Protective effects of photobiomodulation against resistance exercise-induced muscle damage and inflammation in rats.

We investigated whether low-level laser therapy (LLLT) prior to or post resistance exercise could attenuate muscle damage and inflammation. Female Wistar rats were assigned to non-LLLT or LLLT groups. An 830-nm DMC Laser Photon III was used to irradiate their hind legs with 2J, 4J, and 8J doses. Irradiations were performed prior to or post (4J) resistance exercise bouts. Resistance exercise consisted of four maximum load climbs. The load work during a resistance exercise bout was similar between Control (non-LLLT, 225 ± 10 g), 2J (215 ± 8 g), 4J (210 ± 9 g), and 8J (226 ± 9 g) groups. Prior LLLT did not induce climbing performance improvement, but exposure to 4J irradiation resulted in lower blood lactate levels post-exercise. The 4J dose decreased creatine kinase and lactic dehydrogenase levels post-exercise regardless of the time of application. Moreover, 4-J irradiation exposure significantly attenuated tumor necrosis factor alpha, interleukin-6, interleukin-1ß, cytokine-induced neutrophil chemoattractant-1, and monocyte chemoattractant protein-1. There was minor macrophage muscle infiltration in 4J-exposed rats. These data indicate that LLLT prior to or post resistance exercise can reduce muscle damage and inflammation, resulting in muscle recovery improvement. We attempted to determine an ideal LLLT dose for suitable results, wherein 4J irradiation exposure showed a significant protective role.

Examining the impact of varying low-level laser dose on cardiac failure.

Low-level laser therapy (LLLT) has been targeted as a promising tool that can mitigate post-infarction cardiac remodeling. However, there is no gold standard energy delivered to the heart and few studies have evaluated the impact of LLLT on cardiac performance. This study evaluated effects of repeated LLLT applications with different energies delivered to the infarcted myocardium. Echocardiography and hemodynamic measurements were applied to evaluate left ventricular (LV) performance in rats with large infarcts. ELISA, Western blot and biochemical assays were used to assess LV inflammation and oxidative stress. An 830-nm Laser Photon III semiconductor aluminum gallium arsenide diode (DMC, São Carlos, SP, Brazil) was applied transthoracically three times a week for 4 weeks based on the energy (i.e., 10J, 20J, and 40J; respectively). LLLT on 10J and 20J had a similar action in attenuating pulmonary congestion and myocardial fibrosis. Moreover, 10J and 20J attenuated LV end-diastolic pressure and improved +dP/dt and -dP/dt. All LLLT groups had lower levels of inflammatory mediators, but only the 10J group had normalized oxidative stress. All LLLT doses improved superoxide dismutase levels; however, only the 20J group showed a high content of the catalase. There was a lower level of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a in the infarcted myocardium, which it was normalized in the 20J and 40J groups. A higher phospholamban content was found in the 10J group. This study supports the beneficial LLLT role post-infarction. Apparently, the 10J and 20J doses show to be chosen for clinical translation.

Photobiomodulation therapy combined with carvedilol attenuates post-infarction heart failure by suppressing excessive inflammation and oxidative stress in rats.

The post-myocardial infarction heart failure (HF) still carries a huge burden since current therapy is unsuccessful to abrogate poor prognosis. Thus, new approaches are needed, and photobiomodulation therapy (PBMt) may be a way. However, it is not known whether PBMt added to a standard HF therapy provides additional improvement in cardiac remodeling in infarcted rats. This study sought to determine the combined carvedilol-drug and PBMt with low-level laser therapy value in HF. Rats with large infarcts were treated for 30 days. The functional fitness was evaluated using a motorized treadmill. Echocardiography and hemodynamic measurements were used for functional evaluations of left ventricular (LV). ELISA, Western blot and biochemical assays were used to evaluate inflammation and oxidative stress in the myocardium. Carvedilol and PBMt had a similar action in normalizing pulmonary congestion and LV end-diastolic pressure, attenuating LV dilation, and improving LV systolic function. Moreover, the application of PBMt to carvedilol-treated rats inhibited myocardial hypertrophy and improved +dP/dt of LV. PBMt alone prevented inflammation with a superior effect than carvedilol. Carvedilol and PBMt normalized 4-hydroxynonenal (a lipoperoxidation marker) levels in the myocardium. However, importantly, the addition of PBMt to carvedilol attenuated oxidized protein content and triggered a high activity of the anti-oxidant catalase enzyme. In conclusion, these data show that the use of PBMt plus carvedilol therapy results in a significant additional improvement in HF in a rat model of myocardial infarction. These beneficial effects were observed to be due, at least in part, to decreased myocardial inflammation and oxidative stress.

