L. S. Terada
University of Colorado Denver
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Publication
Featured researches published by L. S. Terada.
Journal of Clinical Investigation | 1988
Anita Patt; Alden H. Harken; L K Burton; T C Rodell; D Piermattei; W J Schorr; N B Parker; E M Berger; I R Horesh; L. S. Terada
The contribution of toxic O2 metabolites to cerebral ischemia reperfusion injury has not been determined. We found that gerbils subjected to temporary unilateral carotid artery occlusion (ischemia) consistently developed neurologic deficits during ischemia with severities that correlated with increasing degrees of brain edema and brain H2O2 levels after reperfusion. In contrast, gerbils treated just before reperfusion (after ischemia) with dimethylthiourea (DMTU), but not urea, had decreased brain edema and brain H2O2 levels. In addition, gerbils fed a tungsten-rich diet for 4, 5, or 6 wk developed progressive decreases in brain xanthine oxidase (XO) and brain XO + xanthine dehydrogenase (XD) activities, brain edema, and brain H2O2 levels after temporary unilateral carotid artery occlusion and reperfusion. In contrast to tungsten-treated gerbils, allopurinol-treated gerbils did not have statistically significant decreases in brain XO or XO + XD levels, and reduced brain edema and brain H2O2 levels occurred only in gerbils developing mild but not severe neurologic deficits during ischemia. Finally, gerbils treated with DMTU or tungsten all survived, while greater than 60% of gerbils treated with urea, allopurinol, or saline died by 48 h after temporary unilateral carotid artery occlusion and reperfusion. Our findings indicate that H2O2 from XO contributes to reperfusion-induced edema in brains subjected to temporary ischemia.
Journal of Clinical Investigation | 1988
J. M. Brown; L. S. Terada; M. A. Grosso; G J Whitmann; S E Velasco; Anita Patt; Alden H. Harken; John E. Repine
Three lines of investigation indicated that hydrogen peroxide (H2O2) from xanthine oxidase (XO) contributes to cardiac dysfunction during reperfusion after ischemia. First, addition of dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger (but not urea) simultaneously with reperfusion improved recovery of ventricular function as assessed by ventricular developed pressure (DP), contractility (+dP/dt), and relaxation rate (-dP/dt) in isolated Krebs-Henseleit-perfused rat hearts subjected to global normothermic ischemia. Second, hearts from rats fed tungsten or treated with allopurinol had negligible XO activities (less than 0.5 mU/g wet myocardium compared with greater than 6.0 mU/g in control hearts) and increased ventricular function after ischemia and reperfusion. Third, myocardial H2O2-dependent inactivation of catalase occurred after reperfusion following ischemia, but not after ischemia without reperfusion or perfusion without ischemia. In contrast, myocardial catalase did not decrease during reperfusion of ischemic hearts treated with DMTU, tungsten, or allopurinol.
Inflammation | 1989
J. M. Brown; Connie J. Beehler; Elaine M. Berger; M. A. Grosso; Glenn J.R. Whitman; L. S. Terada; John A. Leff; Alden H. Harken; John E. Repine
Perfusion with human serum albumin decreased myocardial hydrogen peroxide (H2O2) levels (as assessed by inactivation of myocardial catalase activities following ammotriazole pretreatment) and increased myocardial ventricular developed pressures (DP), contractility (+dP/dt) but not relaxation rate (-dP/dt) in isolated crystalloid perfused rat hearts subjected to normothermic global ischemia (20 min) and then reperfusion (40 min). Albumin also decreased H2O2 concentrations in vitro. The findings support the possibility that albumin may act as a protective O2 metabolite scavenger in vivo.
American Journal of Physiology-regulatory Integrative and Comparative Physiology | 1991
Benjamin O. Anderson; Denis D. Bensard; J. M. Brown; John E. Repine; Paul F. Shanley; J. A. Leff; L. S. Terada; Anirban Banerjee; Alden H. Harken
Bacterial lipopolysaccharide (LPS) and an N-formyl peptide, N-formyl-neoleucyl-leucyl-phenylalanine (FNLP), synergistically promote lung injury in rats as measured by 125I-labeled albumin flux. Concomitantly, neutrophils are sequestered in the lung. We hypothesized that LPS-FNLP-induced lung injury is mediated both by neutrophil-dependent and -independent mechanisms. Rats were depleted of circulating and marginating neutrophils with vinblastine. LPS-FNLP-induced lung protein leak was partially decreased in these neutrophil-depleted animals, although a component of lung injury remained. We hypothesized that LPS-FNLP-induced lung injury was also mediated by xanthine oxidase (XO). Rats were fed a tungsten-enriched diet that inactivates molybdenum-dependent oxidase systems. LPS-FNLP-induced lung leak was partially decreased in these animals as well. When tungsten-fed rats were also neutrophil depleted with vinblastine, no increase in 125I-albumin flux was observed in response to LPS-FNLP. In parallel experiments, lungs from vinblastine-pretreated rats were isolated and perfused. FNLP infusion into the LPS-primed, crystalloid-perfused lungs caused increased 125I-albumin flux, which was prevented by oxidase inhibition. We conclude that LPS-FNLP-induced lung injury is both neutrophil mediated and neutrophil independent. The nonneutrophil component of the LPS-FNLP-induced lung injury appears to be pulmonary XO derived and dependent.
Proceedings of the National Academy of Sciences of the United States of America | 1989
J. M. Brown; M. A. Grosso; L. S. Terada; Glenn J.R. Whitman; Anirban Banerjee; Carl W. White; Alden H. Harken; John E. Repine
Proceedings of the National Academy of Sciences of the United States of America | 1990
J. M. Brown; Carl W. White; L. S. Terada; M. A. Grosso; Paul F. Shanley; David W. Mulvin; Anirban Banerjee; Glenn J.R. Whitman; Alden H. Harken; John E. Repine
American Journal of Physiology-lung Cellular and Molecular Physiology | 1992
L. S. Terada; J. J. Dormish; Paul F. Shanley; J. A. Leff; B. O. Anderson; John E. Repine
Proceedings of the National Academy of Sciences of the United States of America | 1993
Richard M. Wright; Gisela M. Vaitaitis; Cory M. Wilson; Thomas B. Repine; L. S. Terada; John E. Repine
Journal of Applied Physiology | 1991
B. O. Anderson; Ernest E. Moore; F. A. Moore; J. A. Leff; L. S. Terada; Alden H. Harken; John E. Repine
American Journal of Physiology-lung Cellular and Molecular Physiology | 1996
Robert Shenkar; Michael D. Schwartz; L. S. Terada; John E. Repine; Joe M. McCord; Edward Abraham
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Cooperative Institute for Research in Environmental Sciences
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