UNLABELLED: Abstract Objective: Myocardial reperfusion injury can induce further cardiomyocyte death and contribute to adverse cardiovascular outcomes after myocardial ischemia, cardiac surgery, or circulatory arrest. Exposure to near-infrared (NIR) light at the time of reoxygenation protects neonatal rat cardiomyocytes and HL-1 cells from injury. We hypothesized that application of NIR at 670 nm would protect the heart against ischemia-reperfusion injury. METHODS: We assessed the protective role of NIR in in vivo and in vitro rat models of ischemia-reperfusion injury. RESULTS: NIR application had no effect on the function of the nonischemic isolated heart, and had no effect on infarct size when applied during global ischemia. In the in vivo model, NIR commencing immediately before reperfusion decreased infarct size by 40%, 33%, 38%, and 77%, respectively, after regional ischemic periods of 30, 20, 15, and 10 min. Serum cardiac troponin I (cTnI) was significantly reduced in the 15 min group, whereas creatine kinase (CK) and lactate dehydrogenase (LDH) levels were not affected. CONCLUSIONS: We have demonstrated the safety of NIR application in an in vitro rat isolated model. In addition, we have demonstrated safety and efficacy when using NIR for cardioprotection in an in vivo rat ischemia model, and that this cardioprotection is dependent upon some factor present in blood, but not in perfusion buffer. RESULTS show potential for cTnI, but not CK or LDH, as a biomarker for cardioprotection by NIR. NIR may have therapeutic utility in providing myocardial protection from ischemia-reperfusion injury.
UNLABELLED: Abstract Objective: Myocardial reperfusion injury can induce further cardiomyocyte death and contribute to adverse cardiovascular outcomes after myocardial ischemia, cardiac surgery, or circulatory arrest. Exposure to near-infrared (NIR) light at the time of reoxygenation protects neonatal rat cardiomyocytes and HL-1 cells from injury. We hypothesized that application of NIR at 670 nm would protect the heart against ischemia-reperfusion injury. METHODS: We assessed the protective role of NIR in in vivo and in vitro rat models of ischemia-reperfusion injury. RESULTS: NIR application had no effect on the function of the nonischemic isolated heart, and had no effect on infarct size when applied during global ischemia. In the in vivo model, NIR commencing immediately before reperfusion decreased infarct size by 40%, 33%, 38%, and 77%, respectively, after regional ischemic periods of 30, 20, 15, and 10 min. Serum cardiac troponin I (cTnI) was significantly reduced in the 15 min group, whereas creatine kinase (CK) and lactate dehydrogenase (LDH) levels were not affected. CONCLUSIONS: We have demonstrated the safety of NIR application in an in vitro rat isolated model. In addition, we have demonstrated safety and efficacy when using NIR for cardioprotection in an in vivo ratischemia model, and that this cardioprotection is dependent upon some factor present in blood, but not in perfusion buffer. RESULTS show potential for cTnI, but not CK or LDH, as a biomarker for cardioprotection by NIR. NIR may have therapeutic utility in providing myocardial protection from ischemia-reperfusion injury.
Authors: U Oron; T Yaakobi; A Oron; D Mordechovitz; R Shofti; G Hayam; U Dror; L Gepstein; T Wolf; C Haudenschild; S B Haim Journal: Circulation Date: 2001-01-16 Impact factor: 29.690
Authors: E M Antman; M J Tanasijevic; B Thompson; M Schactman; C H McCabe; C P Cannon; G A Fischer; A Y Fung; C Thompson; D Wybenga; E Braunwald Journal: N Engl J Med Date: 1996-10-31 Impact factor: 91.245
Authors: Jennifer L Strande; Michael E Widlansky; Nikos E Tsopanoglou; Jidong Su; JingLi Wang; Anna Hsu; Kasi V Routhu; John E Baker Journal: Cardiovasc Res Date: 2009-04-20 Impact factor: 10.787