ArticleBritish journal of pharmacology1999
Regional haemodynamic responses to infusion of lipopolysaccharide in conscious rats: effects of pre- or post-treatment with glibenclamide.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 60 citations in OpenAlex.
- A Protective Role of Glibenclamide in Inflammation-Associated Injury.Mediators of inflammation · 2017Review
- Cystathionine β-synthase-derived hydrogen sulfide regulates lipopolysaccharide-induced apoptosis of the BRL rat hepatic cell line in vitro.Experimental and therapeutic medicine · 2012Article
- Early potassium channel blockade improves sepsis-induced organ damage and cardiovascular dysfunction.British journal of pharmacology · 2011Article
- Early physiologic responses to hemorrhagic hypotension.Translational research : the journal of laboratory and clinical medicine · 2010Article
- Lipopolysaccharides up-regulate Kir6.1/SUR2B channel expression and enhance vascular KATP channel activity via NF-kappaB-dependent signaling.The Journal of biological chemistry · 2010Article
- Renal blood flow in sepsis.Critical care (London, England) · 2005Review
- The pore-forming subunit of the K(ATP) channel is an important molecular target for LPS-induced vascular hyporeactivity in vitro.British journal of pharmacology · 2005Article
- Role of hydrogen sulphide in haemorrhagic shock in the rat: protective effect of inhibitors of hydrogen sulphide biosynthesis.British journal of pharmacology · 2004Article
- Cannabinoid antagonist SR-141716 inhibits endotoxic hypotension by a cardiac mechanism not involving CB1 or CB2 receptors.American journal of physiology. Heart and circulatory physiology · 2004Article
- Science Review: Vasopressin and the cardiovascular system part 2 - clinical physiology.Critical care (London, England) · 2004Review
- Dexamethasone improves vascular hyporeactivity induced by LPS in vivo by modulating ATP-sensitive potassium channels activity.British journal of pharmacology · 2003Article
- Synthesis of Amino-ADT Provides Access to Hydrolytically Stable Amide-Coupled Hydrogen Sulfide Releasing Drug Targets.Synlett : accounts and rapid communications in synthetic organic chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. To determine the putative contribution of K(ATP)-channels to the haemodynamic sequelae of endotoxaemia, three experiments were carried out in different groups of conscious, chronically-instrumented, unrestrained, male Long Evans rats. 2. In the first experiment, pretreatment with the K(ATP)-channel antagonist, glibenclamide, abolished the initial hypotension, but not the renal vasodilatation caused by LPS infusion. Subsequently, however, in the presence of glibenclamide and LPS there was a significant increase in mean arterial blood pressure, and a bradycardia, in contrast to the fall in mean arterial blood pressure and the tachycardia seen in the presence of vehicle and LPS. The pressor and bradycardic changes in the presence of glibenclamide and LPS were accompanied by significant reductions in hindquarters flow and vascular conductance, and these were significantly greater than those seen in the presence of vehicle and LPS, or glibenclamide and saline. 3. Administration of glibenclamide 6 h after the onset of saline and LPS infusion, or 6 h after the onset of saline and LPS infusion in the presence of the AT(1)-receptor antagonist, losartan, and the ET(A)-, ET(B)- receptor antagonist, SB 209670, in the absence or presence of dexamethasone, caused a significant increase in mean arterial blood pressure and reductions in renal, mesenteric and hindquarters conductances, although the latter was the only vascular bed in which there was a reduction in flow. 4. The results are consistent with a contribution from K(ATP)-channels to the vasodilatation caused by LPS, particularly in the hindquarters vascular bed.
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