Dexmedetomidine Attenuates Renal and Myocardial Ischaemia/Reperfusion Injury in a Dose-dependent Manner by Inhibiting Inflammatory Response

2016 ◽  
Author(s):  
F Ji ◽  
HY Zhao ◽  
J Du ◽  
X-G Zhou ◽  
B Zhang
Keyword(s):  
Inflammatory Response ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Dependent Manner ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Dose Dependent

scholarly journals The Role of Redox Dysregulation in the Inflammatory Response to Acute Myocardial Ischaemia-reperfusion Injury - Adding Fuel to the Fire

2018 ◽  
Vol 25 (11) ◽  
pp. 1275-1293 ◽  
Author(s):  
Sauri Hernandez-Resendiz ◽  
Kroekkiat Chinda ◽  
Sang-Bing Ong ◽  
Hector Cabrera-Fuentes ◽  
Cecilia Zazueta ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Time Course ◽  
Critical Role ◽  
Experimental Studies ◽  
Left Ventricular ◽  
Molecular Techniques ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

Background: The inflammatory response to acute myocardial ischaemia/ reperfusion injury (IRI) plays a critical role in determining myocardial infarct (MI) size, and subsequent post-MI left ventricular (LV) remodelling, making it a potential therapeutic target for improving clinical outcomes in patients presenting with an acute myocardial infarction (AMI). Recent experimental studies using advanced imaging and molecular techniques, have yielded new insights into the mechanisms through which reactive oxygen species (ROS) contribute to the inflammatory response induced by acute myocardial IRI - “adding fuel to the fire”. The infiltration of inflammatory cells into the MI zone, leads to elevated myocardial concentrations of ROS, cytokine release, and activation of apoptotic and necrotic death pathways. Anti-oxidant and anti-inflammatory therapies have failed to protect the heart against acute myocardial IRI. This may be, in part, due to a lack of understanding of the time course, nature and mechanisms of the inflammation and redox dysregulation, which occur in the setting of acute myocardial IRI. Conclusion: In this article, we examine the inflammatory response and redox dysregulation induced by acute myocardial IRI, and highlight potential therapeutic options for targeting redox dysregulation, in order to attenuate the detrimental effects of the inflammatory response following an AMI, so as to reduce MI size and prevent heart failure.

Leucocyte depletion in cardiopulmonary bypass: a comparison of four strategies

Perfusion ◽  
2003 ◽  
Vol 18 (2) ◽  
pp. 95-105 ◽  
Author(s):  
Piya Samankatiwat ◽  
Ioannis Samartzis ◽  
Panuwat Lertsithichai ◽  
Demetrios Stefanou ◽  
Prakash P Punjabi ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Inflammatory Response ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Troponin I ◽  
Neutrophil Activation ◽  
Controlled Study ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Group A

Leucocytes have been shown to play a fundamental role in the pathophysiology of inflammation. This prospective, randomized, controlled study was designed to identify the most advantageous leucocyte depletion technique in terms of reduction in systemic inflammatory response syndrome and myocardial ischaemia reperfusion injury associated with cardiopulmonary bypass (CPB). Forty consecutive patients undergoing elective coronary artery bypass graft (CABG) surgery were randomly allocated to one of four groups. The four groups consisted of a control group, a systemic leucocyte depletion (SLD) group, a cardioplegic leucocyte depletion (CLD) group and a total leucocyte depletion (TLD) group. There were 10 patients in each group. Lactoferrin (marker of neutrophil activation) and troponin-I (marker of myocardial ischaemia reperfusion injury) were measured at six time points: post induction, 5 min on CPB, 5 min before releasing the aortic crossclamp, 15 min after releasing the clamp and 1 and 24 hours after the discontinuation of CPB. Plasma lactoferrin levels increased rapidly in every group after the commencement of CPB, subsequently reached a peak after releasing the aortic crossclamp and gradually declined after the discontinuation of CPB. The lowest lactoferrin concentration was observed in the TLD (range 2.15-141.9 ng/mL) and CLD groups (7.469-114.6 ng/mL). Regarding myocardial injury, plasma cardiac troponin-I levels did not differ significantly between groups; but troponin-I concentrations rose dramatically after releasing the aortic crossclamp in all groups. Nevertheless, the CLD group had the lowest troponin-I level (1.37-5.55 ng/mL). In conclusion, it is believed that myocardial ischaemia is probably a major contributor to the inflammatory response. Although there is no clear statistical significance shown in this pilot study, the data tend to support the cardioplegic leucocyte depletion strategy as the optimal method for attenuating neutrophil activation and myocardial ischaemia reperfusion injury.

Nitrite and myocardial ischaemia reperfusion injury. Where are we now?

2021 ◽  
Vol 223 ◽  
pp. 107819
Author(s):  
Kayleigh Griffiths ◽  
Jordan J. Lee ◽  
Michael P. Frenneaux ◽  
Martin Feelisch ◽  
Melanie Madhani
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion
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