title: Effects of hyperoxia on local and remote microcirculatory inflammatory response after splanchnic ischemia and reperfusion.
abstract: Splanchnic ischemia-reperfusion (I/R) causes tissue hypoxia that triggers local and systemic microcirculatory inflammatory responses. We evaluated the effects of hyperoxia in I/R induced by 40-min superior mesenteric artery (SMA) occlusion and 120-min reperfusion in four groups of rats: 1) control (anesthesia only), 2) sham operated (all surgical procedures without vascular occlusion; air ventilation), 3) SMA I/R and air, 4) SMA I/R and 100% oxygen ventilation started 10 min before reperfusion. Leukocyte rolling and adhesion in mesenteric microvessels, pulmonary microvascular blood flow velocity (BFV), and macromolecular (FITC-albumin) flux into lungs were monitored by intravital videomicroscopy. We also determined pulmonary leukocyte infiltration. SMA I/R caused marked decreases in mean arterial blood pressure (MABP) and blood flow to the splanchnic and hindquarters vascular beds and pulmonary BFV and shear rates, followed by extensive increase in leukocyte rolling and adhesion and plugging of >50% of the mesenteric microvasculature. SMA I/R also caused marked increase in pulmonary sequestration of leukocytes and macromolecular leak with concomitant decrease in circulating leukocytes. Inhalation of 100% oxygen maintained MABP at significantly higher values (P < 0.001) but did not change regional blood flows. Oxygen therapy attenuated the increase in mesenteric leukocyte rolling and adherence (P < 0.0001) and maintained microvascular patency at values not significantly different from sham-operated animals. Hyperoxia also attenuated the decrease in pulmonary capillary BFV and shear rates, reduced leukocyte infiltration in the lungs (P < 0.001), and prevented the increase in pulmonary macromolecular leak (P < 0.001), maintaining it at values not different from sham-operated animals. The data suggest that beneficial effects of normobaric hyperoxia in splanchnic I/R are mediated by attenuation of both local and remote inflammatory microvascular responses.
authors.affiliation: Department of Medicine, Carmel Medical Center, Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, 7 Michal St., Haifa 34362, Israel.
authors.forename: Dan
authors.initials: D
authors.lastname: Waisman
authors.forename: Vera
authors.initials: V
authors.lastname: Brod
authors.forename: Rafael
authors.initials: R
authors.lastname: Wolff
authors.forename: Edmond
authors.initials: E
authors.lastname: Sabo
authors.forename: Mark
authors.initials: M
authors.lastname: Chernin
authors.forename: Zalman
authors.initials: Z
authors.lastname: Weintraub
authors.forename: Avi
authors.initials: A
authors.lastname: Rotschild
authors.forename: Haim
authors.initials: H
authors.lastname: Bitterman
mesh_terms: D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects / Q000276:immunology; D006400:Hematocrit; D018496:Hyperoxia / Q000276:immunology* / Q000503:physiopathology*; D007962:Leukocytes / Q000276:immunology; D008168:Lung / Q000276:immunology / Q000503:physiopathology; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D018715:Microscopy, Video; D009102:Multiple Organ Failure / Q000276:immunology / Q000503:physiopathology; D010100:Oxygen / Q000097:blood / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000276:immunology* / Q000503:physiopathology*; D013152:Splanchnic Circulation / Q000187:drug effects / Q000502:physiology*; D013314:Stress, Mechanical; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014657:Vasculitis / Q000276:immunology / Q000503:physiopathology
chemical_list: D010100:Oxygen