Atrial fibrillation promotion in a rat model of heart failure induced by left ventricle radiofrequency ablation.

BACKGROUND: Atrial fibrillation (AF) frequently coexists with congestive heart failure (CHF). The increased susceptibility to AF in CHF has been attributed to a variety of structural and electrophysiological changes in the atria, particularly dilation and interstitial fibrosis. We evaluated atrial remodeling and AF vulnerability in a rat model of CHF induced by left ventricle (LV) radiofrequency (RF) ablation. METHODS: Wistar rats were divided into 3 groups: RF-induced CHF (Ab, n = 36), CHF animals treated with spironolactone (AbSpi, n = 20) and sham controls (Sham, n = 29). After 12 weeks, animals underwent echocardiographic and electrophysiological evaluation and were sacrificed for histological (atrial fibrosis) and Western blotting (TGF-ß1, collagen I/III, connexin 43 and CaV1.2) analysis. RESULTS: Mild LV dysfunction and marked atrial enlargement were noted in both ablated groups. AF inducibility (episodes ≥2 s) increased in the Ab group compared to sham animals (31/36, 86%; vs. 15/29, 52%; p = 0.005), but did not differ from the AbSpi group (16/20, 80%; p = NS). Sustained AF (>30 s) was also more frequent in the Ab group compared to shams (56% vs. 28%; p = 0.04). Spironolactone reduced atrial fibrosis (p < 0.01) as well as TGF-ß1 (p < 0.01) and collagen I/III (p < 0.01) expression but did not affect connexin 43 and CaV1.2 expression. CONCLUSIONS: Rats with RF-induced CHF exhibit pronounced atrial structural remodeling and enhanced AF vulnerability. This model may be useful for studying AF substrate in CHF.

Swimming Training Improves Myocardial Mechanics, Prevents Fibrosis, and Alters Expression of Ca2+ Handling Proteins in Older Rats.

Exercise training effects on the contractility of aged myocardium have been investigated for more than 20 years, but the data are still unclear. This study evaluated the hypothesis that a swimming training (ST) may improve myocardial inotropism in older rats. Male Wistar rats aged 4 (young)-and 21 (old)-months-old were divided into young untrained (YNT), old untrained (ONT), and old trained (OTR; 6 weeks of ST) groups. Echocardiography and hemodynamic were employed to assess left ventricular morphology and function. Myocardial mechanics was evaluated on papillary muscles. Histological and immunoblotting were carried out to evaluate fibrosis and proteins that modulate the myocardial function and calcium handling. We found that older rats did not show cardiac dysfunction, but ONT group showed lower physical performance during a swimming test (YNT: 5 ± 2; ONT: -16 ± 0.4; OTR: 51 ± 3; Δ%, sec). Moreover, ONT group showed worse myocardial inotropism, in which it was reversed by ST (Peak developed tension: YNT: 6.2 ± 0.7; ONT: 3.9 ± 0.3; OTR: 6.9 ± 0.9; g/mm2). The ST was associated with preserved collagen content (YNT: 0.38 ± 0.05; ONT: 0.78 ± 0.12; OTR: 0.34 ± 0.09; %). Exercise partially mitigated the effects of aging on intracellular Ca2+-regulating protein (eg, L-Ca2+ channel and phospholamban) and ß-isoform of myosin. Thus, we propose that these molecular alterations together with inhibition of collagen increase contribute to improved myocardial performance in older rats.

Low-Level Laser Application in the Early Myocardial Infarction Stage Has No Beneficial Role in Heart Failure.

