Effects of aminoguanidine administration on vascular hyporeactivity in thoracic aorta from endotoxaemic rats

Erol, Ayşe; Koşay, Sezen

doi:10.1016/s0014-2999(00)00764-0

Cited by 13 publications

(11 citation statements)

References 44 publications

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“…Evidence in the literature suggests that induction of iNOS activity by LPS causes prolonged production of large amount of NO that contributes signi® cantly to the vascular hyporeactivity characteristic of endotoxic shock (Thiemermann & Vane 1990 ;Erol & Kosay 2000). In this regard, experiments examining the role of NO in the decreased vascular contractility in endotoxaemic rats have used aminoguanidine which shown some bene® cial eOE ects in this study.…”

Section: Discussionmentioning

confidence: 91%

Evodia rutaecarpaprotects against circulation failure and organ dysfunction in endotoxaemic rats through modulating nitric oxide release

Chiou

Chen

et al. 2002

Journal of Pharmacy and Pharmacology

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Using a rat model of septic shock we studied the effects of Evodia rutaecarpa, a Chinese herbal medicine with antimicrobial and anti-inflammatory activity, on haemodynamic parameters, biochemical markers of organ function and nitric oxide (NO) production. Anaesthetized rats challenged with a high dosage of endotoxin (Escherichia coli lipopolysaccharide; LPS; 50 mg kg(-1), i.v.) for 6 h showed a severe decrease in mean arterial pressure. This was accompanied by delayed bradycardia, vascular hyporeactivity to phenylephrine and increase in plasma levels of lactate dehydrogenase, aspartate aminotransferase, bilirubin and creatinine, as well as NOx (NO2- plus NO3-). Pretreatment with ethanol extract of E. rutaecarpa (25, 50 and 100 mg kg(-1), i.v.), 1 h before LPS, dose-dependently prevented the circulation failure, vascular hyporeactivity to phenylephrine, prevented liver dysfunction and reduced the NOx over-production in plasma in endotoxaemic rats. A selective inducible NO-synthase (iNOS) inhibitor, aminoguanidine (15 mg kg(-1), i.v.), also effectively ameliorated the above pathophysiological phenomenon associated with endotoxaemia so that the normal condition was approached. Endotoxaemia for 6 h resulted in a significant increase in iNOS activity in the liver homogenate, which was attenuated significantly by E. rutaecarpa pretreatment. In summary, E. rutaecarpa, at the dosages used, exerted these beneficial effects probably through inhibition of iNOS activity and subsequent modulation of the release of NO. These significant results may offer E. rutaecarpa as a candidate for the treatment of this model of endotoxaemia.

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Section: Discussionmentioning

confidence: 91%

Evodia rutaecarpaprotects against circulation failure and organ dysfunction in endotoxaemic rats through modulating nitric oxide release

Chiou

Chen

et al. 2002

Journal of Pharmacy and Pharmacology

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“…4 Several pathologies are associated with vascular dysfunction including attenuation of endothelium-dependent vasodilatation, alteration of responsiveness of vascular smooth muscle to vasoconstrictor stimuli, or both. For instance, in inflammatory disorders such as cirrhosis, portal hypertension, 19 or sepsis 20 both vascular hypo-responsiveness to vasoconstrictors and reduced endothelium-dependent relaxation have been reported. We have previously shown that the same type of MPs used in the present study is able to induce endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Proinflammatory Proteins Through NF-κB Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity

