Author + information
- Received November 20, 1995
- Revision received February 23, 1996
- Accepted March 4, 1996
- Published online July 1, 1996.
- Jacob Gurevitch, MD1,∗,
- Inna Frolkis, MD, PhD1,
- Yael Yuhas, PhD∗,
- Yosi Paz, MD1,
- Menachem Matsa, MD1,
- Rephael Mohr, MD1 and
- Vladimir Yakirevich, MD1
- ↵∗Address for correspondence: Dr. Jacob Gurevitch, Department of Thoracic and Cardiovascular Surgery, Ichilov Hospital, 6 Weizman Street, Tel-Aviv 64239, Israel.
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.
☆ This study was supported by the Research Fund of the Department of Thoracic and Cardiovascular Surgery, Elias Souraski-Tel-Aviv Medical Center.
- Received November 20, 1995.
- Revision received February 23, 1996.
- Accepted March 4, 1996.