Low-level laser therapy (LLLT) has been targeted as a promising approach that can mitigate post-infarction cardiac remodeling. There is some interesting evidence showing that the beneficial role of the LLLT could persist long-term even after the end of the application, but it remains to be systematically evaluated. Therefore, the present study aimed to test the hypothesis that LLLT beneficial effects in the early post-infarction cardiac remodeling could remain in overt heart failure even with the disruption of irradiations. Female Wistar rats were subjected to the coronary occlusion to induce myocardial infarction or Sham operation. A single LLLT application was carried out after 60 s and 3 days post-coronary occlusion, respectively. Echocardiography was performed 3 days and at the end of the experiment (5 weeks) to evaluate cardiac function. After the last echocardiographic examination, LV hemodynamic evaluation was performed at baseline and on sudden afterload increases. Compared with the Sham group, infarcted rats showed increased systolic and diastolic internal diameter as well as a depressed shortening fraction of LV. The only benefit of the LLLT was a higher shortening fraction after 3 days of infarction. However, treated-LLLT rats show a lower shortening fraction in the 5th week of study when compared with Sham and non-irradiated rats. A worsening of cardiac function was confirmed in the hemodynamic analysis as evidenced by the higher LV end-diastolic pressure and lower +dP/dt and -dP/dt with five weeks of study. Cardiac functional reserve was also impaired by infarction as evidenced by an attenuated response of stroke work index and cardiac output to a sudden afterload stress, without LLLT repercussions. No significant differences were found in the myocardial expression of Akt1/VEGF pathway. Collectively, these findings illustrate that LLLT improves LV systolic function in the early post-infarction cardiac remodeling. However, this beneficial effect may be dependent on the maintenance of phototherapy. Long-term studies with LLLT application are needed to establish whether these effects ultimately translate into improved cardiac remodeling.

Are there gender differences in left ventricular remodeling after myocardial infarction in rats?

OBJECTIVE: An unclear issue is whether gender may influence at cardiac remodeling after myocardial infarction (MI). We evaluated left ventricle remodeling in female and male rats post-MI. METHODS: Rats were submitted to anterior descending coronary occlusion. Echocardiographic evaluations were performed on the first and sixth week post-occlusion to determine myocardial infarction size and left ventricle systolic function (FAC, fractional area change). Pulsed Doppler was applied to analyze left ventricle diastolic function using the following parameters: E wave, A wave, E/A ratio. Two-way ANOVA was applied for comparisons, complemented by the Bonferroni test. A P≤=0.05 was considered significant. RESULTS: There were no significant differences between genders for morphometric parameters on first (MI [Female (FE): 44.0 ± 5.0 vs. Male (MA): 42.0 ± 3.0%]; diastolic [FE: 0.04 ± 0.003 vs. MA: 0.037 ± 0.005, mm/g] and systolic [FE: 0.03 ± 0.0004 vs. MA: 0.028 ± 0.005, mm/g] diameters of left ventricle) and sixth (MI [FE: 44.0 ± 5.0 vs. MA: 42.0 ± 3.0, %]; diastolic [FE: 0.043 ± 0.01 vs. MA: 0.034 ± 0.005, mm/g] and systolic [FE: 0.035 ± 0.01 vs. MA: 0.027 ± 0.005, mm/g] of LV) week. Similar findings were reported for left ventricle functional parameters on first (FAC [FE: 34.0 ± 6.0 vs. MA: 32.0 ± 4.0, %]; wave E [FE: 70.0 ± 18.0 vs. MA: 73.0 ± 14.0, cm/s]; wave A [FE: 20.0 ± 12.0 vs. MA: 28.0 ± 13.0, cm/s]; E/A [FE: 4.9 ± 3.4 vs. MA: 3.3 ± 1.8]) and sixth (FAC [FE: 29.0 ± 7.0 vs. MA: 31.0 ± 7.0, %]; wave E [FE: 85.0 ± 18.0 vs. MA: 87.0 ± 20.0, cm/s]; wave A [FE: 20.0 ± 11.0 vs. MA: 28.0 ± 17.0, cm/s]; E/A [FE: 6.2 ± 4.0 vs. MA: 4.6 ± 3.4]) week. CONCLUSION: Gender does not influence left ventricle remodeling post-MI in rats.

Are there gender differences in left ventricular remodeling after myocardial infarction in rats? / Há diferenças entre os gêneros no remodelamento ventricular esquerdo após infarto do miocárdio em ratos?

