Exercise training improves metabolic response after ischemia in isolated working rat heart

1994 ◽  
Vol 76 (4) ◽  
pp. 1608-1614 ◽  
Author(s):  
D. K. Bowles ◽  
J. W. Starnes
Keyword(s):  
Metabolic Response ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Sedentary Control ◽  
Free Radical Production ◽  
Radical Production ◽  
Diastolic Stiffness ◽  
Working Heart ◽  
Retrograde Reperfusion ◽  
Working Rat Heart

Hearts from treadmill-trained and sedentary rats were perfused in the working heart mode. Mechanical and metabolite status was evaluated before ischemia, after 25 min of global ischemia, and after 30 min of retrograde reperfusion. After reperfusion, hearts from trained rats were found to have better recovery of contractile function, lower diastolic stiffness, greater efficiency of work, and greater extracellular calcium responsiveness than hearts from sedentary rats. Training had no significant impact on bioenergetic status before or at the end of ischemia. However, after reperfusion, both phosphocreatine and ATP were significantly higher in hearts from trained rats than from sedentary control rats. Mitochondrial function in both subsarcolemmal and intermyofibrillar subpopulations was unaffected by ischemia-reperfusion. 45Ca2+ uptake during reperfusion was significantly higher in hearts from sedentary rats than from exercise-trained rats. No differences were found in free radical production or tolerance due to training. Therefore, hearts from exercise-trained rats demonstrated an increased metabolic tolerance to ischemic-reperfusion damage, which may contribute to the improved postischemic functional recovery.

Glucose-6-phosphate dehydrogenase deficiency and cardiac surgery

Perfusion ◽  
2010 ◽  
Vol 25 (6) ◽  
pp. 417-421 ◽  
Author(s):  
N. Dogra ◽  
GD Puri ◽  
SS Rana
Keyword(s):  
Cardiac Surgery ◽  
Blood Cells ◽  
Perioperative Management ◽  
Dehydrogenase Deficiency ◽  
Ischemia Reperfusion ◽  
Anaesthetic Management ◽  
Whole Body ◽  
Free Radical Production ◽  
Radical Production ◽  
Glucose 6 Phosphate Dehydrogenase

Cardiac surgery involving cardiopulmonary bypass (CPB) in its conventional form involves many processes leading to free radical production, such as perioperative ischemia, reperfusion, circulation of whole body blood through the CPB circuit, hypothermia and acidosis. The red blood cells of a glucose-6-phosphate dehydrogenase (G6PD)-deficient person are unable to scavenge these free radicals, resulting in haemolysis. Here, we describe the successful anaesthetic management of two G6PD-deficient children who underwent cardiac surgery, on and off CPB, without any obvious haemolytic reaction, followed by a discussion of the disorder, with specific consideration of perioperative management of such cases.

Glibenclamide improves postischemic recovery of myocardial contractile function in trained and sedentary rats

2001 ◽  
Vol 91 (4) ◽  
pp. 1545-1554 ◽  
Author(s):  
Korinne N. Jew ◽  
Russell L. Moore
Keyword(s):  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Diastolic Stiffness ◽  
Pressure Development ◽  
Increased Sensitivity ◽  
Developed Pressure

In this study, we sought to determine whether there was any evidence for the idea that cardiac ATP-sensitive K+ (KATP) channels play a role in the training-induced increase in the resistance of the heart to ischemia-reperfusion (I/R) injury. To do so, the effects of training and an KATP channel blocker, glibenclamide (Glib), on the recovery of left ventricular (LV) contractile function after 45 min of ischemia and 45 min of reperfusion were examined. Female Sprague-Dawley rats were sedentary (Sed; n = 18) or were trained (Tr; n = 17) for >20 wk by treadmill running, and the hearts from these animals used in a Langendorff-perfused isovolumic LV preparation to assess contractile function. A significant increase in the amount of 72-kDa class of heat shock protein was observed in hearts isolated from Tr rats. The I/R protocol elicited significant and substantial decrements in LV developed pressure (LVDP), minimum pressure (MP), rate of pressure development, and rate of pressure decline and elevations in myocardial Ca2+ content in both Sed and Tr hearts. In addition, I/R elicited a significant increase in LV diastolic stiffness in Sed, but not Tr, hearts. When administered in the perfusate, Glib (1 μM) elicited a normalization of all indexes of LV contractile function and reductions in myocardial Ca2+content in both Sed and Tr hearts. Training increased the functional sensitivity of the heart to Glib because LVDP and MP values normalized more quickly with Glib treatment in the Tr than the Sed group. The increased sensitivity of Tr hearts to Glib is a novel finding that may implicate a role for cardiac KATP channels in the training-induced protection of the heart from I/R injury.

scholarly journals Blocking Free Radical Production via Adenoviral Gene Transfer Decreases Cardiac Ischemia–Reperfusion Injury

2000 ◽  
Vol 2 (5) ◽  
pp. 470-475 ◽  
Author(s):  
Henry L. Zhu ◽  
Allan S. Stewart ◽  
Matthew D. Taylor ◽  
C. Vijayasarathy ◽  
Timothy J. Gardner ◽  
...  
Keyword(s):  
Free Radical ◽  
Gene Transfer ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Free Radical Production ◽  
Adenoviral Gene Transfer ◽  
Radical Production

Loss of exercise-induced cardioprotection after cessation of exercise

2004 ◽  
Vol 96 (4) ◽  
pp. 1299-1305 ◽  
Author(s):  
Shannon L. Lennon ◽  
John Quindry ◽  
Karyn L. Hamilton ◽  
Joel French ◽  
Jessica Staib ◽  
...  
Keyword(s):  
Myocardial Stunning ◽  
Time Course ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Antioxidant Enzyme Activity ◽  
Male Rats ◽  
Sedentary Control ◽  
Cardiac Work ◽  
Exercise Induced ◽  
Working Heart

Endurance exercise provides cardioprotection against ischemia-reperfusion (I/R) injury. Exercise-induced cardioprotection is associated with increases in cytoprotective proteins, including heat shock protein 72 (HSP72) and increases in antioxidant enzyme activity. On the basis of the reported half-life of these putative cardioprotective proteins, we hypothesized that exercise-induced cardioprotection against I/R injury would be lost within days after cessation of exercise. To test this, male rats (4 mo) were randomly assigned to one of five experimental groups: 1) sedentary control, 2) exercise followed by 1 day of rest, 3) exercise followed by 3 days of rest, 4) exercise followed by 9 days of rest, and 5) exercise followed by 18 days of rest. Exercise-induced increases ( P < 0.05) in left ventricular catalase activity and HSP72 were evident at 1 and 3 days postexercise. However, at 9 days postexercise, myocardial HSP72 and catalase levels declined to sedentary control values. To evaluate cardioprotection during recovery from I/R, hearts were isolated, placed in working heart mode, and subjected to 20.5 min of global ischemia followed by 30 min of reperfusion. Compared with sedentary controls, exercised animals sustained less I/R injury as evidenced by maintenance of a higher ( P < 0.05) percentage of preischemia cardiac work during reperfusion at 1, 3, and 9 days postexercise. The exercise-induced cardioprotection vanished by 18 days after exercise cessation. On the basis of the time course of the loss of cardioprotection and the return of HSP72 and catalase to preexercise levels, we conclude that HSP72 and catalase are not essential for exercise-induced protection during myocardial stunning. Therefore, other cytoprotective molecules are responsible for providing protection during I/R.

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