Endothelial dysfunction in myocardial ischemia and reperfusion: role of oxygen-derived free radicals

1991 ◽  
pp. 109-116 ◽  
Author(s):  
Allan M. Lefer ◽  
D. J. Lefer
Keyword(s):  
Free Radicals ◽  
Endothelial Dysfunction ◽  
Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion ◽  
Oxygen Derived Free Radicals

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.

Renal sympathetic nerve activity during cardiac ischemia and reperfusion in rats

1996 ◽  
Vol 271 (4) ◽  
pp. R1033-R1040 ◽  
Author(s):  
E. E. Ustinova ◽  
H. D. Schultz
Keyword(s):  
Free Radicals ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ischemia And Reperfusion ◽  
Nerve Activity ◽  
Myocardial Ischemia And Reperfusion ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Oxygen Derived Free Radicals ◽  
Renal Sympathetic

We studied the role played by prostaglandins and oxygen-derived free radicals in mediating reflex changes in renal sympathetic nerve activity (RSNA) during myocardial ischemia and reperfusion. Ligation of the left coronary artery for 20 min and reperfusion for 10 min were performed in anesthetized rats with sinoaortic denervation and with intact cardiac afferent nerves (control, n = 7), with cardiac sympathetic denervation (SD, n = 6), with vagal denervation (VD, n = 7), and with combined SD + VD (n = 6). In control rats, RSNA decreased by 10 +/- 3% from baseline (P < 0.05) during the first minute of ischemia and increased above baseline after 5 min of ischemia, with the maximum increase at the first minute of reperfusion. In rats with SD, RSNA decreased by 19 +/- 4% from baseline (P < 0.05) at the first minute of ischemia and remained depressed during the entire ischemic and reperfusion periods. In rats with VD, RSNA increased by 26 +/- 5% from baseline (P < 0.05) at the first minute of ischemia, and the increase in RSNA at the end of the ischemic period and at reperfusion was greater than in control rats. No changes in RSNA during ischemia and reperfusion were observed with combined SD + VD. Reflex changes in RSNA that occurred at the onset of ischemia in both VD (n = 7) and SD (n = 7) rats were abolished by indomethacin (5 mg/kg i.v., 20 min before ischemia). Reflex changes in RSNA after prolonged ischemia (> 10 min) and during reperfusion in both VD (n = 7) and SD (n = 7) rats were abolished by the antioxidant deferoxamine (20 mg/kg i.v., 20 min before ischemia). Deferoxamine also diminished the increase of RSNA at the onset of ischemia in VD rats. Thus, in rats, the vagal afferent reflex predominates during early ischemia and the sympathetic afferent reflex predominates during prolonged ischemia and reperfusion. Reflex changes in RSNA that occur at the onset of ischemia are mediated by activation of vagal and sympathetic afferent endings by prostaglandins. Reflex changes in RSNA after prolonged ischemia and during reperfusion are mediated by activation of vagal and sympathetic afferent endings by oxygen-derived free radicals.

Sign in / Sign up

Export Citation Format

Share Document