[HTML][HTML] Tumor necrosis factor-alpha is released from the isolated heart undergoing ischemia and reperfusion
J Gurevitch, I Frolkis, Y Yuhas, Y Paz, M Matsa… - Journal of the American …, 1996 - Elsevier
J Gurevitch, I Frolkis, Y Yuhas, Y Paz, M Matsa, R Mohr, V Yakirevich
Journal of the American College of Cardiology, 1996•ElsevierObjectives. The purpose of this study was to examine whether tumor necrosis factor-alpha
(TNF-alpha) is released directly from the ischemic myocardium undergoing reperfusion.
Background. Tumor necrosis factor-alpha is a protein hormone produced by systemic
leukocytes (primarily by activated macrophages). It has been implicated as a systemic
mediator in the development of septic shock and other pathologic conditions. Serum TNF-
alpha has also been detected in a variety of cardiac disease states and after myocardial …
(TNF-alpha) is released directly from the ischemic myocardium undergoing reperfusion.
Background. Tumor necrosis factor-alpha is a protein hormone produced by systemic
leukocytes (primarily by activated macrophages). It has been implicated as a systemic
mediator in the development of septic shock and other pathologic conditions. Serum TNF-
alpha has also been detected in a variety of cardiac disease states and after myocardial …
Objectives
The purpose of this study was to examine whether tumor necrosis factor-alpha (TNF-alpha) is released directly from the ischemic myocardium undergoing reperfusion.
Background
Tumor necrosis factor-alpha is a protein hormone produced by systemic leukocytes (primarily by activated macrophages). It has been implicated as a systemic mediator in the development of septic shock and other pathologic conditions. Serum TNF-alpha has also been detected in a variety of cardiac disease states and after myocardial ischemia-reperfusion injury.
Methods
Nine isolated rat hearts undergoing 30 min of perfusion, followed by warm cardioplegic arrest, 1 h of global ischemia and 30 min of reperfusion, were investigated using the modified Langendorff model.
Results
Significant amounts of TNF-alpha (752 ± 212 pmol/ml) were detected in the effluent during the first minute of reperfusion. Tumor necrosis factor-alpha levels correlated with postischemic deterioration in peak systolic pressures (r = 0.7882, p = 0.012), dP/dt max (r = 0.6795, p = 0.044), time-pressure integral (r = 0.7661, p = 0.0016) and postischemic creatine kinase levels (r = 0.8367, p = 0.005). The deterioration in coronary flow, however, was inversely correlated with TNF-alpha levels (r = −0.7581, p = 0.018).
Conclusions
To our knowledge, this study is the first to suggest that the isolated rat myocardium synthesizes and releases TNF-alpha in response to ischemia and reperfusion, which directly correlates with the postischemic deterioration in myocardial mechanical performance and the amount of cellular necrosis.
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