ArticleThe Journal of experimental medicine1998
Essential role of induced nitric oxide in the initiation of the inflammatory response after hemorrhagic shock.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 473 citations in OpenAlex.
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- Fluid sparing and norepinephrine use in a rat model of resuscitated haemorrhagic shock: end-organ impact.Intensive care medicine experimental · 2018Article
- Gender-differences of in vitro colonic motility after chemo- and radiotherapy in humans.BMC pharmacology & toxicology · 2018Article
- Experimental Hemorrhagic Shock Protocol in Swine Models: The Effects of 21-Aminosteroid on the Small Intestine.Current therapeutic research, clinical and experimental · 2018Article
- The role of NIGMS P50 sponsored team science in our understanding of multiple organ failure.The journal of trauma and acute care surgery · 2017Article
- Preliminary profiling of blood transcriptome in a rat model of hemorrhagic shock.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- Inhibition of BTK protects lungs from trauma-hemorrhagic shock-induced injury in rats.Molecular medicine reports · 2017Article
- New progress in roles of nitric oxide during hepatic ischemia reperfusion injury.World journal of gastroenterology · 2017Review
- Inducible Nitric Oxide Synthase (iNOS) Is a Novel Negative Regulator of Hematopoietic Stem/Progenitor Cell Trafficking.Stem cell reviews and reports · 2017Article
- Inhaled hydrogen ameliorates endotoxin-induced bowel dysfunction.Acute medicine & surgery · 2017Article
- Exacerbation of Mild Hypoxia on Acute Radiation Syndrome and Subsequent Mortality.Adaptive medicine · 2017Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Resuscitation from hemorrhagic shock induces profound changes in the physiologic processes of many tissues and activates inflammatory cascades that include the activation of stress transcriptional factors and upregulation of cytokine synthesis. This process is accompanied by acute organ damage (e.g., lungs and liver). We have previously demonstrated that the inducible nitric oxide synthase (iNOS) is expressed during hemorrhagic shock. We postulated that nitric oxide production from iNOS would participate in proinflammatory signaling. Using the iNOS inhibitor N6-(iminoethyl)-L-lysine or iNOS knockout mice we found that the activation of the transcriptional factors nuclear factor kappaB and signal transducer and activator of transcription 3 and increases in IL-6 and G-CSF messenger RNA levels in the lungs and livers measured 4 h after resuscitation from hemorrhagic shock were iNOS dependent. Furthermore, iNOS inhibition resulted in a marked reduction of lung and liver injury produced by hemorrhagic shock. Thus, induced nitric oxide is essential for the upregulation of the inflammatory response in resuscitated hemorrhagic shock and participates in end organ damage under these conditions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.