| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 110 Francis St, Lowry Medical Office Bldg, Suite 2A, Boston, MA 02215
(Email: jfeng{at}caregroup.harvard.edu; fsellke{at}caregroup.harvard.edu).
The use of cardiopulmonary bypass (CPB) during cardiac surgery induces innate and adaptive pro-inflammatory responses [1, 2]. Numerous cytokines and chemokines are released and activated after CPB. Many procedures including off-pump surgery have been clinically used to suppress these pro-inflammatory consequences. Recent studies have reported that soluble heat shock protein (HSP) 70 is also significantly elevated in the blood after CPB [3, 4]. The present study of Szerafin and colleagues [5] extended these previous findings by measuring various molecular weights of soluble HSPs, such as HSP 27, 60, 70, and 90 alpha, in blood after on-pump and off-pump surgery [5]. In addition, they also tested soluble 20S immune-proteasome. They concluded that the innate immune system is activated due to spillage of known immunomodulatory and apoptosis-associated proteins.
Comparing serum HSP levels after on-pump with those after off-pump surgery is a very interesting clinical investigation. This original study provides novel insights into the possible role of these stress proteins in activating inflammation and the innate immune system after CPB. Many experimental and clinical studies suggest that upregulation of intracellular HSPs may have potential protective or anti-apoptotic effects [6]. In contrast, extracellular HSPs may indicate cell death, such as necrosis and apoptosis [3]. The results of this study are compatible with the suggestion that extracellular HSPs and 20S immune-proteasome may be potential "risk factors" during CPB related trauma.
However, the present study did not investigate the sources of these soluble HSPs. The circulating HSPs may derived not only from damaged tissues and cells of various organs stressed by hypothermia, cardioplegia, ischemia and reperfusion, surgical trauma, and tissue stretch, but also from blood cells damaged when circulating through polyethylene tubing, blood suction, and the heart-lung machine. In addition, the authors did not explain why only soluble HSP60 remained unchanged after on-pump and off-pump surgery. One possible explanation is the existence of HSP60 antibody in circulating blood [3]. Furthermore, in comparison with a previous study [4], the present data failed to show the correlations between spilled HSPs or 20 proteasome and secretion of the pro-inflammatory cytokine interleukin-6 after on-pump surgery. These discrepancies may be due to different blood sampling times, such as 3 to 6 hours versus 24 hours after CPB. In addition, the investigators did not measure these HSP levels of local tissues or cells. Finally, it still remains uncertain if the outcomes after on-pump or off-pump CABG are different to any clinically significant degree for the vast majority of patients. Therefore, more bench and clinical work needs to be done before drawing the conclusion that circulating soluble HSPs are the pro-inflammatory markers during CPB and cardiac surgery.
 |
References |
|---|
 Top References |
|---|
, and 20S proteasome in on-pump versus off-pump coronary artery bypass graft patients Ann Thorac Surg 2008;85:80-88.Related Article
, and 20S Proteasome in On-Pump Versus Off-Pump Coronary Artery Bypass Graft Patients
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
