Long-term effect of low energy laser irradiation on infarction and reperfusion injury in the rat heart.

Low-energy laser irradiation (LELI) has been found to modulate biological processes. The present study investigated the effect of LELI on infarct size after chronic myocardial infarction (MI) and ischemia-reperfusion injury in rats. The left anterior descending (LAD) coronary artery was ligated in 83 rats to create MI or ischemia-reperfusion injury. The hearts of the laser-irradiated (LI) rats received irradiation after LAD coronary artery occlusion and 3 days post-MI. At 14, 21, and 45 days post-LAD coronary artery permanent occlusion, infarct sizes (percentage of left ventricular volume) in the non-laser-irradiated (NLI) rats were 52 +/- 12 (SD), 47 +/- 11, and 34 +/- 7%, respectively, whereas in the LI rats they were significantly lower, being 20 +/- 8, 15 +/- 6, and 10 +/- 4%, respectively. Left ventricular dilatation (LVD) in the chronic infarcted rats was significantly reduced (50-60%) in LI compared with NLI rats. LVD in the ischemia-reperfusion-injured LI rats was significantly reduced to a value that did not differ from intact normal noninfarcted rats. Laser irradiation caused a significant 2.2-fold elevation in the content of inducible heat shock proteins (specifically HSP70i) and 3.1-fold elevation in newly formed blood vessels in the heart compared with NLI rats. It is concluded that LELI caused a profound reduction in infarct size and LVD in the rat heart after chronic MI and caused complete reduction of LVD in ischemic-reperfused heart. This phenomenon may be partially explained by the cardioprotective effect of the HSP70i and enhanced angiogenesis in the myocardium after laser irradiation.

Attenuation of infarct size in rats and dogs after myocardial infarction by low-energy laser irradiation.

BACKGROUND AND OBJECTIVE: The aim of the present study was to investigate the possibility that low-energy laser irradiation attenuates infarct size formation after induction of chronic myocardial infarction (MI) in small and large experimental animals. STUDY DESIGN/MATERIALS AND METHODS: Laser irradiation was applied to the infarcted area of rats and dogs at various power densities (2.5 to 20 mW/cm(2)) after occlusion of the coronary artery. RESULTS: In infarcted laser-irradiated rats that received laser irradiation immediately and 3 days after MI at energy densities of 2.5, 6, and 20 mW/cm(2), there was a 14%, 62% (significant; P < 0.05), and 2.8% reduction of infarct size (14 days after MI) relative to non--laser-irradiated rats, respectively. In dogs, a 49% (significant; P < 0.01) reduction of infarct size was achieved. CONCLUSION: The results of the present study indicate that delivery of low-energy laser irradiation to infarcted myocardium in rats and dogs has a profound effect on the infarct size after MI.

Low-energy laser irradiation reduces formation of scar tissue after myocardial infarction in rats and dogs.

BACKGROUND: Low-energy laser irradiation (LELI) has been found to attenuate various biological processes in tissue culture and experimental animal models. The aim of the present study was to investigate the effect of LELI on the formation of scar tissue in experimentally induced chronic infarct in rats and dogs. METHODS AND RESULTS: Myocardial infarction (MI) was induced in 50 dogs and 26 rats by ligation of the left anterior descending coronary artery. After induction of MI, the laser-irradiated (LI) group received laser irradiation (infrared laser, 803-nm wavelength) epicardially. Control MI-induced non-laser irradiated (NLI) dogs were sham-operated, and laser was not applied. All dogs were euthanized at 5 to 6 weeks after MI. Infarct size was determined by TTC staining and histology. The laser treatment (P:<0.05) lowered mortality significantly, from 30% to 6.5%, after induction of MI. The infarct size in the LI dogs was reduced significantly (P:<0.0001) (52%) compared with NLI dogs. Histological observation of the infarct revealed a typical scar tissue in NLI dogs and cellularity in most of the LI dogs. Only 14+/-3% of the mitochondria in the cardiomyocytes in the ischemic zone (4 hours after MI) of LI MI-induced rats were severely damaged, compared with 36+/-1% in NLI rats. Accordingly, ATP content in that zone was 7.6-fold (significantly) higher in LI than in NLI rats. CONCLUSIONS: Our observations indicate that epicardial LELI of rat and dog hearts after chronic MI caused a marked reduction in infarct size, probably due to a cardioprotective effect of the LELI.

Promotion of bone repair in the cortical bone of the tibia in rats by low energy laser (He-Ne) irradiation.

The effect of low energy laser (He-Ne) irradiation on bone repair in the cortical part of the tibia of the rat was investigated using biochemical and radioactive labeling methods. A fixed round hole was created in the lateral aspect of the tibia and the newly formed tissue was collected from the gap in the cortical bone. Alkaline phosphatase (ALP) and calcium progressively accumulated at the site of injury, peaking at 9 and 13 days postinjury, respectively. Direct irradiation of the hole injury with He-Ne laser on days 5 and 6 postinjury altered osteoblastic activity at the injured site as reflected by alkaline phosphatase activity. The laser irradiation also caused a significant increase ( approximately 2-fold) in calcium accumulation at the site of injury for 9-18 days postinjury. The rate of calcium deposition, measured by radioactive calcium, was significantly higher (approximately 2-fold) in the laser-irradiated rats as compared with controls. It is concluded that the process of bone repair in a hole created in the rat tibia is markedly enhanced by direct He-Ne laser irradiation of the injured site at the optimal energy level and time postinjury.

Effect of low-energy laser (He-Ne) irradiation on the process of bone repair in the rat tibia.

The effect of low-energy laser (He-Ne) irradiation on bone repair in the tibia of the rat after hole injury was investigated using biochemical and quantitative histomorphometrical methods. The activity of alkaline phosphatase (ALP) showed a sharp peak at 6 days post-injury and a lower peak at 12 days. The overall kinetics of tartrate-resistant acid phosphatase (TRAP) activity coincided with that of ALP but with the higher peak at 12 days postoperatively. Calcium accumulated progressively at the site of injury, peaking at 11 days and then declining. The histological evaluation revealed filling of the intramedullary canal with woven bone at the site of injury at 6 days after surgery, and progressive filling of the hole-injury gap in the cortical bone by membranous ossification. Direct irradiation of the hole injury with He-Ne laser at 5 and 6 days after injury altered the osteoblast and osteoclast cell populations, as reflected by the significant 2.2-fold increase in ALP enzymatic activity over control, nonirradiated rats at 10 days post-injury, and a significant decrease of 40% in TRAP activity at 11 days. Histomorphometrical analysis revealed a more rapid accumulation of reparative new bone in the hole injury of the laser-irradiated rats. The volume fraction (percent of total volume of the injured zone) of the new reparative compact bone was 27 +/- 9%, 88 +/- 9%, and 94 +/- 6% at 10, 13, and 15 days after injury, respectively, in the laser-irradiated rats; respective control values were 9 +/- 7%, 44 +/- 9%, and 58 +/- 5% for the same time intervals.(ABSTRACT TRUNCATED AT 250 WORDS)