Hypoxia causes leukocyte adherence to mesenteric venules in nonacclimatized, but not in acclimatized, rats

1999 ◽  
Vol 87 (3) ◽  
pp. 873-881 ◽  
Author(s):  
John G. Wood ◽  
Leone F. Mattioli ◽  
Norberto C. Gonzalez
Keyword(s):  
Nitric Oxide ◽  
Ischemia Reperfusion ◽  
Acute Hypoxia ◽  
Oxide Formation ◽  
Nitric Oxide Formation ◽  
Systemic Hypoxia ◽  
Adhesive Interactions ◽  
Acclimatization Period ◽  
Oxide Synthase

Although the effects of ischemia-reperfusion have received considerable attention, few studies have directly evaluated the microcirculatory response to systemic hypoxia. The overall objective of this study was to assess the effect of environmental hypoxia on adhesive interactions of circulating leukocytes with rat mesenteric venules by using intravital microscopy. Experiments were designed to 1) characterize the adhesive interactions of circulating leukocytes to venules during acute hypoxia produced by a reduction in inspired[Formula: see text], 2) evaluate the role of nitric oxide in these adhesive interactions, 3) determine whether the effect of hypoxia on leukocyte adhesive interactions differs between acclimatized and nonacclimatized rats, and 4) assess whether compensatory changes in nitric oxide formation contribute to this difference. The results showed that acute hypoxia promotes leukocyte-endothelial adherence in mesenteric venules of nonacclimatized rats. The mechanism of this response is consistent with depletion of nitric oxide within the microcirculation. In contrast, no leukocyte-endothelial adherence occurred during hypoxia in rats acclimatized to hypobaric hypoxia. The results are consistent with increased nitric oxide formation due to expression of inducible nitric oxide synthase during the acclimatization period. Further studies are needed to establish the cause of nitric oxide depletion during acute hypoxia as well as to define the compensatory responses that attenuate hypoxia-induced leukocyte-endothelial adherence in the microvasculature of acclimatized rats.

scholarly journals Nitric oxide formation from nitroglycerin: role of cysteine

1995 ◽  
Vol 67 ◽  
pp. 182
Author(s):  
Yoko Aniva ◽  
Naoko Uehara ◽  
Toshihiro Matsuzaki ◽  
Matao Sakanashi
Keyword(s):  
Nitric Oxide ◽  
Oxide Formation ◽  
Nitric Oxide Formation

The role of differnt isoforms of nitric oxide synthase (NOS) in hepatic ischemia-reperfusion infjury in mice

2001 ◽  
Vol 120 (5) ◽  
pp. A549
Author(s):  
Shigeyuki Kawachi ◽  
Motohide Shimazu ◽  
Masaki Kitajima ◽  
Matthew B. Grisham
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Oxide Synthase

Inhibition of nitric oxide formation and superoxide generation during reduction of LY83583 by neuronal nitric oxide synthase

1998 ◽  
Vol 360 (2-3) ◽  
pp. 213-218 ◽  
Author(s):  
Yoshito Kumagai ◽  
Kazumi Midorikawa ◽  
Yumi Nakai ◽  
Toshikazu Yoshikawa ◽  
Kazuki Kushida ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Formation ◽  
Superoxide Generation ◽  
Nitric Oxide Formation ◽  
Oxide Synthase

Alternative pathways of nitric oxide formation in Lactobacilli: Evidence for nitric oxide synthase activity by EPR

Microbiology ◽  
2006 ◽  
Vol 75 (6) ◽  
pp. 634-638 ◽  
Author(s):  
D. R. Yarullina ◽  
O. N. Il’inskaya ◽  
A. V. Aganov ◽  
N. I. Silkin ◽  
D. G. Zverev
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxide Formation ◽  
Alternative Pathways ◽  
Nitric Oxide Formation ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

scholarly journals Nitric oxide and cyclic GMP formation induced by interleukin 1β in islets of Langerhans. Evidence for an effector role of nitric oxide in islet dysfunction

1992 ◽  
Vol 287 (1) ◽  
pp. 229-235 ◽  
Author(s):  
J A Corbett ◽  
J L Wang ◽  
J H Hughes ◽  
B A Wolf ◽  
M A Sweetland ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Synthesis ◽  
Insulin Secretion ◽  
Time Dependent ◽  
Oxide Formation ◽  
Nitric Oxide Formation ◽  
Iron Nitrosyl ◽  
Dependent Inhibition ◽  
Glucose Stimulated Insulin Secretion ◽  
Oxide Synthase

