Ischemic Injury

Photomed Laser Surg. 2005 Jun;23(3):273-7.

Protection of skeletal muscles from ischemic injury: low-level laser therapy increases antioxidant activity.

Avni D, Levkovitz S, Maltz L, Oron U.

Department of Zoology, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv, Israel.

Objective: The aim of this study was to investigate the effect of low-level laser therapy (LLLT) on ischemic-reperfusion (I-R) injury in the gastrocnemius muscle of the rat.

Background Data: Ischemic injury in skeletal muscle is initiated during hypoxia and is aggravated by reoxygenation during blood reperfusion and accumulation of cytotoxic reactive oxygen superoxides. LLLT has been found to biostimulate various biological processes, such as attenuation of ischemic injury in the heart.

Materials and Methods: The injury was induced in the gastrocnemius muscles of 106 rats by complete occlusion of the blood supply for 3 h, followed by reperfusion. Another group of intact rats served to investigate the effect of LLLT on intact nonischemic muscles. Creatine phosphokinase, acid phosphatase, and heat shock protein were determined 7 days after I-R injury and antioxidant levels 2 h after reperfusion.

Results: Laser irradiation (Ga-As, 810 nm) was applied to the muscles immediately and 1 h following blood supply occlusion. It was found that laser irradiation markedly protects skeletal muscles from degeneration following acute I-R injury. This was evident by significantly (p < 0.05) higher content of creatine phosphokinase activity and lower (p < 0.05) activity of acid phosphatase in the LLLT-treated muscles relative to the injured non-irradiated ones. The content of antioxidants and heat shock proteins was also higher (p < 0.05) in the LLLT-treated muscles relative to that of injured non-irradiated muscles.

Conclusion: The present study describes for the first time the ability of LLLT to significantly prevent degeneration following ischemia / reperfusion injury in skeletal muscles, probably by induction of synthesis of antioxidants and other cytoprotective proteins, such as hsp-70i. The elevation of antioxidants was also evident in intact muscle following LLLT. The above phenomenon may also be of clinical relevance in scheduled surgery or microsurgery requiring extended tourniquet applications to skeletal muscle followed by reperfusion.

Zhong Xi Yi Jie He Xue Bao. 2005 Mar;3(2):128-31.

Protective effect of low-level irradiation on acupuncture points combined with iontophoresis against focal cerebral ischemia-reperfusion injury in rats.

[Article in Chinese]

Dai JY, Ge LB, Zhou YL, Wang L.

Acupuncture Clinic, Institute of Qigong, Shanghai University of Traditional Chinese Medicine, Shanghai 200030, China. djysh2002@yahoo.com.cn

OBJECTIVE: To investigate the effects of low-level laser irradiation on acupuncture points combined with iontophoresis against brain damage after middle cerebral artery occlusion (MCAO) in rats.

METHODS: Sixty-nine SD rats were randomly divided into five groups, including normal group, sham operation group, model group, electro-acupuncture group and low-level laser irradiation on acupuncture points combined with iontophoresis group (LLLI group). The cerebral ischemia-reperfusion (I/R) model was established by thread embolism of middle cerebral artery. The rats in the LLLI group, as well as the electro-acupuncture group were given treatment as soon as the occlusion finished (0 hour) and 12, 24 hours after the occlusion. We observed the changes of neurological deficit scores and the body weight of the rats at different time. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the ratos brain tissue were tested.

RESULTS: The neurological deficit score of the LLLI group was significantly lower than that of the model group. The body weight and the activity of SOD of the rats decreased slightly, and the content of MDA decreased significantly after the treatment.

CONCLUSION: The low-level laser irradiation on acupuncture points combined with iontophoresis can prevent focal cerebral ischemia-reperfusion injury. One of its mechanisms may be increasing the activity of SOD and decreasing the damage of the oxidation products to the body.