Inflammation and oxygen free radical formation during pulmonary ischemia-reperfusion injury

Abstract

In a companion study, we showed that 2 h of warm unilateral lung ischemia followed by reperfusion resulted in bilateral tissue injury, indicated by increases in extravascular density (EVD) and permeability, measured as the pulmonary transcapillary escape rate (PTCER) for radiolabeled transferrin. EVD and PTCER measurements were obtained with the quantitative imaging technique of positron emission tomography (PET). In the current study, we evaluated this increase in EVD histologically and correlated EVD and PTCER with measurements of oxidant-reactive sulfhydryls (RSH) in plasma as a marker of oxygen free radical (OFR) formation. Histologically edema, leukocyte infiltration, and hemorrhage were all present on the ischemic side, but only after reperfusion, whereas only neutrophil infiltration was observed on the nonischemic side. Histology scores correlated with EVD (r = 0.81) and PTCER (r = 0.75), but permeability was abnormal at times even in the absence of neutrophil infiltration. Plasma RSH concentration from the ischemic lung decreased significantly (P less than 0.05) during pulmonary ischemia (i.e., before reperfusion) and returned to baseline on reperfusion. The degree of RSH oxidation did not correlate with the severity of injury as measured by PET or histology. Thus pulmonary ischemia-reperfusion injury is characterized by inflammation, hemorrhage, edema, and OFR formation. Injury occurred after reperfusion, not after ischemia alone. In addition, injury to the contralateral nonischemic lung suggests a neutrophil-independent circulating mediator of injury.

Effects of Gabexate Mesilate (FOY) on Ischemia–Reperfusion-Induced Acute Lung Injury in Dogs

“…We determined 90 min ischemic time to be adequate in the present model according to the results of our pilot investigation. We believe 6 h reperfusion is too short, but 12 to 18 h will be enough to demonstrate the significant injury because of the leukocyteendothelium interaction and related free radical and cytokine reaction which take effect within this period [27,28]. In the present study, most of the injury parameters maintained a relatively stable plateau level at 18 h after reperfusion, thus proving our hypothesis.…”

Association of Increased Immunostaining for Inducible Nitric Oxide Synthase and Nitrotyrosine With Fibroblast Growth Factor Transformation in Pancreatic Cancer

“…23 Previous in vitro studies have demonstrated that FGF-1 is released from cells in response to oxidative stress, 16,23,24 a pathologic condition that may involve inflammatory-mediated production of reactive oxygen-nitrogen species. 39,57,58 Our results demonstrate the increased immunoappearance of iNOS and nitrotyrosine in the ductal epithelium of pancreatic tumor tissue. This observation predicts that endogenous production of reactive nitrogen species, as evidenced by markers for NO and peroxynitrite, induces oxidative stress in the ductal epithelium of pancreatic adenocarcinoma.…”

The effect of one-lung ventilation upon pulmonary inflammatory responses during lung resection

“…This could explain the underlying mechanisms of inflammation in both the dependent lung and the nondependent lung [3,34]. The nondependent lung remains completely atelectatic for a period of time, which is accompanied by hypoperfusion due to hypoxic vasoconstriction.…”