Nitric oxide modulates pancreatic edema formation in rat caerulein-induced pancreatitis

1995 ◽  
Vol 30 (5) ◽  
pp. 636-642 ◽  
Author(s):  
Takashi Abe ◽  
Tooru Shimosegawa ◽  
Akihiko Satoh ◽  
Reishi Abe ◽  
Yoshifumi Kikuchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Edema Formation ◽  
Pancreatic Edema

Hypoxia compared with normoxia alters the effects of nitric oxide in ischemia-reperfusion lung injury

1997 ◽  
Vol 273 (3) ◽  
pp. L504-L512 ◽  
Author(s):  
Y. C. Huang ◽  
P. W. Fisher ◽  
E. Nozik-Grayck ◽  
C. A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Average Rate ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
No Production ◽  
Protective Effects ◽  
Lung Weight ◽  
Edema Formation ◽  
No Donors

Because both the biosynthesis of nitric oxide (NO.) and its metabolic fate are related to molecular O2, we hypothesized that hypoxia would alter the effects of NO. during ischemia-reperfusion (IR) in the lung. In this study, buffer-perfused lungs from rabbits underwent either normoxic IR (AI), in which lungs were ventilated with 21% O2 during ischemia and reperfusion, or hypoxic IR (NI), in which lungs were ventilated with 95% N2 during ischemia followed by reoxygenation with 21% O2. Lung weight gain (WG) and pulmonary artery pressure (Ppa) were monitored continuously, and microvascular pressure (Pmv) was measured after reperfusion to calculate pulmonary vascular resistance. We found that both AI and NI produced acute lung injury, as shown by increased WG and Ppa during reperfusion. In AI, where perfusate PO2 was > 100 mmHg, the administration of the NO. synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) before ischemia worsened WG and Ppa. Pmv also increased, suggesting a hydrostatic mechanism involved in edema formation. The effects of L-NAME could be attenuated by giving L-arginine and exogenous NO. donors before ischemia or before reperfusion. Partial protection was also provided by superoxide dismutase. In contrast, lung injury in NI at perfusate PO2 of 25-30 mmHg was attenuated by L-NAME; this effect could be reversed by L-arginine. Exogenous NO. donors given either before ischemia or before reperfusion, however, did not increase lung injury. NO. production was measured by quantifying the total nitrogen oxides (NOx) accumulating in the perfusate. The average rate of NOx accumulation was greater in AI than in NI. We conclude that hypoxia prevented the protective effects of NO on AI lung injury. The effects of hypoxia may be related to lower NO. production relative to oxidant stress during IR and/or altered metabolic fates of NO.-mediated production of peroxynitrite by hypoxic ischemia.

scholarly journals Inhaled Nitric Oxide Reduces Secondary Brain Damage after Traumatic Brain Injury in Mice

2012 ◽  
Vol 33 (2) ◽  
pp. 311-318 ◽  
Author(s):  
Nicole A Terpolilli ◽  
Seong-Woong Kim ◽  
Serge C Thal ◽  
Wolfgang M Kuebler ◽  
Nikolaus Plesnila
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Brain Regions ◽  
Lesion Volume ◽  
Effective Treatment Option ◽  
Secondary Brain Damage ◽  
Edema Formation ◽  
Regional Ischemia

Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood–brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.

The Role of Nitric Oxide in Edema Formation in L-Arginine-Induced Acute Pancreatitis

Pancreas ◽  
2002 ◽  
Vol 25 (3) ◽  
pp. 277-282 ◽  
Author(s):  
Tamás Takács ◽  
László Czakó ◽  
Éva Morschl ◽  
Ferenc László ◽  
László Tiszlavicz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Pancreatitis ◽  
Edema Formation

Superoxide dismutase potentiates platelet-activating factor-induced injury in perfused lung

1994 ◽  
Vol 266 (3) ◽  
pp. L246-L254 ◽  
Author(s):  
Y. C. Huang ◽  
E. S. Nozik ◽  
C. A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Superoxide Dismutase ◽  
Lung Injury ◽  
Platelet Activating Factor ◽  
Anion Channel ◽  
Lung Edema ◽  
Rabbit Lung ◽  
Edema Formation ◽  
Nitric Oxide Synthase Inhibitor

Platelet-activating factor (PAF) causes pulmonary hypertension and lung edema in animals and isolated perfused lungs by poorly understood mechanisms. Because oxidative mechanisms have been implicated in PAF-mediated cellular injury, we tested the hypothesis that superoxide anion (O2-.) contributes to PAF-induced lung injury by determining whether superoxide dismutase (SOD) could prevent the lung injury. Isolated rabbit lungs were perfused with PAF (100 nM) at a dose that caused transient hypertension and mild edema. Lungs pretreated with Cu,Zn SOD (100 U/ml) for 10 min developed persistent pulmonary hypertension and more lung edema formation in response to PAF. Enhanced responses to PAF also were observed in lungs perfused with 200 U/ml Cu,Zn SOD, but not with 10 or 40 U/ml Cu,Zn SOD. The higher doses of SOD also decreased thromboxane B2 levels in the perfusate. Potentiation of the PAF effect by Cu,Zn SOD was eliminated if the enzyme was inactivated or if the lung was treated with an anion channel blocker. The augmented PAF response in the presence of SOD was not altered by catalase (200 U/ml) or by nitric oxide synthase inhibitor. The data suggest that excessive Cu,Zn SOD enzyme activity potentiates PAF-induced injury in perfused rabbit lung presumably by overscavenging extracellular O2.- generated from intercellular sources. The augmented responses to PAF are not directly attributable to increased hydrogen peroxide, nitric oxide-related products, or thromboxane A2 production. These results suggest the new hypothesis that a balance between O2-. production and its metabolism determines vascular and endothelial responses to PAF.

