scholarly journals Direct measurement of nitric oxide release in gastric mucosa during ischemia-reperfusion in rats

1998 ◽  
Vol 274 (3) ◽  
pp. G465-G471 ◽  
Author(s):  
Kouichirou Wada ◽  
Yoshinori Kamisaki ◽  
Tsuyoshi Ohkura ◽  
Gaku Kanda ◽  
Kentaro Nakamoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Superoxide Radical ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Celiac Artery ◽  
Radical Scavenger ◽  
Gastric Mucosal Lesions ◽  
Nitric Oxide Release ◽  
Pentobarbital Sodium Anesthesia

Nitric oxide (NO) generation in the rat gastric mucosa during ischemia-reperfusion was measured using an NO-sensitive electrode. Under pentobarbital sodium anesthesia, an electrode was inserted into the submucosa from the serous membrane side in the fundus. After steady-state baseline recording, the celiac artery was clamped for 30 min, and then ischemia-reperfusion was achieved by removing the clamp. The clamping of the celiac artery caused a decrease in blood flow and an increase in NO level in the gastric tissue. Just after the removal of the clamp, the NO level rapidly fell and returned to the baseline level. Administration of N G-nitro-l-arginine methyl ester (an NO synthase inhibitor, 30 mg/kg ip) before ischemia significantly attenuated both the increase in NO level during ischemia and the formation of acute gastric mucosal lesions observed after 60 min reperfusion. Administration of superoxide dismutase (a superoxide radical scavenger, 10,000 U/kg iv) at the end of ischemia inhibited both the rapid decrease in NO level during the reperfusion and the gastric mucosal erosions. Because NO and superoxide radical produce a highly reactive peroxynitrite, it can be argued that NO has an important pathological role in acute gastric mucosal injury induced by ischemia-reperfusion. Our conclusion was strongly supported by immunohistochemical staining of nitrotyrosine residues, an indication of peroxynitrite formation.

scholarly journals A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

2015 ◽  
Vol 51 (3) ◽  
pp. 637-642 ◽  
Author(s):  
Seyyed Ali Mard ◽  
Zahra Nikraftar ◽  
Yaghoob Farbood ◽  
Esrafil Mansouri
Keyword(s):  
Gastric Mucosa ◽  
Protein Expression ◽  
Protective Effect ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Celiac Artery ◽  
Male Rats ◽  
Gastric Mucosal Lesions ◽  
Inflammatory Protein

The aim of the present study was to investigate the protective effect of crocin on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rats. Thirty-two male rats were randomly divided into sham, I/R, I/R + crocin pretreatment and crocin alone groups. To induce I/R lesions, the celiac artery was clamped for 30 min, and the clamp was then removed to allow reperfusion for 3 h. Crocin-pretreated rats received crocin (15 mg/kg, i.p.) 30 min prior to the induction of I/R injury. Samples of gastric mucosa were collected to quantify the protein expression of caspase-3, an apoptotic factor, and inducible nitric oxide synthase (iNOS), a pro-inflammatory protein, by Western blot. Pretreatment with crocin decreased the total area of gastric lesions and decreased the protein expression levels of caspase-3 and iNOS induced by I/R injury. Our findings showed a protective effect of crocin in gastric mucosa against I/R injury. This effect of crocin was mainly mediated by reducing the protein expression of iNOS and caspase-3.

Protective effect ofl-citrulline against acute gastric mucosal lesions induced by ischemia–reperfusion in rats

2011 ◽  
Vol 89 (5) ◽  
pp. 317-327 ◽  
Author(s):  
Lingshan Gou ◽  
Ling Zhang ◽  
Cui Yin ◽  
Genguang Jia ◽  
Xiaoxing Yin ◽  
...  
Keyword(s):  
Protective Effect ◽  
Ischemia Reperfusion ◽  
Neutrophil Infiltration ◽  
Mucosal Injury ◽  
Celiac Artery ◽  
Myeloperoxidase Activity ◽  
Gastric Mucus ◽  
Gastric Mucosal Lesions ◽  
Oxide Synthase ◽  
Inducible Nos

The present study investigated the protective effect of l-citrulline on gastric mucosal injury induced by ischemia–reperfusion (IR) in rats. Under anesthesia, the celiac artery was clamped for 30 min, and then the clamp was removed for 60 min reperfusion. Sixty minutes before ischemia, l-citrulline was administered intragastrically at doses of 300, 600, and 900 mg/kg. After the experiment, the stomachs were removed for biochemical and histological examinations. Pretreatment with l-citrulline (300, 600, and 900 mg/kg) significantly ameliorated the gastric damage caused by IR. Moreover, l-citrulline prevented the production of lipid peroxidation and inhibited the increase of myeloperoxidase activity. The elevation in total nitric oxide synthase (NOS) activity, inducible NOS activity, and inducible NOS protein expression as well as the decrease in constitutive NOS activity and gastric mucus level in the gastric mucosa induced by IR were significantly prevented. However, the protective effect mediated by l-citrulline was significantly antagonized by coadministration of l-nitroarginine methyl ester (10 mg/kg, s.c.). These results suggest that part of the mechanism of gastric protection by l-citrulline might be through inhibiting neutrophil infiltration and preserving gastric mucus synthesis and secretion in rats, functions that are closely related to the maintenance of constitutive NOS activity.