Objective: An unclear issue is whether gender may influence at cardiac remodeling after myocardial infarction (MI). We evaluated left ventricle remodeling in female and male rats post-MI. Methods: Rats were submitted to anterior descending coronary occlusion. Echocardiographic evaluations were performed on the first and sixth week post-occlusion to determine myocardial infarction size and left ventricle systolic function (FAC, fractional area change). Pulsed Doppler was applied to analyze left ventricle diastolic function using the following parameters: E wave, A wave, E/A ratio. Two-way ANOVA was applied for comparisons, complemented by the Bonferroni test. A P≤=0.05 was considered significant. Results: There were no significant differences between genders for morphometric parameters on first (MI [Female (FE): 44.0±5.0 vs. Male (MA): 42.0±3.0%]; diastolic [FE: 0.04±0.003 vs. MA: 0.037±0.005, mm/g] and systolic [FE: 0.03±0.0004 vs. MA: 0.028±0.005, mm/g] diameters of left ventricle) and sixth (MI [FE: 44.0±5.0 vs. MA: 42.0±3.0, %]; diastolic [FE: 0.043±0.01 vs. MA: 0.034±0.005, mm/g] and systolic [FE: 0.035±0.01 vs. MA: 0.027±0.005, mm/g] of LV) week. Similar findings were reported for left ventricle functional parameters on first (FAC [FE: 34.0±6.0 vs. MA: 32.0±4.0, %]; wave E [FE: 70.0±18.0 vs. MA: 73.0±14.0, cm/s]; wave A [FE: 20.0±12.0 vs. MA: 28.0±13.0, cm/s]; E/A [FE: 4.9±3.4 vs. MA: 3.3±1.8]) and sixth (FAC [FE: 29.0±7.0 vs. MA: 31.0±7.0, %]; wave E [FE: 85.0±18.0 vs. MA: 87.0±20.0, cm/s]; wave A [FE: 20.0±11.0 vs. MA: 28.0±17.0, cm/s]; E/A [FE: 6.2±4.0 vs. MA: 4.6±3.4]) week. Conclusion: Gender does not influence left ventricle remodeling post-MI in rats. .

Objetivo: A influência do gênero no remodelamento cardíaco após o infarto do miocárdio é uma questão em intenso debate. Nós avaliamos o remodelamento ventricular esquerdo em ratos infartados de ambos os gêneros. Métodos: O infarto do miocárdio foi induzido por oclusão da artéria coronária descendente anterior (fêmeas [FM]; machos [MC]). A ecocardiografia foi realizada na primeira e sexta semana pós-oclusão para determinar o tamanho do infarto do miocárdio e a função sistólica do ventricular esquerdo (mudança na área fracional [FAC]). A função diastólica derivou dos seguintes parâmetros: onda E; onda A; razão E/A. ANOVA duas vias com pós-teste de Bonferroni foi aplicado nas comparações (P≤=0,05). Resultados: Todas variáveis morfométricas foram similares (P>0,05) entre os gêneros com uma (infarto do miocárdio [FM: 44,0±5,0 vs. MC: 42,0±3,0, %]; diâmetro diastólico [FM: 0,04±0,003 vs. MC: 0,037±0,005, mm/g] e sistólico [FM: 0,03±0,0004 vs. MC: 0,028±0,005, mm/g] do VE) e seis (IM [FM: 44,0±5,0 vs. MC: 42,0±3,0, %]; diâmetro diastólico [FM: 0,043±0,01 vs. MC: 0,034±0,005, mm/g] e sistólico [FM: 0,035±0,01 vs. MC: 0,027±0,005, mm/g] do ventricular esquerdo) semanas. Achado similar ocorreu para os dados funcionais com uma (FAC [FM: 34,0±6,0 vs. MC: 32,0±4,0, %]; onda E [FM: 70,0±18,0 vs. MC: 73,0±14,0, cm/s]; onda A [FM: 20,0±12,0 vs. MC: 28,0±13,0, cm/s]; E/A [FM: 4,9±3,4 vs. MC: 3,3±1,8]) e seis (FAC [FM: 29,0±7,0 vs. MC: 31,0±7,0, %]; onda E [FM: 85,0±18,0 vs. MC: 87,0±20,0, cm/s]; onda A [FM: 20,0±11,0 vs. MC: 28,0±17,0 cm/s]; E/A [FM: 6,2±4,0 vs. MC: 4,6±3,4]) semanas. Conclusão: O gênero não é determinante para o remodelamento ventricular esquerdo pós-infarto do miocárdio em ratos. .