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 nearinfrared (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 ischemiareperfusion 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.
A 32-month-old boy, born at term, presented with progressive developmental regression from 14 months of age. On examination, he had horizontal nystagmus, diminished gag reflex, hypertonicity, and depressed reflexes. Brain MRI revealed symmetric T2/fluid-attenuated inversion recovery confluent hyperintensities in the periventricular white matter, corpus callosum, and centrum semiovale (sparing subcortical U fibers) with enhancement of multiple cranial nerves (figure). The characteristic leopard-like appearance of the hyperintensities prompted further evaluation for metachromatic leukodystrophy (MLD). 1,2 Arylsulfatase A enzyme activity was found to be low, and the patient had a homozygous pathogenic variant in the ARSA gene (c.465+1G), confirming MLD. Study funding No targeted funding reported.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.