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Pediatric emergency care 05/2013; 29(5):690. · 0.92 Impact Factor
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European journal of emergency medicine: official journal of the European Society for Emergency Medicine 04/2013; 20(2):142-4. · 0.73 Impact Factor
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Anesthesiology 04/2013; 118(4):991-2. · 5.36 Impact Factor
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The Lancet 02/2013; 381(9865):445-6. · 38.28 Impact Factor
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Anesthesiology 02/2013; 118(2):462-3. · 5.36 Impact Factor
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Annals of emergency medicine 12/2012; 60(6):817-8. · 4.23 Impact Factor
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Saudi medical journal 12/2012; 33(12):1355-6. · 0.52 Impact Factor
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Anesthesiology 10/2012; 117(4):914-5. · 5.36 Impact Factor
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The American journal of emergency medicine 09/2012; · 1.54 Impact Factor
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Critical care (London, England) 07/2012; 16(4):441. · 4.61 Impact Factor
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ABSTRACT: To assess effects of postconditioning with the vagal stimulation (VS) on the local and systematic inflammatory responses to acute myocardial ischemia reperfusion injury (IRI).
Sixty male Sprague-Dawley rats were randomly allocated into three groups: sham group, ischemia reperfusion group (IR group), and postconditioning with the VS group (POVS group). Serum levels of inflammatory cytokines during reperfusion and myocardial levels of inflammatory cytokines in both ischemic and non-ischemic regions at the end of the experiment were assayed. The infarct size was assessed by Evans blue and triphenyltetrazolium chloride staining.
The infarct size was significantly reduced in the POVS group compared to the IR group. Serum levels of TNF-α at 30, 60, and 120 min of reperfusion and serum levels of HMGB-1, ICAM-1, IL-1, and IL-6 at 120 min of reperfusion were significantly lower in the POVS group than in the IR group. Myocardial levels of TNF-α, HMGB-1, ICAM-1, IL-1, and IL-6 in both ischemic and non-ischemic regions were also significantly reduced in the POVS group compared with the IR group.
Postconditioning with the VS can significantly attenuate the local and systemic inflammatory responses to myocardial IRI, and provide an obvious cardioprotection.
Agents and Actions 07/2012; 61(11):1273-82. · 1.59 Impact Factor
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Surgery for Obesity and Related Diseases 06/2012; 8(5):655-6. · 3.93 Impact Factor
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Pediatric Anesthesia 06/2012; 22(6):607-8. · 2.10 Impact Factor
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European Journal of Anaesthesiology 05/2012; 29(10):496-7. · 2.23 Impact Factor
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New England Journal of Medicine 05/2012; 366(20):1943; author reply 1944. · 53.30 Impact Factor
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Internal and Emergency Medicine 03/2012; 7(4):389-91; author reply 393-4. · 2.06 Impact Factor
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ABSTRACT: The inflammatory response plays a major role in ischemia-reperfusion injury (IRI). Considering that cholinergic stimulation can inhibit inflammatory response through the cholinergic anti-inflammatory pathway (CAP) and the α subunit-containing nicotinic acetylcholine receptor(α7nAChR) expressed by immune cells is an important component of CAP, we assessed the effect of postconditioning with α7nAChR agonist on systemic inflammatory response during the myocardial ischemia-reperfusion process in an in vivo rat model. Thirty Sprague Dawley rats were randomly divided into three groups: sham group, control group, and postconditioning with α7nAChR agonist group (PP group). In the groups other than the sham group, the left anterior descending coronary artery was ligated for 30 min followed by a 180-min reperfusion. At the end of the experiment, the serum levels of troponin I, tumor necrosis factor α, interleukin-6, and high-mobility group box 1 were assayed, and the infarct size was assessed. The results showed that postconditioning with α7nAChR agonist significantly attenuated the systemic inflammatory response to myocardial IRI, as evidenced by decreased serum levels of tumor necrosis factor α and high-mobility group box 1. Also, this treatment protected against myocardial IRI, as shown by reduced infarct size and serum troponin I level.
Inflammation 03/2012; 35(4):1357-64. · 1.75 Impact Factor
