Role of Nitric Oxide in Hemorrhagic Shock-Induced Bacterial Translocation

2000 ◽  
Vol 93 (2) ◽  
pp. 247-256 ◽  
Author(s):  
Teng Choo Hua ◽  
Shabbir M. Moochhala
Keyword(s):  
Nitric Oxide ◽  
Hemorrhagic Shock ◽  
Bacterial Translocation

PHYSIOLOGIC AND MOLECULAR CHARACTERIZATION OF THE ROLE OF NITRIC OXIDE IN HEMORRHAGIC SHOCK

Shock ◽  
1997 ◽  
Vol 7 (3) ◽  
pp. 157-163 ◽  
Author(s):  
Edward Kelly ◽  
Nishit S. Shah ◽  
Nathan N. Morgan ◽  
Simon C. Watkins ◽  
Andrew B. Peitzman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hemorrhagic Shock ◽  
Molecular Characterization

PP235 ROLE OF ARGININE AND INDUCIBLE NITRIC OXIDE SYNTHASE ON BACTERIAL TRANSLOCATION

2010 ◽  
Vol 5 (2) ◽  
pp. 114-115
Author(s):  
I.E.P. Quirino ◽  
R.G.C. Santos ◽  
V.N. Cardoso ◽  
J.I.A. Leite ◽  
M.I.T.D. Correia
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Bacterial Translocation ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Allicin ameliorates intraintestinal bacterial translocation after trauma/hemorrhagic shock in rats: The role of mesenteric lymph node dendritic cell

Surgery ◽  
2017 ◽  
Vol 161 (2) ◽  
pp. 546-555 ◽  
Author(s):  
Yun Zhang ◽  
Jian Zhang ◽  
Tao Xu ◽  
Wei Wu ◽  
Fang-Fang Huang ◽  
...  
Keyword(s):  
Lymph Node ◽  
Dendritic Cell ◽  
Hemorrhagic Shock ◽  
Bacterial Translocation ◽  
Mesenteric Lymph Node ◽  
Mesenteric Lymph

Hemorrhagic Shock-induced Bacterial Translocation: The Role of Neutrophils and Hydroxyl Radicals

1990 ◽  
Vol 30 (8) ◽  
pp. 942-952 ◽  
Author(s):  
EDWIN A. DEITCH ◽  
WILLIAM BRIDGES ◽  
LI MA ◽  
RODNEY BERG ◽  
ROBERT D. SPECIAN ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Hydroxyl Radicals ◽  
Bacterial Translocation

Reduction of shock-induced gastric damage by a nitric oxide-releasing aspirin derivative: role of neutrophils

1997 ◽  
Vol 273 (6) ◽  
pp. G1246-G1251 ◽  
Author(s):  
John L. Wallace ◽  
Webb McKnight ◽  
Tammy L. Wilson ◽  
Piero Del Soldato ◽  
Giuseppe Cirino
Keyword(s):  
Nitric Oxide ◽  
Hemorrhagic Shock ◽  
Gastric Damage ◽  
Leukocyte Adherence ◽  
Inhibitory Effects ◽  
Neutrophil Adherence ◽  
Nitric Oxide Releasing ◽  
Derivatives Of ◽  
Ncx 4016

The gastric damage associated with hemorrhagic shock appears to occur, at least in part, through neutrophil-dependent mechanisms. Nitric oxide (NO)-releasing derivatives of aspirin have been shown to spare the gastrointestinal tract of injury. As NO can inhibit neutrophil adherence, it is possible that such a derivative of aspirin (NCX-4016) would exert inhibitory effects on neutrophil adherence and therefore be capable of protecting the stomach against shock-induced gastric damage. This hypothesis was tested in this study. Oral administration of NCX-4016 or glyceryl trinitrate or depletion of circulating neutrophils with antineutrophil serum significantly reduced the extent of gastric damage induced by hemorrhagic shock, whereas aspirin had no effect. NCX-4016 and antineutrophil serum pretreatment resulted in significant preservation of gastric blood flow during the shock period. Moreover, NCX-4016, but not aspirin, was capable of inhibiting N-formyl-Met-Leu-Phe-induced leukocyte adherence to postcapillary mesenteric venules. These results suggest that an NO-releasing aspirin derivative reduces the susceptibility of the stomach to shock-induced damage through inhibitory effects on neutrophil adherence to the vascular endothelium.

Role of Nitric Oxide in Gastric Injury Induced by Hemorrhagic Shock in Rats

Pharmacology ◽  
2000 ◽  
Vol 61 (2) ◽  
pp. 106-112 ◽  
Author(s):  
Arzu Denizbaşı ◽  
Cumhur Yegen ◽  
Melek Öztürk ◽  
Berrak Yegen
Keyword(s):  
Nitric Oxide ◽  
Hemorrhagic Shock ◽  
Gastric Injury

Evidence for a Role of Nitric Oxide in Hypovolemic Hemorrhagic Shock

1992 ◽  
Vol 19 (6) ◽  
pp. 982-986 ◽  
Author(s):  
Basilia Zingarelli ◽  
Francesco Squadrito ◽  
Domenica Altavilla ◽  
Gioacchino Calapai ◽  
Giuseppe M. Campo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hemorrhagic Shock

Abstract P200: Role of Macula Densa Neuronal Nitric Oxide Synthase in Control of Renin Release and Blood Pressure Recovery Following Hemorrhagic Shock

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Lei Wang ◽  
Shaohui Wang ◽  
Jacentha Buggs ◽  
Jie Zhang ◽  
Jin Wei ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Radio Telemetry ◽  
Macula Densa ◽  
Pressure Recovery ◽  
Renin Release ◽  
Limiting Factor ◽  
Sodium Diet

Renin is a rate limiting factor for generation of angiotensin II, which is essential for blood pressure regulation. The role of macula densa nitric oxide (NO) in renin release is not conclusive. The goal of this study was to elucidate the role of macula densa neuronal NO synthase (NOS1) in control of renin release in response to sodium challenges and hemorrhagic shock, as well as in blood pressure recovery after hemorrhagic shock. C57BL/6L mice and macula densa specific NOS1 knockout (MD-NOS1KO) mice were given 10 days of low (0.1% NaCl), normal (0.4% NaCl) and high (1.4% NaCl) sodium diet. Hemorrhagic shock was induced by withdrawing 0.4 ml whole blood from the right retro-orbital sinus. Mean arterial pressure (MAP) in conscious mice was monitored by radio-telemetry system. Plasma renin concentration (PRC) was determined by radioimmunoassay. Low sodium diet stimulated PCR by 29% (from 685 ± 32 to 883 ± 112 ng/ml/hr) in WT mice and by 16% (from 652 ± 24 to 756 ± 124 ng/ml/hr) in the MD-NOS1KO mice (n=5/group, p<0.01 vs WT). PCR was not significantly different between the WT and MD-NOS1KO mice fed a normal or high salt diet. As shown in Fig1A, following removal of 0.4ml of blood, MAP dropped to about 40mmHg in the WT mice and 35mmHg in the MD-NOS1KO mice. MAP recovered faster in WT mice than the MD-NOS1KO mice. In Fig1B, PRC increased over 200% of the basal value in WT mice, but only increased about 26% in the MD-NOS1KO mice (n=4/group, p<0.01 vs WT). We conclude that NOS1 in the macula densa facilitates renin release. Lack of macula densa NO generation impairs blood pressure recovery, which may be mediated by limiting renin release during hemorrhagic shock.

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