scholarly journals Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model

Biomolecules ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 101
Author(s):  
Suhail Al-Salam ◽  
Elhadi H. Aburawi ◽  
Suleiman Al-Hammadi ◽  
Sekhar Dhanasekaran ◽  
Mohamed Shafiuallah ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mast Cell ◽  
Mast Cells ◽  
Small Bowel ◽  
Nitric Oxide Synthase ◽  
Rat Model ◽  
Anaphylactic Shock ◽  
Wistar Rat ◽  
Severe Hypotension ◽  
Oxide Synthase

Anaphylactic shock (AS) is a life-threatening, multisystem disorder arising from sudden release of mast cell- and basophil-derived mediators into the circulation. In this study, we have used a Wistar rat model to investigate AS-associated histopathologic changes in various organs. Rats were sensitized with ovalbumin (1 mg s.c), and AS was induced by intravenous injection of ovalbumin (1 mg). Experimental groups included nonallergic rats (n = 6) and allergic rats (n = 6). Heart rate and blood pressure were monitored during one hour. Organs were harvested at the end of the experiment and prepared for histologic and immunohistochemical studies. Lung, small bowel mucosa and spleen were found to undergo heavy infiltration by mast cells and eosinophils, with less prominent mast cell infiltration of cardiac tissue. The mast cells in lung, small bowel and spleen exhibited increased expression of tryptase, c-kit and induced nitric oxide synthase (iNOS). Increased expression of endothelial nitric oxide synthase (eNOS) by vascular endothelial cells was noted principally in lung, heart and small bowel wall. The Wistar rat model of AS exhibited accumulation of mast cells and eosinophils in the lung, small bowel, and spleen to a greater extent than in the heart. We conclude that lung and gut are principal inflammatory targets in AS, and likely contribute to the severe hypotension of AS. Targeting nitric oxide (NO) production may help reduce AS mortality.

Impaired pulmonary artery contractile responses in a rat model of microgravity: role of nitric oxide

2002 ◽  
Vol 92 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Daniel Nyhan ◽  
Soonyul Kim ◽  
Stacey Dunbar ◽  
Dechun Li ◽  
Artin Shoukas ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pulmonary Artery ◽  
Lung Tissue ◽  
Rat Model ◽  
Orthostatic Intolerance ◽  
Volume Distribution ◽  
Contractile Responses ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Vascular contractile hyporesponsiveness is an important mechanism underlying orthostatic intolerance after microgravity. Baroreceptor reflexes can modulate both pulmonary resistance and capacitance function and thus cardiac output. We hypothesized, therefore, that pulmonary vasoreactivity is impaired in the hindlimb-unweighted (HLU) rat model of microgravity. Pulmonary artery (PA) contractile responses to phenylephrine (PE) and U-46619 (U4) were significantly decreased in the PAs from HLU vs. control (C) animals. N G-nitro-l-arginine methyl ester (10−5 M) enhanced the contractile responses in the PA rings from both C and HLU animals and completely abolished the differential responses to PE and U4 in HLU vs. C animals. Vasorelaxant responses to ACh were significantly enhanced in PA rings from HLU rats compared with C. Moreover, vasorelaxant responses to sodium nitroprusside were also significantly enhanced. Endothelial nitric oxide synthase (eNOS) and soluble guanlyl cyclase expression were significantly enhanced in PA and lung tissue from HLU rats. In marked contrast, the expression of inducible nitric oxide synthase was unchanged in lung tissue. These data support the hypothesis that vascular contractile responsiveness is attenuated in PAs from HLU rats and that this hyporesponsiveness is due at least in part to increased nitric oxide synthase activity resulting from enhanced eNOS expression. These findings may have important implications for blood volume distribution and attenuated stroke volume responses to orthostatic stress after microgravity exposure.