Treatment of pancreatic islets with interleukin 1 (IL-1) results in a time-dependent inhibition of glucose-stimulated insulin secretion which has recently been demonstrated to be dependent on the metabolism of L-arginine to nitric oxide. In this report IL-1 beta is shown to induce the accumulation of cyclic GMP (cGMP) in a time-dependent fashion that mimics the time-dependent inhibition of insulin secretion by IL-1 beta. The accumulation of cGMP is dependent on nitric oxide synthase activity, since NG-monomethyl-L-arginine (a competitive inhibitor of nitric oxide synthase) prevents IL-1 beta-induced cGMP accumulation. cGMP formation and nitrite production induced by IL-1 beta pretreatment of islets are also blocked by the protein synthesis inhibitor, cycloheximide. The formation of cGMP does not appear to mediate the inhibitory effects of IL-1 beta on insulin secretion since a concentration of cycloheximide (1 microM) that blocks IL-1 beta-induced inhibition of glucose-stimulated insulin secretion and nitric oxide formation does not prevent cGMP accumulation, thus dissociating the two events. By using e.p.r. spectroscopy, IL-1 beta is shown to induce the formation of a g = 2.04 iron-nitrosyl feature in islets which is prevented by cycloheximide, demonstrating the requirement of protein synthesis for IL-1 beta-induced nitric oxide formation. Iron-nitrosyl complex-formation by islets confirms that IL-1 beta induces the generation of nitric oxide by islets, and provides evidence indicating that nitric oxide mediates destruction of iron-sulphur clusters of iron-containing enzymes. Consistent with the destruction of iron-sulphur centres is the finding that pretreatment of islets with IL-1 beta results in an approx. 60% inhibition of mitochondrial oxidation of D-glucose to CO2. Inhibition of islet glucose oxidation appears to be mediated by nitric oxide since both NMMA and cycloheximide prevent IL-1 beta-induced inhibition of glucose oxidation. These results show that IL-1 beta-induced nitric oxide formation parallels the ability of IL-1 beta to inhibit glucose-stimulated insulin secretion by islets, and that protein synthesis is required for IL-1 beta-induced nitric oxide formation. These results also suggest that nitric oxide mediates IL-1 beta-induced inhibitory effects on the pancreatic beta-cell by functioning as an effector molecule responsible for the destruction of iron-sulphur centres of iron-containing proteins, resulting in an impairment of mitochondrial function.

scholarly journals Isoform-selective 5′-AMP-activated protein kinase-dependent preconditioning mechanisms to prevent postischemic leukocyte-endothelial cell adhesive interactions

2011 ◽  
Vol 300 (4) ◽  
pp. H1352-H1360 ◽  
Author(s):  
F. Spencer Gaskin ◽  
Kazuhiro Kamada ◽  
Mozow (Yusof) Zuidema ◽  
Allan W. Jones ◽  
Leona J. Rubin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Protein Kinase ◽  
Endothelial Nitric Oxide Synthase ◽  
Ischemia Reperfusion ◽  
Cell Adhesive ◽  
Adhesive Interactions ◽  
Amp Activated Protein Kinase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

We previously demonstrated that preconditioning induced by ethanol consumption at low levels [ethanol preconditioning (EPC)] or with 5-aminoimidazole-4-carboxamide 1-β-d-ribofuranoside (AICAR-PC) 24 h before ischemia-reperfusion prevents postischemic leukocyte-endothelial cell adhesive interactions (LEI) by a mechanism that is initiated by nitric oxide formed by endothelial nitric oxide synthase. Recent work indicates that 1) ethanol increases the activity of AMP-activated protein kinase (AMPK) and 2) AMPK phosphorylates endothelial nitric oxide synthase at the same activation site seen following EPC (Ser1177). In light of these observations, we postulated that the heterotrimeric serine/threonine kinase, AMPK, may play a role in triggering the development of the anti-inflammatory phenotype induced by EPC. Ethanol was administered to C57BL/6J mice by gavage in the presence or absence of AMPK inhibition. Twenty-four hours later, the numbers of rolling and adherent leukocytes in postcapillary venules of the small intestine were recorded using an intravital microscopic approach. Following 45 min of ischemia, LEI were recorded after 30 and 60 min of reperfusion or at equivalent time points in control animals. Ischemia-reperfusion induced a marked increase in LEI relative to sham-operated control mice. The increase in LEI was prevented by EPC, an effect that was lost with AMPK inhibition during the period of ethanol exposure. Studies conducted in AMPK α1- and α2-knockout mice suggest that the anti-inflammatory effects of AICAR are not dependent on which isoform of the catalytic α-subunit is present because a deficiency of either isoform results in a loss of protection. In sharp contrast, EPC appears to be triggered by an AMPK α2-isoform-dependent mechanism.

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