Tesse¹,

Martínez²,

Hugel³

et al. 2005

ATVB

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Objective-Microparticles are membrane vesicles with procoagulant and proinflammatory properties released during cell activation, including apoptosis. The present study was designed in dissecting the effects evoked by microparticles on vascular reactivity. Methods and Results-Microparticles from either apoptotic T lymphocytic cells or from plasma of diabetic patients with vascular complications induced vascular hyporeactivity in response to vasoconstrictor agents in mouse aorta. Hyporeactivity was reversed by nitric oxide (NO) synthase plus cyclooxygenase-2 inhibitors, and associated with an increased production of vasodilatory products such as NO and prostacyclin. Microparticles induced an upregulation of proinflammatory protein expressions, inducible NO-synthase and cyclooxygenase-2, mainly in the medial layer of the vessels as evidenced by immunochemical staining. In addition, microparticles evoke NF-B activation probably through the interaction with the Fas/Fas Ligand pathway. Finally, in vivo treatment of mice with lymphocyte-derived MPs induces vascular hyporeactivity, which was reversed by the combination of NO and cyclooxygenase-2 inhibitors. Conclusion-These data provide a rationale to explain the paracrine role of microparticles as vectors of transcellular exchange of message in promoting vascular dysfunction during inflammatory diseases. (Arterioscler Thromb Vasc Biol. 2005;25:2522-2527.)Key Words: Fas/Fas Ligand Ⅲ microvesicles Ⅲ proinflammatory proteins Ⅲ vascular dysfunction Ⅲ vasoactivity R ecent data suggest that inflammation play a central role in the origin and complications of cardiovascular disease. For instance, inflammation has a pivotal role in the development of atherosclerosis and the acute activation of the vascular wall with consecutive local thrombosis and altered vasoactivity. This process is orchestrated by the interactions between inflammatory cells, such as leukocytes and vascular cells, endothelial cells, and smooth muscle cells, which under activation or apoptosis, for example, lead to the release of circulating microparticles (MPs). MPs are vesicles shed from the blebbing plasma membrane of various cell types, such as platelets, T and B cells, monocytes, and endothelial cells during activation by agonists, shear stress, 1,2 or apoptosis. 3,4 MPs harbor cell surface proteins and contain cytoplasmic components of the original cell. They exhibit negatively charged phospholipids, chiefly phosphatidylserine, at their surface accounting for their procoagulant character 1 and proinflammatory properties. 5 Elevated levels of circulating MPs have been detected under pathological states, such as atherosclerosis, acute coronary syndrome, diabetes, preeclampsia, and sepsis. 4,6 -9 Furthermore, these pathologies are associated with vascular dysfunction including attenuation of endothelium-dependent vasodilatation, alteration of responsiveness of vascular smooth muscle to vasoconstrictor stimuli, or both. However, the mechanisms triggering the modifications of the vessel contraction/relaxati...

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“…Previous studies have also shown that high K + -induced contractions were also reduced in inflamed segments of the jejunum (Hara & Szurszewski 1986), ileum (Martinolle et al 1997), and colon (Depoortere et al 1999). The KCl contractile response decreases after LPS incubation (1 lg mL )1 for 6 h) and after treatment with endotoxin (6 or 18 h) in rat aorta (Takakura et al 1994, Donaldson & Myers 1996, Ho et al 1996, Erol & Kosay 2000. The LPS also reduces ACh-induced contractions in small intestine segments of LPS-treated rabbits (Rebollar et al 2000) and relaxes phenylephrine-induced contractions in rat aorta (Hall et al 1996).…”

Section: Discussionmentioning

confidence: 92%

“…1994, Donaldson & Myers 1996, Ho et al. 1996, Erol & Kosay 2000). The LPS also reduces ACh‐induced contractions in small intestine segments of LPS‐treated rabbits (Rebollar et al.…”

Section: Discussionmentioning

confidence: 99%

Role of prostaglandins in lipopolysaccharide effects on K⁺‐induced contractions in rabbit small intestine

Rebollar

Guerrero‐Lindner

Arruebo

et al. 2003

Acta Physiologica Scandinavica

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Effects of aminoguanidine administration on vascular hyporeactivity in thoracic aorta from endotoxaemic rats

Cited by 13 publications

References 44 publications

Evodia rutaecarpaprotects against circulation failure and organ dysfunction in endotoxaemic rats through modulating nitric oxide release

Evodia rutaecarpaprotects against circulation failure and organ dysfunction in endotoxaemic rats through modulating nitric oxide release

Upregulation of Proinflammatory Proteins Through NF-κB Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity

Role of prostaglandins in lipopolysaccharide effects on K⁺‐induced contractions in rabbit small intestine

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Effects of aminoguanidine administration on vascular hyporeactivity in thoracic aorta from endotoxaemic rats

Cited by 13 publications

References 44 publications

Evodia rutaecarpaprotects against circulation failure and organ dysfunction in endotoxaemic rats through modulating nitric oxide release

Evodia rutaecarpaprotects against circulation failure and organ dysfunction in endotoxaemic rats through modulating nitric oxide release

Upregulation of Proinflammatory Proteins Through NF-κB Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity

Role of prostaglandins in lipopolysaccharide effects on K+‐induced contractions in rabbit small intestine

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Role of prostaglandins in lipopolysaccharide effects on K⁺‐induced contractions in rabbit small intestine