scholarly journals Nitric Oxide

2007 ◽  
Vol 107 (5) ◽  
pp. 822-842 ◽  
Author(s):  
Noboru Toda ◽  
Hiroshi Toda ◽  
Yoshio Hatano ◽  
David C. Warltier
Keyword(s):  
Nitric Oxide ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Nitric Oxide Release ◽  
Blood Flows ◽  
Anesthetic Agents ◽  
Regional Blood Flows ◽  
Peripheral Arterial

There has been an explosive increase in the amount of interesting information about the physiologic and pathophysiologic roles of nitric oxide in cardiovascular, nervous, and immune systems. The possible involvement of the nitric oxide-cyclic guanosine monophosphate pathway in the effects of anesthetic agents has been the focus of many investigators. Relaxations of cerebral and peripheral arterial smooth muscle as well as increases in cerebral and other regional blood flows induced by anesthetic agents are mediated mainly via nitric oxide released from the endothelium and/or the nitrergic nerve and also via prostaglandin I2 or endothelium-derived hyperpolarizing factor. Preconditioning with volatile anesthetics protects against ischemia-reperfusion-induced myocardial dysfunction and cell death or neurotoxicity, possibly through nitric oxide release. Inhibition of nitric oxide synthase decreases the anesthetic requirement. Involvement of nitric oxide in the effects of volatile, intravenous, and local anesthetics differs. This review article includes a summary of information about the sites and mechanisms by which various anesthetic agents interact with the nitric oxide-cyclic guanosine monophosphate system.

scholarly journals Participation of nitric oxide in the mucosal injury of intestine induced by ischemia-reperfusion in rats

1997 ◽  
Vol 73 ◽  
pp. 223
Author(s):  
Kohei Takada ◽  
Kimihirio Yamashita ◽  
Masaya Yoshimura ◽  
Yasuko Sakurai-Yamashita ◽  
Kohtaro Taniyama
Keyword(s):  
Nitric Oxide ◽  
Ischemia Reperfusion ◽  
Mucosal Injury

scholarly journals S-Nitroso Human Serum Albumin Treatment Reduces Ischemia/Reperfusion Injury in Skeletal Muscle via Nitric Oxide Release

Circulation ◽  
2002 ◽  
Vol 105 (25) ◽  
pp. 3032-3038 ◽  
Author(s):  
Seth Hallström ◽  
Harald Gasser ◽  
Christoph Neumayer ◽  
Alexander Fügl ◽  
Joseph Nanobashvili ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Human Serum Albumin ◽  
Serum Albumin ◽  
Human Serum ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Release

Effect of a free radical scavenger on nitric oxide release in microvessels

2013 ◽  
Vol 58 (1-2) ◽  
pp. 134-139 ◽  
Author(s):  
Tsutomu Yamashita ◽  
Kumi Sakamoto ◽  
Hiroshi Yamanishi ◽  
Nagao Totani ◽  
Junichiro Yamamoto
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Nitric Oxide Release

scholarly journals Activation of Pak1/Akt/eNOS signaling following sphingosine-1-phosphate release as part of a mechanism protecting cardiomyocytes against ischemic cell injury

2011 ◽  
Vol 301 (4) ◽  
pp. H1487-H1495 ◽  
Author(s):  
Emmanuel Eroume A. Egom ◽  
Tamer M. A. Mohamed ◽  
Mamas A. Mamas ◽  
Ying Shi ◽  
Wei Liu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Myocytes ◽  
Coronary Sinus ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Protective Effects ◽  
Lactate Dehydrogenase Activity ◽  
Nitric Oxide Release ◽  
Sphingosine 1 Phosphate

We investigated whether plasma long-chain sphingoid base (LCSB) concentrations are altered by transient cardiac ischemia during percutaneous coronary intervention (PCI) in humans and examined the signaling through the sphingosine-1-phosphate (S1P) cascade as a mechanism underlying the S1P cardioprotective effect in cardiac myocytes. Venous samples were collected from either the coronary sinus ( n = 7) or femoral vein ( n = 24) of 31 patients at 1 and 5 min and 12 h, following induction of transient myocardial ischemia during elective PCI. Coronary sinus levels of LCSB were increased by 1,072% at 1 min and 941% at 5 min ( n = 7), while peripheral blood levels of LCSB were increased by 579% at 1 min, 617% at 5 min, and 436% at 12 h ( n = 24). In cultured cardiac myocytes, S1P, sphingosine (SPH), and FTY720, a sphingolipid drug candidate, showed protective effects against CoCl induced hypoxia/ischemic cell injury by reducing lactate dehydrogenase activity. Twenty-five nanomolars of FTY720 significantly increased phospho-Pak1 and phospho-Akt levels by 56 and 65.6% in cells treated with this drug for 15 min. Further experiments demonstrated that FTY720 triggered nitric oxide release from cardiac myocytes is through pertussis toxin-sensitive phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase signaling. In ex vivo hearts, ischemic preconditioning was cardioprotective in wild-type control mice (Pak1f/f), but this protection appeared to be ineffective in cardiomyocyte-specific Pak1 knockout (Pak1cko) hearts. The present study provides the first direct evidence of the behavior of plasma sphingolipids following transient cardiac ischemia with dramatic and early increases in LCSB in humans. We also demonstrated that S1P, SPH, and FTY720 have protective effects against hypoxic/ischemic cell injury, likely a Pak1/Akt1 signaling cascade and nitric oxide release. Further study on a mouse model of cardiac specific deletion of Pak1 demonstrates a crucial role of Pak1 in cardiac protection against ischemia/reperfusion injury.

