Abstract 17692: Arrhythmogenic Mechanisms in Hemorrhagic Shock-induced Heart and Comparable Effect of Different Hemoglobin Concentration of Two Artificial Oxygen Carriers

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bonpei Takase ◽  
Yuko Higashimura ◽  
Yoshihiro Tanaka ◽  
Kenichi Hashmoto
Keyword(s):  
Hemorrhagic Shock ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Electrophysiological Study ◽  
Hemoglobin Concentration ◽  
Conduction Delay ◽  
Oxygen Carriers ◽  
Artificial Oxygen Carriers ◽  
Ventricular Electrical Remodeling

Lethal ventricular arrhythmias (VT/VF) are serious complications after resuscitation of severe hemorrhagic shock (HS). To investigate mechanisms of arrhythmogenesis after HS and a role of two different concentration of oxygenated liposome-encapsulated human hemoglobin (LHb [Hgb=6g] or HbV [Hgb=10g]), optical mapping analysis (OMP) and electrophysiological study (EPS) were performed using rat HS model. HS was induced by withdrawing 30% blood from aorta (shock alone). Rats were resuscitated by transfusing saline, 5% albumin (5%ALB), LHb, HbV or oxygenated autologous washed red blood cells (wRBC: n=7, per group). After excising heart, OMP and EPS were performed in isolated Langendorff-perfused hearts. OMP revealed abnormal ventricular conduction delay (VCD) with impaired action potential duration dispersion (APDd) in both ventricles in shock alone, saline, and 5%ALB whereas VCD and APDd were substantially attenuated in LHb, HbV or wRBC (a). VT/VF was easily provoked by burst pacing stimulus to LV in saline and 5%ALB while few VT/VF was induced in LHb, LbV or wRBC (b). Conclusion: Ventricular electrical remodeling of abnormal VCD and APDd after HS causes VT/VF. LHb, LbV and wRBC comparably prevent VT/VF possible by attenuating ischemia-reperfusion injury in HS. Especially, even low concentration of hemoglobin in LHb is comparably effective with closely normal concentration of HbV.

Abstract 340: Cardiac Autonomic Activity, Cardiac Function and Arrhythmogenic Property in Heart in Hemorrhagic Shock: Effect of Artificial Oxygen Carrier

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Bonpei Takase ◽  
Yoshihiro Tanaka
Keyword(s):  
Cardiac Function ◽  
Hemorrhagic Shock ◽  
Ischemia Reperfusion ◽  
Electrophysiological Study ◽  
Oxygen Carrier ◽  
Conduction Delay ◽  
Autonomic Activity ◽  
Artificial Oxygen Carrier ◽  
Fatty Acid Binding ◽  
Cardiac Autonomic Activity

Lethal ventricular arrhythmias (VT/VF) is serious complications in severe hemorrhagic shock (HS). Cardiac autonomic imbalance and dysfunction are well known unfavorable conditions. However, the effect of oxygenation including artificial oxygen carrier is not fully understood. To investigate the role of oxygenation in lethal HS, cardiac autonomic activity measures, cardiac function test, optical mapping analysis (OMP), and electrophysiological study (EPS) were performed in rats lethal HS. Methods and Results: 1) Over the course of 150 min, rats were subjected to blood withdrawal (0.2 mL/min; total 85% bleeding) and simultaneously transfused with washed rat red blood cells (wRBC), liposome-encapsulated hemoglobin (LHb) or 5% albumin (5%ALB). Temporal changes in cardiac function by 2-D Echocardiography, heart-type fatty acid-binding protein (hFAB) levels, plasma levels of catecholamines, heart rate variability (HRV), and hypoxia-inducible factor 1α expression (HIF1) were measured. As results, > 85% of the rats transfused with either LHb or wRBC survived for 8 days. LHb transfusion suppressed HIF1 expression in the heart, maintained low levels of hFAB, and attenuated sympathetic nerve activity as reflected by changes in HRV and catecholamines. 2) After cannulating 22G catheter into the abdominal aorta, acute HS was induced by withdrawing 30% of total blood for 25 min. After HS, the rats were immediately resuscitated by transfusing the same amount of wRBC, LHb, or 5%ALB. After excising the heart, OMP and EPS were performed in Langendorff-perfused hearts. OMP revealed abnormal ventricular conduction delay in conjunction with impaired action potential duration (APD) dispersion in 5%ALB. In contrast, myocardial conduction velocity and APD dispersion were substantially attenuated in wRBC or LHb. Sustained VT/VF was easily provoked by burst pacing stimulus to the LV in 5%ALB whereas no VT/VF was induced with wRBC or LHb. Conclusions: The results indicate that wRBC and LHb attenuates cardiac dysfunction and sympathetic overactivity during lethal HS. Oxygenated hemoglobin transfusion by using either wRBC or LHb prevents VT/VF by preserving myocardial electrical structures caused by ischemia-reperfusion injury in HS.

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

Role of JNK phosphorylation in intestinal ischemia/reperfusion injury in mice

2010 ◽  
Vol 30 (2) ◽  
pp. 140-143
Author(s):  
De-yi ZHENG ◽  
Jian-ming WNAG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Kai-yang LU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

The role of microRNA in hepatic ischemia/reperfusion injury

MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
Chrysanthos D. Christou ◽  
Georgios Tsoulfas
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Clinical Manifestations ◽  
Diagnostic Procedures ◽  
Clinical Tool ◽  
Hepatic Ischemia ◽  
Humoral Factors ◽  
Early Graft ◽  
Hepatic Ischemia Reperfusion

Introduction: Ischemia-reperfusion (I/R) injuries are caused by complex interrelated mechanisms and pathways. Regarding the liver, I/R injuries and their clinical manifestations are crucial for the surgical outcome. Despite its importance, there is no broadly accepted therapy either for the prevention or for the management of I/R injury. I/R injury of the liver can occur either during hepatic surgery (warm) or during the transplantation procedure (cold). MicroRNAs play a pivotal role in the mechanism of I/R injury, as they regulate the expression of the cellular participants and humoral factors associated with I/R injury. Objective: In this review, we highlight the microRNAs that are involved in the I/R injury of the liver, and the molecular pathways that they regulate. In addition, we discuss the potential role of circulating microRNAs as biomarkers and their role as pharmacological targets in the prevention, diagnosis and treatment of I/R injuries. Method: We conducted a comprehensive review of the PubMed bibliographic database regarding microRNAs and I/R injuries of the liver. Results: In diagnostics, microRNA panels could replace invasive diagnostic procedures, relieving patients of the associated complications. In therapeutics, microRNA agomirs, antagomirs and other drugs can be used to shift the balance between proapoptotic and survival pathways, to alleviate the liver damage caused by I/R. In transplantation procedures, microRNA profiling could decrease the incidence of early graft dysfunction, especially regarding marginal grafts. Conclusion: Although microRNAs seem a very promising clinical tool in the management of I/R injuries, further research is required, until microRNAs become a novel tool in the diagnosis and monitoring of an I/R injury of the liver.

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