Clonidine pre-treatment prevents hemorrhagic shock-induced endotoxemia and oxidative stress in the gut, liver, and lungs of the rat

Filos, Kriton S.; Panteli, Eleftheria S; Fligou, Foteini; Papamichail, Chrysaygi; Papapostolou, Ioannis; Zervoudakis, George; Spiliopoulou, Iris; Georgiou, Christos D.

doi:10.1179/1351000212y.0000000029

Cited by 6 publications

(6 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The five studies were all in rats, four dexmedetomidine [19, 24, 27, 43] and one clonidine [39]. Study size ranged from 30 to 80 animals.…”

Section: Resultsmentioning

confidence: 99%

“…Filos et al used a haemorrhage model and studied the effects of clonidine pre-treatment (150 μg/kg subcutaneously) on circulating endotoxin and tissue superoxide radicals, finding both were reduced [39]. Uysal et al used a femoral artery/vein clamp model to study effects of dexmedetomidine 10 and 30 μg/kg on an epigastric island skin flap 12 h and 7 days post-IRI finding both doses reduced tissue NO, MDA, and MPO at both time points, and reduced flap necrosis area [19].…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

The effect of dexmedetomidine and clonidine on the inflammatory response in critical illness: a systematic review of animal and human studies

et al. 2019

View full text Add to dashboard Cite

BackgroundThe α2 agonists, dexmedetomidine and clonidine, are used as sedative drugs during critical illness. These drugs may have anti-inflammatory effects, which might be relevant to critical illness, but a systematic review of published literature has not been published. We reviewed animal and human studies relevant to critical illness to summarise the evidence for an anti-inflammatory effect from α2 agonists.MethodsWe searched PubMed, the Cochrane library, and Medline. Animal and human studies published in English were included. Broad search terms were used: dexmedetomidine or clonidine, sepsis, and inflammation. Reference lists were screened for additional publications. Titles and abstracts were screened independently by two reviewers and full-text articles obtained for potentially eligible studies. Data extraction used a bespoke template given study diversity, and quality assessment was qualitative.ResultsStudy diversity meant meta-analysis was not feasible so descriptive synthesis was undertaken. We identified 30 animal studies (caecal ligation/puncture (9), lipopolysaccharide (14), acute lung injury (5), and ischaemia-reperfusion syndrome (5)), and 9 human studies. Most animal (26 dexmedetomidine, 4 clonidine) and all human studies used dexmedetomidine. In animal studies, α2 agonists reduced serum and/or tissue TNFα (20 studies), IL-6 (17 studies), IL-1β (7 studies), NFκB (6 studies), TLR4 (6 studies), and a range of other mediators. Timing and doses varied widely, but in many cases were not directly relevant to human sedation use. In human studies, dexmedetomidine reduced CRP (4 studies), TNFα (5 studies), IL-6 (6 studies), IL-1β (3 studies), and altered several other mediators. Most studies were small and low quality. No studies related effects to clinical outcomes.ConclusionEvidence supports potential anti-inflammatory effects from α2 agonists, but the relevance to clinically important outcomes is uncertain. Further work should explore whether dose relationships with inflammation and clinical outcomes are present which might be separate from sedation-mediated effects.

show abstract

“…The five studies were all in rats, four dexmedetomidine [19, 24, 27, 43] and one clonidine [39]. Study size ranged from 30 to 80 animals.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

The effect of dexmedetomidine and clonidine on the inflammatory response in critical illness: a systematic review of animal and human studies

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Thus, it is not surprising to see the “paradoxical effect” of stimulant treatment, which causes oxidative stress (El-Tawil, Abou-Hadeed, El-Bab, & Shalaby, 2011; Martins et al, 2006) but is also neuroprotective (Volz, 2008) and is an effective treatment for ADHD (Faraone & Buitelaar, 2010). In contrast, clonidine, which is also an effective treatment for ADHD, reduces oxidative stress in rats (Filos et al, 2012; Nik Yusoff, Mustapha, Govindasamy, & Sirajudeen, 2013). Whether this is an alternative mechanism of action for this drug is unknown.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress and ADHD

et al. 2013

View full text Add to dashboard Cite

Objective To clarify the role of oxidative stress and antioxidant activity in ADHD. Method We examined the association of ADHD and oxidative stress by applying random effects meta-analysis to studies of oxidative stress and antioxidant status in medication naive patients with ADHD and controls. Results Six studies of a total of 231 ADHD patients and 207 controls met our selection criteria. The association between ADHD and antioxidant status was not significant. We found a significant association between ADHD and oxidative stress that could not be accounted for by publication bias. The significant association lost significance after correcting for intrastudy clustering. No one observation accounted for the positive result. Conclusion These results are preliminary given the small number of studies. They suggest that patients with ADHD have normal levels of antioxidant production, but that their response to oxidative stress is insufficient, leading to oxidative damage.

show abstract

“…Few studies have shown that the prognosis of HS closely relates to the enterogenous endotoxemia, which cannot be reverted by intravenous fluid resuscitation [28,29]. Therefore, reducing the concentration of the enterogenous endotoxin will help to improve the prognosis of HS.…”

Section: Discussionmentioning

confidence: 99%

Dai Huang Fu Zi Tang could ameliorate intestinal injury in a rat model of hemorrhagic shock by regulating intestinal blood flow and intestinal expression of p-VASP and ZO-1

Kang

Zhan

et al. 2014

BMC Complement Altern Med

View full text Add to dashboard Cite

BackgroundDai Huang Fu Zi Tang (DHFZT), an oriental herbal formula, has long been used clinically in treatment of intestinal obstruction, acute pancreatitis, cholecystalgia and chronic diarrhea for thousands of years. Recent studies have demonstrated that DHFZT can reduce intestinal pathological injury and the concentration of enterogenous endotoxin in an animal model. But the underlying mechanism has not been fully elucidated.MethodsSD male rats in adult were used to model HS and treated with DHFZT. The serum concentration of endotoxin were analyzed by dynamic turbidimetric method. In addition, the blood flow of small intestine were measured using laser speckle technique. Phosphorylated vasodilator-stimulated phosphoprotein (p-VASP) and zonula occludens (ZO)-1 protein, intestinal fatty acid binding protein (IFABP) were measured by Western Blotting, RT-PCR, ELISA respectively.ResultsPresent study showed that DHFZT markedly elevated the blood flow of small intestine, protected the intestinal barrier function by up-regulating the expression of ZO-1 protein and down-regulating expression of p-VASP, and notely decreased serum concentration of IFABP and endotoxin in HS.ConclusionsThese results reveal that DHFZT improves intestinal blood flow, protects the intestinal barrier function, and ameliorates intestinal endotoxaemia in rats with HS.

show abstract

Clonidine pre-treatment prevents hemorrhagic shock-induced endotoxemia and oxidative stress in the gut, liver, and lungs of the rat

Cited by 6 publications

References 44 publications

The effect of dexmedetomidine and clonidine on the inflammatory response in critical illness: a systematic review of animal and human studies

The effect of dexmedetomidine and clonidine on the inflammatory response in critical illness: a systematic review of animal and human studies

Oxidative Stress and ADHD

Dai Huang Fu Zi Tang could ameliorate intestinal injury in a rat model of hemorrhagic shock by regulating intestinal blood flow and intestinal expression of p-VASP and ZO-1

Contact Info

Product

Resources

About