Polymorphonuclear leukocyte infiltration into gastric mucosa after ischemia-reperfusion

1994 ◽  
Vol 266 (1) ◽  
pp. G48-G54 ◽  
Author(s):  
F. J. Andrews ◽  
C. Malcontenti-Wilson ◽  
P. E. O'Brien
Keyword(s):  
Gastric Mucosa ◽  
Reperfusion Injury ◽  
Polymorphonuclear Leukocytes ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Immunoperoxidase Staining ◽  
Immunoperoxidase Technique ◽  
Gastric Ischemia

Polymorphonuclear leukocytes (PMN) have been implicated in the pathogenesis of ischemia-reperfusion injury. The objective of this study was to investigate PMN infiltration and distribution within the gastric mucosa of rats subjected to 30 min gastric ischemia followed by reperfusion. Sections of mucosa were stained for PMN using an immunoperoxidase technique, and injury was assessed by quantitative histology. In control animals, there were 4 +/- 2 PMN/mm2 in the superficial and 9 +/- 4 PMN/mm2 in the deep mucosa. This increased significantly to 67 +/- 9 PMN/mm2 (P < 0.05) and 160 +/- 53 PMN/mm2 (P < 0.01) respectively at 15 min of reperfusion. The percentage of these PMN which were extravasated was 83 +/- 4% in the superficial mucosa and 82 +/- 4% in the deep mucosa (P < 0.001 compared with control levels of 0% in superficial and 10% in deep mucosa). Significant PMN infiltration occurred before full expression of mucosal injury and treatment of rats with anti-PMN antisera blocked reperfusion injury (treated 10.7 +/- 1.4% mucosa damaged, controls 33.5 +/- 2.4%; P < 0.001). Treatment with allopurinol (100 mg/kg) significantly reduced the number of infiltrating PMN (superficial 7 +/- 1/mm2, deep 16 +/- 2/mm2; P < 0.01) and the percentage of extravasating PMN (superficial 40 +/- 10%, deep 30 +/- 15%; P < 0.01) while also significantly reducing tissue injury (21.9 +/- 1.9% mucosa damaged, P < 0.01 compared with controls). We conclude that the immunoperoxidase staining provides a simple means of identifying PMN in histological sections. Furthermore, our results support a role for PMN in gastric ischemia-reperfusion injury.

Role of nitric oxide in restitution of injured guinea pig gastric mucosa in vitro

1995 ◽  
Vol 268 (6) ◽  
pp. G933-G942 ◽  
Author(s):  
A. Yanaka ◽  
H. Muto ◽  
H. Fukutomi ◽  
S. Ito ◽  
W. Silen
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Guinea Pig ◽  
Electrical Resistance ◽  
Mucosal Injury ◽  
Luminal Surface ◽  
Morphological Examination ◽  
Mannitol Flux

The role of nitric oxide (NO) in restitution was examined in intact sheets of in vitro guinea pig gastric mucosae after mucosal injury induced by exposure of the luminal surface to 1.25 M NaCl for 10 min. The recovery of transmucosal electrical resistance and [3H]mannitol flux after the injury were significantly greater at luminal pH (pH1) 7.0 than 3.0. The recovery was abolished by pretreatment with 1 mM NG-nitro-L-arginine methyl ester (L-NAME), only at pHL 3.0, an effect reversed by 1 mM L-arginine. Enhancement of the recovery by L-arginine at pHL 3.0 was abolished by 50 microM methylene blue (MB), an effect restored by 1 mM N6,2'-O-dibutyryl guanosine 3',5'-cyclic monophosphate (DBcGMP). In L-arginine- but not L-NAME-treated tissues, recovery was enhanced further by an increase in serosal [HCO3-] and was inhibited by 5% N-acetyl-L-cysteine in the luminal solution or by the removal of serosal HCO3-. Morphological examination showed the formation of a thick "mucoid cap" in L-arginine-but not L-NAME-treated tissues. These results suggest that, in the presence of luminal acid, endogenous NO contributes to restitution in injured gastric mucosa at least in part by facilitating the formation of the mucoid cap.

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