scholarly journals Nitric oxide inhalation reduces brain damage, prevents mortality, and improves neurological outcome after subarachnoid hemorrhage by resolving early pial microvasospasms

2016 ◽  
Vol 36 (12) ◽  
pp. 2096-2107 ◽  
Author(s):  
Nicole A Terpolilli ◽  
Sergej Feiler ◽  
Ari Dienel ◽  
Frank Müller ◽  
Nicole Heumos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Neurological Outcome ◽  
Autologous Blood ◽  
Microvascular Dysfunction ◽  
Inhaled Nitric Oxide ◽  
Large Artery ◽  
Stroke Subtype ◽  
Edema Formation ◽  
Pial Arterioles

Subarachnoid hemorrhage is a stroke subtype with particularly bad outcome. Recent findings suggest that constrictions of pial arterioles occurring early after hemorrhage may be responsible for cerebral ischemia and – subsequently – unfavorable outcome after subarachnoid hemorrhage. Since we recently hypothesized that the lack of nitric oxide may cause post-hemorrhagic microvasospasms, our aim was to investigate whether inhaled nitric oxide, a treatment paradigm selectively delivering nitric oxide to ischemic microvessels, is able to dilate post-hemorrhagic microvasospasms; thereby improving outcome after experimental subarachnoid hemorrhage. C57BL/6 mice were subjected to experimental SAH. Three hours after subarachnoid hemorrhage pial artery spasms were quantified by intravital microscopy, then mice received inhaled nitric oxide or vehicle. For induction of large artery spasms mice received an intracisternal injection of autologous blood. Inhaled nitric oxide significantly reduced number and severity of subarachnoid hemorrhage-induced post-hemorrhage microvasospasms while only having limited effect on large artery spasms. This resulted in less brain-edema-formation, less hippocampal neuronal loss, lack of mortality, and significantly improved neurological outcome after subarachnoid hemorrhage. This suggests that spasms of pial arterioles play a major role for the outcome after subarachnoid hemorrhage and that lack of nitric oxide is an important mechanism of post-hemorrhagic microvascular dysfunction. Reversing microvascular dysfunction by inhaled nitric oxide might be a promising treatment strategy for subarachnoid hemorrhage.

scholarly journals Roots ofErigeron annuusAttenuate Acute Inflammation as Mediated with the Inhibition of NF-κB-Associated Nitric Oxide and Prostaglandin E2production

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Mi Jeong Jo ◽  
Jong Rok Lee ◽  
Il Je Cho ◽  
Young Woo Kim ◽  
Sang Chan Kim
Keyword(s):  
Nitric Oxide ◽  
Proinflammatory Cytokines ◽  
Acute Inflammation ◽  
Inflammatory Diseases ◽  
Inflammatory Cells ◽  
Prostaglandin E ◽  
Concomitant Treatment ◽  
Edema Formation ◽  
Erigeron Annuus ◽  
Naturalized Plant

Erigeron annuusis a naturalized plant belonging to Compositae (asteraceae) family, which is called the annual fleabane, and commonly found at meadows and roadside. This study investigated the anti-inflammatory effects of the extract ofE. annuusroots (EER), as assessed by the paw edema formation and histological analysis in rat, and the productions of nitric oxide (NO), prostaglandin E2(PGE2), and pro-inflammatory cytokines in Raw264.7 murine macrophages. Carrageenan treatment promoted infiltration of inflammatory cells and caused swelling in the hind paw. Oral administrations of EER (0.3 g/kg and 1 g/kg) attenuated acute inflammation similar to the result using dexamethasone (1 mg/kg). Treatment of macrophages with lipopolysaccharide (LPS) simulated inflammatory condition: LPS significantly increased the productions of NO, PGE2, and proinflammatory cytokines. EER suppressed activation of macrophages, preventing the induction of iNOS and COX-2 protein expressions. LPS treatment induced phosphorylation of I-κBαand increased the level of nuclear NF-κB protein, both of which were suppressed by concomitant treatment of EER. In conclusion, EER ameliorated acute inflammation in rats, and the induction of NO, PGE2, and proinflammatory cytokines in Raw264.7 cells. EER’s effects may be associated with its inhibition of NF-κB activation, suggesting its effect on inflammatory diseases.

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