestinal mucosa during ischemia and after reperfusion. To determine whether PMNs mediate the increased microvascular permeability produced by ischemia-reperfusion (I/R) we treated cats with either saline, antineutrophil serum (ANS), or a monoclonal antibody specific for the beta-chain of the CD18 complex (MoAb 60.3) that prevents neutrophil adherence and extravasation. Intestinal microvascular permeability to plasma proteins was measured in control preparations (0.08 +/- 0.007), in preparations subjected to 1 h of ischemia then reperfusion (I/R, 0.32 +/- 0.02), I/R preparations treated with ANS (0.13 +/- 0.01), and I/R preparations treated with MoAb (0.12 +/- 0.003). Our results indicate that both PMN depletion (to less than 10% control) and prevention of PMN adherence significantly attenuate the increased microvascular permeability induced by I/R. These findings, coupled to previous results obtained from this model, support the hypothesis that neutrophils, which accumulate in the mucosa in response to xanthine oxidase activation, mediate the oxyradical-dependent injury produced by reperfusion of the ischemic bowel.
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D002199:Capillary Permeability; D002415:Cats; D002448:Cell Adhesion; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000503:physiopathology*; D009504:Neutrophils / Q000502:physiology*; D010100:Oxygen / Q000633:toxicity*; D010477:Perfusion
chemical_list: D000911:Antibodies, Monoclonal; D010100:Oxygen