Mechanisms of activation of lipid free-radical peroxidation during regional ischemia followed by reperfusion of the heart

1981 ◽  
Vol 92 (3) ◽  
pp. 1170-1172 ◽  
Author(s):  
P. F. Litvitskii ◽  
A. Kh. Kogan ◽  
A. N. Kudrin ◽  
L. O. Luk'yanova
Keyword(s):  
Free Radical ◽  
Regional Ischemia ◽  
Lipid Free Radical

Molecular and Cellular Mechanisms of Myocardial Stunning

1999 ◽  
Vol 79 (2) ◽  
pp. 609-634 ◽  
Author(s):  
Roberto Bolli ◽  
Eduardo Marbán
Keyword(s):  
Free Radical ◽  
Myocardial Stunning ◽  
Recovery Of Function ◽  
Myocardial Dysfunction ◽  
Calcium Overload ◽  
Global Ischemia ◽  
Stunned Myocardium ◽  
Common Mechanism ◽  
Regional Ischemia

The past two decades have witnessed an explosive growth of knowledge regarding postischemic myocardial dysfunction or myocardial “stunning.” The purpose of this review is to summarize current information regarding the pathophysiology and pathogenesis of this phenomenon. Myocardial stunning should not be regarded as a single entity but rather as a “syndrome” that has been observed in a wide variety of experimental settings, which include the following: 1) stunning after a single, completely reversible episode of regional ischemia in vivo; 2) stunning after multiple, completely reversible episodes of regional ischemia in vivo; 3) stunning after a partly reversible episode of regional ischemia in vivo (subendocardial infarction); 4) stunning after global ischemia in vitro; 5) stunning after global ischemia in vivo; and 6) stunning after exercise-induced ischemia (high-flow ischemia). Whether these settings share a common mechanism is unknown. Although the pathogenesis of myocardial stunning has not been definitively established, the two major hypotheses are that it is caused by the generation of oxygen-derived free radicals (oxyradical hypothesis) and by a transient calcium overload (calcium hypothesis) on reperfusion. The final lesion responsible for the contractile depression appears to be a decreased responsiveness of contractile filaments to calcium. Recent evidence suggests that calcium overload may activate calpains, resulting in selective proteolysis of myofibrils; the time required for resynthesis of damaged proteins would explain in part the delayed recovery of function in stunned myocardium. The oxyradical and calcium hypotheses are not mutually exclusive and are likely to represent different facets of the same pathophysiological cascade. For example, increased free radical formation could cause cellular calcium overload, which would damage the contractile apparatus of the myocytes. Free radical generation could also directly alter contractile filaments in a manner that renders them less responsive to calcium (e.g., oxidation of critical thiol groups). However, it remains unknown whether oxyradicals play a role in all forms of stunning and whether the calcium hypothesis is applicable to stunning in vivo. Nevertheless, it is clear that the lesion responsible for myocardial stunning occurs, at least in part, after reperfusion so that this contractile dysfunction can be viewed, in part, as a form of “reperfusion injury.” An important implication of the phenomenon of myocardial stunning is that so-called chronic hibernation may in fact be the result of repetitive episodes of stunning, which have a cumulative effect and cause protracted postischemic dysfunction. A better understanding of myocardial stunning will expand our knowledge of the pathophysiology of myocardial ischemia and provide a rationale for developing new therapeutic strategies designed to prevent postischemic dysfunction in patients.

Spectrofluorescent detection of malonaldehyde as a measure of lipid free radical damage in response to ethanol potentiation of spinal cord trauma

Lipids ◽  
1977 ◽  
Vol 12 (11) ◽  
pp. 945-950 ◽  
Author(s):  
Myron L. Seligman ◽  
Eugene S. Flamm ◽  
Bernard D. Goldstein ◽  
Richard G. Poser ◽  
Harry B. Demopoulos ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Free Radical ◽  
Spinal Cord Trauma ◽  
Free Radical Damage ◽  
Radical Damage ◽  
Lipid Free Radical

scholarly journals Pelatihan pencegahan intoksikasi kadmium pada pekerja bengkel las di Kota Mataram

2021 ◽  
Vol 2 (2) ◽  
pp. 45-47
Author(s):  
Bayu Tirta Dirja ◽  
Devi Rahmadhona ◽  
Decky Aditya Zulkarnaen
Keyword(s):  
Heavy Metal ◽  
Free Radical ◽  
Human Health ◽  
Air Pollutants ◽  
Posttest Score ◽  
The Body ◽  
Cadmium Exposure ◽  
Pretest Score ◽  
The Impact ◽  
Lipid Free Radical

Cadmium (Cd) is a nephrotoxic heavy metal which endangers human health, especially welding workers. Cadmium can enter the body through inhalation of formed air pollutants. Cadmium would then bind with metallotionins, binds Cd+Mt, which would be deposited in the kidneys and induces the formation of lipid-free radical peroxidation that damages the kidneys, characterized by an increase of creatinine and β2 microglobulins. This service aims to educate welding workers about the impact of cadmium intoxication on the body and the prevention against cadmium exposure. The methods used are demonstration and playback of a video about prevention against cadmium exposure. This activity was carried out on May 6th, 2021 at the CV. Rigansa Mataram welding workshop. The activity was attended by ten participants. The results are an increase of knowledge from a mean pretest score of 50 to a mean posttest score of 90

Myocardial response to regional ischemia and reperfusion in vivo in rat heart

1993 ◽  
Vol 71 (10-11) ◽  
pp. 811-817 ◽  
Author(s):  
L. L. Ji ◽  
R. G. Fu ◽  
T. G. Waldrop ◽  
K. J. Liu ◽  
H. M. Swartz
Keyword(s):  
Free Radical ◽  
Degradation Products ◽  
Electron Paramagnetic Resonance Spectroscopy ◽  
Ischemia Reperfusion ◽  
High Energy ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Regional Ischemia ◽  
Nucleotide Degradation

Ischemia–reperfusion-induced myocardial oxidative changes were investigated in open-chest hearts of anesthetized rats. Surgical occlusion of the left anterior descending coronary artery for 30 min followed by 15 min reperfusion resulted in a significant decrease of reduced glutathione, an increase in glutathione disulfide, and an enhanced lipid peroxidation in rapidly frozen left ventricular tissues. Direct electron paramagnetic resonance spectroscopy revealed an increase in free radical concentration in ischemic cardiac tissues reperfused for 45 s, but the increase diminished at 15 min. These alterations were associated with decreased activities of myocardial glutathione peroxidase, glutathione reductase, and catalase. Ischemia resulted in a significant reduction of high-energy phosphate compounds and an accumulation of nucleotide degradation products, particularly adenosine, in the myocardium. Deterioration of cardiovascular function in reperfused animals was also evident. It is concluded that regional ischemia followed by reperfusion in situ can produce biochemical and physiological alterations consistent with free radical injury in rat hearts, and that an increased purine nucleotide degradation and a decreased antioxidant defense may be responsible for the observed changes.Key words: ischemia–reperfusion, myocardium, oxidative damage, glutathione, antioxidant enzyme.

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