A Possible Role for Free Radicals in Tissue Injury During Myocardial Ischemia and Reperfusion

2015 ◽  
pp. 54-70 ◽  
Author(s):  
D. J. Hearse
Keyword(s):  
Free Radicals ◽  
Myocardial Ischemia ◽  
Tissue Injury ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

scholarly journals Myocardial ischemia and reperfusion injury is dependent on both IgM and mannose-binding lectin

2009 ◽  
Vol 297 (5) ◽  
pp. H1853-H1859 ◽  
Author(s):  
Marc N. Busche ◽  
Vasile Pavlov ◽  
Kazue Takahashi ◽  
Gregory L. Stahl
Keyword(s):  
Myocardial Ischemia ◽  
Complement Activation ◽  
Tissue Injury ◽  
Left Ventricular ◽  
Mannose Binding Lectin ◽  
Left Ventricular Ejection ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion ◽  
Mannose Binding ◽  
Binding Lectin

Complement activation has been shown to play an important role in the inflammation and tissue injury following myocardial ischemia and reperfusion (MI/R). Several recent studies from our laboratory demonstrated the importance of mannose-binding lectin (MBL) as the initiation pathway for complement activation and the resulting pathological effects following MI/R. However, other studies from the past suggest an important role of the classical pathway and perhaps natural antibodies. In the present study, we used newly generated genetically modified mice that lack secreted IgM (sIgM), MBL-A, and MBL-C (sIgM/MBL null) in a plasma reconstitution mouse model of MI/R. Following 30 min of ischemia and 4 h of reperfusion, left ventricular ejection fractions were significantly higher in sIgM/MBL null mice reconstituted with MBL null or sIgM/MBL null plasma compared with reconstitution with wild-type (WT) plasma or WT mice reconstituted with WT plasma following MI/R. Serum troponin I concentration, myocardial polymorphonuclear leukocyte infiltration, and C3 deposition were dependent on the combined presence of sIgM and MBL. These results demonstrate that MI/R-induced complement activation, inflammation, and subsequent tissue injury require both IgM and MBL. Thus MBL-dependent activation of the lectin pathway may not be completely antibody independent in I/R models.

scholarly journals Myocardial ischemia and reperfusion: The role of oxygen radicals in tissue injury

1989 ◽  
Vol 2 (6) ◽  
pp. 761-769 ◽  
Author(s):  
Steven W. Werns ◽  
Benedict R. Lucchesi
Keyword(s):  
Myocardial Ischemia ◽  
Oxygen Radicals ◽  
Tissue Injury ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

Effects of a monoclonal antibody directed against P-selectin after myocardial ischemia and reperfusion

1996 ◽  
Vol 270 (1) ◽  
pp. H88-H98 ◽  
Author(s):  
D. J. Lefer ◽  
D. M. Flynn ◽  
A. J. Buda
Keyword(s):  
Monoclonal Antibody ◽  
Blood Flow ◽  
Myocardial Ischemia ◽  
Myocardial Blood Flow ◽  
Myocardial Contractility ◽  
Tissue Injury ◽  
Vehicle Group ◽  
Myeloperoxidase Activity ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

Neutrophils (polymorphonuclear leukocytes, PMNs) play a role in tissue injury after ischemia and reperfusion. We investigated the effects of a monoclonal antibody (MAb), PB1.3, directed against P-selectin in an acute model of myocardial ischemia-reperfusion injury. Dogs were subjected to 120 min of coronary arterial occlusion and 240 min of reperfusion. MAb PB1.3 (1 mg/kg), the nonblocking P-selectin antibody, MAb PNB1.6 (1 mg/kg), or saline was administered 5 min before reperfusion. Dogs treated with saline (n = 7), MAb PB1.3 (n = 7), and MAb PNB1.6 (n = 5) all experienced similar myocardial blood flows during ischemia, and treatment with MAb PB1.3 failed to preserve postischemic myocardial blood flow. Measurement of myocardial contractility failed to demonstrate any beneficial effects of MAb PB1.3 on postischemic myocardial contractility. However, myocardial necrosis (% of area at risk) was significantly reduced (P < 0.01) in dogs receiving MAb PB1.3 (20.8 +/- 4.8%) compared with dogs receiving either normal saline (41.7 +/- 4.5%) or MAb PNB1.6 (46.7 +/- 7.6%). Myocardial myeloperoxidase activity in the ischemic zone was 4.8 +/- 0.6 in the vehicle group and 3.7 +/- 0.5 in the MAb PNB1.6 group compared with 2.0 +/- 0.5 in MAb PB1.3-treated dogs (P < 0.01 vs. saline; P < 0.05 vs. PNB1.6). In summary, treatment with MAb PB1.3 failed to preserve postischemic myocardial blood flow or myocardial contractility. In contrast, P-selectin immunoneutralization reduced PMN accumulation and myocardial tissue injury in a canine model of coronary occlusion and reperfusion.

scholarly journals Metabolism changes and the role of the free radicals on myocardial ischemia

2016 ◽  
pp. 162-7
Author(s):  
Dyana Sarvasti
Keyword(s):  
Free Radicals ◽  
Myocardial Ischemia ◽  
Structural Changes ◽  
Ischemia And Reperfusion ◽  
Negative Consequences ◽  
Ischemia And Reperfusion Injury ◽  
Myocardial Ischemia And Reperfusion ◽  
Clinical Syndromes ◽  
Severe Impairment

Myocardial ischemic results from severe impairment of coronary blood supply and produces a spectrum of clinical syndromes. It results in a characteristic pattern of metabolic and structural changes that leads to extremely complex situations, which have been extensively studied in recent years. A detailed understanding is now available of the complexity of the response of the myocardium to an ischemic insult. Reperfusion is the most effective way to treat the ischaemic myocardial. But, restoration of flow, however, might result in numerous other negative consequences, thus directly influencing the degree of recovery. Much evidence shows that during the period of myocardial ischemia and reperfusion can occur various changes both in terms of metabolic, electrical, histology, structural, and physiological. Pathological changes in the form of metabolic changes and the role of free radicals on the condition of ischemia and reperfusion injury will be discussed. There are several potential manifestations and outcomes associated with myocardial ischemia and reperfusion.

In Vivo MRI Visualization of Acute Myocardial Ischemia and Reperfusion in Ferrets by the Persistent Action of the Contrast Agent Gd(BME-DTTA)

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3549-3559 ◽  
Author(s):  
Tamás Simor ◽  
Wen-Jang Chu ◽  
Lynne Johnson ◽  
Andras Safranko ◽  
Mark Doyle ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Contrast Agent ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

The determination of myocardial viability using Gd-DTPA in a canine model of acute myocardial ischemia and reperfusion

1996 ◽  
Vol 36 (5) ◽  
pp. 684-693 ◽  
Author(s):  
Raoul S. Pereira ◽  
Frank S. Prato ◽  
Gerald Wisenberg ◽  
Jane Sykes
Keyword(s):  
Myocardial Ischemia ◽  
Myocardial Viability ◽  
Canine Model ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

Cardiopulmonary Bypass–Induced Inflammation and Myocardial Ischemia and Reperfusion Injury Stimulates Accumulation of Soluble MER

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Amanda C. Becker ◽  
Connor W. Lantz ◽  
Joseph M. Forbess ◽  
Conrad L. Epting ◽  
Edward B. Thorp
Keyword(s):  
Cardiopulmonary Bypass ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Myocardial Ischemia And Reperfusion
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