On-pump versus off-pump coronary artery bypass grafting: more heat-shock protein 70 is released after on-pump surgery

Dybdahl, Brit; Wahba, Alexander; Haaverstad, Rune; Kirkeby‐Garstad, Idar; Kierulf, Peter; Espevik, Terje; Sundan, Anders

doi:10.1016/j.ejcts.2004.03.002

Cited by 68 publications

(48 citation statements)

References 27 publications

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“…In a study by Pittet and colleagues a significant upregulation in circulating serum Hsp72 can be measured in severely traumatized patients as early as 30 minutes after injury [10]. Increased circulating serum Hsp72 has also been measured in patients after coronary artery bypass grafting [11,12]. Importantly, circulating serum Hsp72 has been suggested as a marker of myocardial damage, and reported to have a role in the inflammatory response after acute myocardial infarction (AMI) [13].…”

Section: Mechanisms Of Hsp Release: Passive Release Hypothesismentioning

confidence: 99%

Initiation of the Immune Response by Extracellular Hsp72: Chaperokine Activity of Hsp72

Asea

2006

CIR

142

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Heat shock proteins exert their beneficial effects via basically two modes of action depending on their relative location within the host. Intracellular heat shock proteins found within cells serve a cytoprotective role by chaperoning naïve, misfolded and/or denatured proteins in response to stressful stimuli by a process known as the stress response. However, stressful stimuli also induce the release of intracellular heat shock proteins into the extracellular milieu and circulation. The extracellular heat shock protein proteins serve a cytostimulatory role by initiating immune responses designed to fend off microbial infection and destroy neoplastic transformed cells. This review will briefly cover recent advances into elucidating the mechanism(s) by which stress induces the release of heat shock proteins into the circulation, how it initiates immune responses and suggest the possible biological significance of circulating Hsp to the host.

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Section: Mechanisms Of Hsp Release: Passive Release Hypothesismentioning

confidence: 99%

Initiation of the Immune Response by Extracellular Hsp72: Chaperokine Activity of Hsp72

Asea

2006

CIR

142

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“…Extracellular Hsp70 (increased serum levels) is evident in a variety of clinical scenarios associated with physiologic stress. For example, increased extracellular Hsp70 levels are noted following strenuous exercise (180,181,(204)(205)(206)(207)(208), following cardio-pulmonary bypass in both adults (209,210) and children (Wheeler, unpublished data), in elderly adults (211,212), and in children with acute lung injury (Wheeler, unpublished data). In addition, increased extracellular Hsp70 concentrations correlate with worse outcome in a variety of inflammatory disease processes, including liver disease (213), coronary artery disease (214)(215)(216)(217), traumatic brain injury secondary to child abuse (218), pre-eclampsia (219), sickle cell disease vasoocclusive crisis (220), septic shock (221), and traumatic brain injury (222).…”

Section: Stress Proteins and Innate Immunitymentioning

confidence: 99%

Heat shock response and acute lung injury☆

Wheeler

Wong

2007

Free Radical Biology and Medicine

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All cells respond to stress through the activation of primitive, evolutionarily conserved genetic programs that maintain homeostasis and assure cell survival. Stress adaptation, which is known in the literature by a myriad of terms, including tolerance, desensitization, conditioning, and reprogramming, is a common paradigm found throughout nature, in which a primary exposure of a cell or organism to a stressful stimulus (e.g., heat) results in an adaptive response by which a second exposure to the same stimulus produces a minimal response. More interesting is the phenomenon of cross-tolerance, by which a primary exposure to a stressful stimulus results in an adaptive response whereby the cell or organism is resistant to a subsequent stress that is different from the initial stress (i.e. exposure to heat stress leading to resistance to oxidant stress). The heat shock response is one of the more commonly described examples of stress adaptation and is characterized by the rapid expression of a unique group of proteins collectively known as heat shock proteins (also commonly referred to as stress proteins). The expression of heat shock proteins is well described in both whole lungs and in specific lung cells from a variety of species and in response to a variety of stressors. More importantly, in vitro data, as well as data from various animal models of acute lung injury, demonstrate that heat shock proteins, especially Hsp27, Hsp32, Hsp60, and Hsp70 have an important cytoprotective role during lung inflammation and injury.

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“…These relatively small studies must be interpreted in the context of the The Coronary Artery Bypass Grafting Surgery Off-or On-pump Revascularisation Study trial, which randomized 4752 patients to on-versus off-pump coronary artery bypass graft and showed no difference in survival or any other meaningful clinical outcome, including new renal failure requiring dialysis (133). It is difficult to explain the failure of OPCAB to reduce AKI rates, especially given the clear effect of cardiopulmonary bypass on inducing inflammatory markers (134,135). One hypothesis is that the increased hemodynamic instability that occurs with OPCAB (132) negates the benefits of avoiding cardiopulmonary bypass.…”

Section: Cardiopulmonary Bypassmentioning

confidence: 99%

AKI Associated with Cardiac Surgery

Thiele¹,

Isbell²,

Rosner

2015

Clinical Journal of the American Society of Nephrology

254

198

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Approximately 18% of patients undergoing cardiac surgery experience AKI (on the basis of modern standardized definitions of AKI), and approximately 2%-6% will require hemodialysis. The development of AKI after cardiac surgery portends poor short-and long-term prognoses, with those developing RIFLE failure or AKI Network stage III having an almost 2-fold increase in the risk of death. AKI is caused by a variety of factors, including nephrotoxins, hypoxia, mechanical trauma, inflammation, cardiopulmonary bypass, and hemodynamic instability, and it may be affected by the clinician's choice of fluids and vasoactive agents as well as the transfusion strategy used. The risk of AKI may be ameliorated by avoidance of nephrotoxins, achievement of adequate glucose control preoperatively, and use of goal-directed therapy hemodynamic strategies. Remote ischemic preconditioning is an exciting future strategy, but more work is needed before widespread implementation. Unfortunately, there are no pharmacologic agents known to reduce the risk of AKI or treat established AKI.

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On-pump versus off-pump coronary artery bypass grafting: more heat-shock protein 70 is released after on-pump surgery

Abstract: Significantly more HSP70 was released into the circulation following conventional than following off-pump CABG. Circulating HSP70 may indicate cellular stress or damage. Furthermore, HSPs are suggested as immunoregulatory agents, and may be important in the host defence postoperatively.

Cited by 68 publications

References 27 publications

Initiation of the Immune Response by Extracellular Hsp72: Chaperokine Activity of Hsp72

Initiation of the Immune Response by Extracellular Hsp72: Chaperokine Activity of Hsp72

Heat shock response and acute lung injury☆

AKI Associated with Cardiac Surgery

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