Inhibition of Inducible Nitric Oxide Synthase Reduces Bacterial Translocation in a Rat Model of Acute Pancreatitis

Pancreas ◽  
2001 ◽  
Vol 23 (3) ◽  
pp. 296-301 ◽  
Author(s):  
Ismail Simsek ◽  
Mehmet Refik ◽  
Mehmet Yasar ◽  
Mustafa Ozyurt ◽  
Ugur Saglamkaya ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Pancreatitis ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Bacterial Translocation ◽  
Rat Model ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Effect of nitric oxide synthase (NOS) inhibition on macro- and microcirculation in a model of rat endotoxic shock

2006 ◽  
Vol 95 (04) ◽  
pp. 720-727 ◽  
Author(s):  
Soni Pullamsetti ◽  
Daniel Maring ◽  
Hossein Ghofrani ◽  
Konstantin Mayer ◽  
Norbert Weissmann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Septic Shock ◽  
Nitric Oxide Synthase ◽  
Rat Model ◽  
Endotoxic Shock ◽  
Nos Inhibitors ◽  
Mucosal Layer ◽  
Lactate Acidosis ◽  
Oxide Synthase

SummaryTreatment of hemodynamic instability in septic shock often demands the administration of vasopressor agents, although these may have deleterious effects on microcirculatory homeostasis. Inhibition of nitric oxide synthase (NOS) has been suggested as an alternative therapeutic approach, as NO formation may be excessively increased in sepsis. To compare the effects of epinephrine titration, non-selective NOS inhibition by L-NMMA and selective inhibition of inducible NOS (iNOS) by 1400W on hemodynamics and on the regulation of microcirculation in a rat model of endotoxic shock, we intravenously injected endotoxin (LPS) or saline to male Wist ar rats and after 2 hours randomized LPS treated rats into four different groups that received either saline, norepinephrine, L-NMMA or 1400W (n=6 per group). Three hours after LPS administration, rats presented with severe systemic arterial hypotension (64 ± 3 vs. 115 ± 4 mmHg, p<0.001), unresponsiveness to volume treatment, lactate acidosis and a marked increase in plasmatic nitrite and nitrate levels (15 ±8 vs. 263 ± 47 µM, p<0.001). Measurement of the tissue oxygenation in the ileum mucosal layer by the Erlangen micro-lightguide spectrophotometer (EMPHO) technique demonstrated marked heterogeneity of hemoglobin saturation, with appearance of low oxygenated areas. Norepinephrine, usually stabilizing blood pressure (99 ±7 vs. 67 ±4 mmHg 60 min after infusion, p<0.01), increased lactate formation (7.9± 0.2 vs. 3.7 ± 0.5 mM, p<0.001) and drastically increased low oxygenated regions in the ileum mucosal layer. L-NMMA similarly increased blood pressure (92 ±6 vs. 67 ±4 mmHg 60 min after infusion, p<0.05), but did not enhance lactate acidosis. However, some further deterioration of mucosa oxygenation was again noted. 1400W forwarded stabilization of blood pressure (88 ± 5 vs. 67 ±4 mmHg 60 min after injection, p<0.05), reduced plasmatic nitrite and nitrate levels similar to L-NMMA, without an aggravation of lactate acidosis. In addition, mucosal oxygenation did not deteriorate in response to this agent. Thereby, we conclude that in a rat model of endotoxic shock selective iNOS inhibitors are superior to non-specific NOS inhibitors and in particular to norepinephrine for the treatment of macro-and microcirculatory abnormalities in experimental septic shock.

Glial activation is associated with l-DOPA induced dyskinesia and blocked by a nitric oxide synthase inhibitor in a rat model of Parkinson's disease

2015 ◽  
Vol 73 ◽  
pp. 377-387 ◽  
Author(s):  
Mariza Bortolanza ◽  
Roberta Cavalcanti-Kiwiatkoski ◽  
Fernando E. Padovan-Neto ◽  
Célia Aparecida da-Silva ◽  
Miso Mitkovski ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nitric Oxide Synthase ◽  
Rat Model ◽  
Glial Activation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Synthase Inhibitor ◽  
Oxide Synthase
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