Ischemic preconditioning: nearly two decades of research. A comprehensive review

Eisen, Alon; Fisman, Enrique Z.; Rubenfire, Melvyn; Freimark, Dov; McKechnie, Ronald; Tenenbaum, Alexander; Motro, Michael; Adler, Yehuda

doi:10.1016/s0021-9150(03)00238-7

Cited by 136 publications

(109 citation statements)

References 146 publications

Supporting

Mentioning

100

Contrasting

Unclassified

Order By: Relevance

“…Preconditioning refers to a mildly injurious event that confers protection against a later, more injurious, event (Gidday 2006;Dirnagl et al 2003;Eisen et al 2004;Ran et al 2005). Demonstrated preconditioning inducers against NIPTS in mice include mild noise, heat stress, restraint, and hypoxia (Yoshida et al 1999;Wang and Liberman 2002;Yoshida and Liberman 2000;Niu and Canlon 2002;Gagnon et al 2007).…”

Section: Sub-chronic Kanamycin As a Form Of Preconditioningmentioning

confidence: 99%

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

Fernandez

Ohlemiller

Gagnon

et al. 2010

JARO

View full text Add to dashboard Cite

Animal studies indicate that a combination of kanamycin (KM) and noise produces a synergistic effect, whereby the threshold shift from the combination is greater than the sum of the shifts caused by either agent alone. Most such studies have focused on adult animals, and it has remained unclear whether younger, presumably more susceptible, animals show an even greater synergistic effect. The present study tested the hypothesis that young CBA/J mice receiving a low dose of KM (300 mg/kg, 2×/day, s.c.) from 20 to 30 days post-gestational age followed by brief noise exposure (110 dB SPL; 4-45 kHz, 30 s) would show greater noise-induced permanent threshold shifts (NIPTS) than mice receiving either treatment alone. Noise exposure produced 30-40 dB of NIPTS and moderate hair cell loss in young saline-treated mice. KM alone at this dose had no effect on thresholds. Surprisingly, mice receiving KM plus noise were protected from NIPTS, showing ABR thresholds not significantly different from unexposed controls. Mice receiving KM prior to noise exposure also showed significantly less outer hair cell loss than saline-treated mice. Additional experiments indicated protection by KM when the noise was applied either 24 or 48 h after the last KM injection. Our results demonstrate a powerful protective effect of subchronic low-dose kanamycin against NIPTS in young CBA/J mice. Repeated kanamycin exposure may establish a preconditioned protective state, the molecular bases of which remain to be determined.

show abstract

Section: Sub-chronic Kanamycin As a Form Of Preconditioningmentioning

confidence: 99%

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

Fernandez

Ohlemiller

Gagnon

et al. 2010

JARO

View full text Add to dashboard Cite

show abstract

“…As well as HSPs, it may be that other mediators of delayed ischemic preconditioning may occur in the myocardium, and these will be the focus of future investigation. These may include investigation of antioxidant enzymes such as superoxide dismustase, nitric oxide synthase and cyclooxygenase (Eisen et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Heat shock protein 27 is increased in cyanotic tetralogy of Fallot myocardium and is associated with improved cardiac output and contraction

Walker¹,

Danton

Peng

et al. 2013

Cell Stress and Chaperones

View full text Add to dashboard Cite

Tetralogy of Fallot (TOF) is a congenital heart condition in which the right ventricle is exposed to cyanosis and pressure overload. Patients have an increased risk of right ventricle dysfunction following corrective surgery. Whether the cyanotic myocardium is less tolerant of injury compared to non-cyanotic is unclear. Heat shock proteins (HSPs) protect against cellular stresses. The aim of this study was to examine HSP 27 expression in the right ventricle resected from TOF patients and determine its relationship with right ventricle function and clinical outcome. Ten cyanotic and ten noncyanotic patients were studied. Western blotting was used to quantify HSP 27 in resected myocardium at (1) baseline (first 15 min of aortic cross clamp and closest representation of preoperative status) and (2) after 15 min during ischemia until surgery was complete. The cyanotic group had significantly increased haematocrit, lower O 2 saturation, thicker interventricular septal wall thickness and released more troponin-I on post-operative day 1 (p<0.05). HSP 27 expression was significantly increased in the <15 min cyanotic compared to the <15 min non-cyanotic group (p00.03). In the cyanotic group, baseline HSP 27 expression also significantly correlated with oxygen extraction ratio (p00.028), post-operative basal septal velocity (p00.036) and mixed venous oxygen saturation (p00.02), markers of improved cardiac output/contraction. Increased HSP 27 expression and associated improved right ventricle function and systemic perfusion supports a cardioprotective effect of HSP 27 in cyanotic TOF.

show abstract

“…Perhaps one of the most discussed mechanisms concerning diabetes and cardiovascular disease is ischemic preconditioning. 12 This refers to a phenomenon by which one or more brief episodes of myocardial ischemia increase the ability of the heart to tolerate a subsequent prolonged period of ischemic injury. Although ischemic preconditioning has been shown to occur in both animal models and humans, the protection has been characterized by various end points of cellular injury.…”

Section: Mechanismsmentioning

confidence: 99%

How to Best Manage Glycemia and Non-Glycemia During the Time of Acute Myocardial Infarction

Hirsch

O’Brien

2012

Diabetes Technology & Therapeutics

View full text Add to dashboard Cite

Acute myocardial infarction (AMI) is common in patients with diabetes. Reasons for this are multifactorial, but all relate to a variety of maladaptive responses to acute hyperglycemia. Persistent hyperglycemia is associated with worse left ventricular function and higher mortality during AMI, but intervention data are far from clear. Although there is a theoretical basis for the use of glucose-insulin-potassium infusion during AMI, lack of outcome efficacy (and inability to reach glycemic targets) in recent randomized trials has resulted in little enthusiasm for this strategy. Based on the increasing understanding of the dangers of hypoglycemia, while at the same time appreciating the role of hyperglycemia in AMI patients, goal glucose levels of 140-180 mg/dL using an intravenous insulin infusion while not eating seem reasonable for most patients and hospital systems. Non-glycemic therapy for patients with diabetes and AMI has benefited from more conclusive data, as this population has greater morbidity and mortality than those without diabetes. For ST-elevation myocardial infarction (STEMI), reperfusion therapy with primary percutaneous coronary intervention or fibrinolysis, antithrombotic therapy to prevent acute stent thrombosis following percutaneous coronary intervention or rethrombosis following thrombolysis, and initiation of b-blocker therapy are the current standard of care. Emergency coronary artery bypass graft surgery is reserved for the most critically ill. For those with non-STEMI, initial reperfusion therapy or fibrinolysis is not routinely indicated. Overall, there have been dramatic advances for the treatment of people with AMI and diabetes. The use of continuous glucose monitoring in this population may allow better ability to safely reach glycemic targets, which it is hoped will improve glycemic control.

show abstract

Ischemic preconditioning: nearly two decades of research. A comprehensive review

Cited by 136 publications

References 146 publications

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

Heat shock protein 27 is increased in cyanotic tetralogy of Fallot myocardium and is associated with improved cardiac output and contraction

How to Best Manage Glycemia and Non-Glycemia During the Time of Acute Myocardial Infarction

Contact Info

Product

Resources

About