Development and evaluation of calcium hydroxide-coated, pericardium-based biomembranes for direct pulp capping.

AIM: The aim of the present study was to develop a bovine pericardium biomembrane (BPB) and to evaluate pulp response in vivo. METHODS: A double-layer bovine BPB/chitosan was manufactured, and the porous chitosan side was coated with calcium hydroxide. The microstructure of the matrices was evaluated with electron microscopy. To test pulp response, cavities were prepared on the occlusal surface of Wistar rats' mandibular left first molars and capped with matrices, followed by appropriate adhesives/composite restorations. The animals were divided into three groups: group 1, calcium hydroxide alone; group 2, BPB without calcium hydroxide; and group 3, BPB coated with calcium hydroxide. Specimens were processed and histologically evaluated at 7, 14, and 30 days, postoperatively. RESULTS: Electron microscopy showed porous chitosan surface and a cohesive calcium hydroxide layer. Histological analysis showed that groups 1 and 3 had mild odontoblast layer disorganization, but normal pulp tissue appearance at 7, 14, and 30 days. At the same time points, group 2 showed a loss of general pulp tissue, pulp necrosis, and periapical abscess in some teeth. CONCLUSION: Coated bovine pericardium-based biomembranes resulted in favorable outcomes in cases of pulp exposure after a 30-day observation period, and might protect against injuries caused by adhesive systems and composites.

Respiratory muscle training decreases diaphragm DNA damage in rats with heart failure.

Respiratory muscle training (RMT) promotes beneficial effects on respiratory mechanics, heart and lung morphological changes, and hemodynamic variables in rats with heart failure (HF). However, the relation between RMT effects and diaphragm oxidative stress remains unclear. Therefore, the aim of this study was to evaluate the RMT effects on diaphragm DNA damage in HF rats. Wistar rats were allocated into 4 groups: sedentary sham (Sed-Sham, n = 8), trained sham (RMT-Sham, n = 8), sedentary HF (Sed-HF, n = 8), and trained HF (RMT-HF, n = 8). The animals underwent a RMT protocol (30 min/day, 5 days/week for 6 weeks), whereas sedentary animals did not exercise. Groups were compared by a two-way ANOVA and Tukey's post hoc tests. In rats with HF, RMT promoted reduction in pulmonary congestion (p < 0.0001) and left ventricular end diastolic pressure (p < 0.0001). Moreover, RMT produced a decrease in the diaphragm DNA damage in HF rats. This was demonstrated through the reduction in the percentage of tail DNA (p < 0.0001), tail moment (p < 0.01), and Olive tail moment (p < 0.001). These findings showed that a 6-week RMT protocol in rats with HF promoted an improvement in hemodynamic function and reduces diaphragm DNA damage.

The influence of low-level laser therapy on parameters of oxidative stress and DNA damage on muscle and plasma in rats with heart failure.

In heart failure (HF), there is an imbalance between the production of reactive oxygen species and the synthesis of antioxidant enzymes, causing damage to the cardiovascular function and increased susceptibility to DNA damage. The aim of this study was to evaluate the influence of low-level laser therapy (LLLT) on parameters of oxidative stress and DNA damage in skeletal muscle and plasma of rats with HF. Wistar rats were allocated into six groups: "placebo" HF rats (P-HF, n = 9), "placebo" Sham rats (P-sham, n = 8), HF rats at a dose 3 J/cm(2) of LLLT (3 J/cm(2)-HF, n = 8), sham rats at a dose 3 J/cm(2) of LLLT (3 J/cm(2)-sham, n = 8), HF rats at a dose 21 J/cm(2) of LLLT (21 J/cm(2)-HF, n = 8) and sham rats at a dose 21 J/cm(2) of LLLT (21 J/cm(2)-sham, n = 8). Animals were submitted to a LLLT protocol for 10 days at the right gastrocnemius muscle. Comparison between groups showed a significant reduction in superoxide dismutase (SOD) activity in the 3 J/cm(2)-HF group (p = 0.03) and the 21 J/cm(2)-HF group (p = 0.01) compared to the P-HF group. 2',7'-Dihydrodichlorofluorescein (DCFH) oxidation levels showed a decrease when comparing 3 J/cm(2)-sham to P-sham (p = 0.02). The DNA damage index had a significant increase either in 21 J/cm(2)-HF or 21 J/cm(2)-sham in comparison to P-HF (p = 0.004) and P-sham (p = 0.001) and to 3 J/cm(2)-HF (p = 0.007) and 3 J/cm(2)-sham (p = 0.037), respectively. Based on this, laser therapy appears to reduce SOD activity and DCFH oxidation levels, changing the oxidative balance in the skeletal muscle of HF rats. Otherwise, high doses of LLLT seem to increase DNA damage.

Low-level laser therapy improves the inflammatory profile of rats with heart failure.

Following heart failure (HF), immune activation leads to an imbalance between pro-inflammatory and anti-inflammatory cytokines. Low-level laser therapy (LLLT) has been used as an anti-inflammatory treatment in several disease conditions. However, the effect of LLLT on the skeletal muscle of rats with HF remains unclear. The present report aimed to evaluate the influence of LLLT on the inflammatory profile of rats with HF. The left coronary artery was ligated to induce HF and a sham operation was performed in the control groups. Male Wistar rats (n=49) were assigned to one of six groups: placebo sham rats (P-Sham; n=8), LLLT at a dose of 3 J/cm(2) sham rats (3 J/cm(2)-Sham; n=8), LLLT at a dose of 21 J/cm(2) sham rats (21 J/cm(2)-Sham; n=8), placebo HF rats (P-HF; n=9), LLLT at a dose of 3 J/cm(2) HF rats (3 J/cm(2)-HF; n=8), and LLLT at a dose of 21 J/cm(2) HF rats (21 J/cm(2)-HF; n=8). Four weeks after myocardial infarction or sham surgery, rats were subjected to LLLT (InGaAlP 660 nm, spot size 0.035 cm(2), output power 20 mW, power density 0.571 W/cm(2), energy density 3 or 21 J/cm(2), exposure time 5.25 s and 36.75 s) on the right gastrocnemius for 10 consecutive days. LLLT reduced plasma IL-6 levels (61.3 %; P<0.01), TNF-α/IL-10 (61.0 %; P<0.01) and IL-6/IL-10 ratios (77.3 %; P<0.001) and increased IL-10 levels (103 %; P<0.05) in the 21 J/cm(2)-HF group. Moreover, LLLT reduced the TNF-α (20.1 % and 21.3 %; both P<0.05) and IL-6 levels (54.3 % and 37.8 %; P<0.01 and P<0.05, respectively) and the IL-6/IL-10 ratio (59.7 % and 42.2 %; P<0.001 and P<0.05, respectively) and increased IL-10 levels (81.0 % and 85.1 %; both P<0.05) and the IL-10/TNF-α ratio (171.5 % and 119.8 %; P<0.001 and P<0.05, respectively) in the gastrocnemius in the 3 J/cm(2)-HF and 21 J/cm(2)-HF groups. LLLT showed systemic and skeletal muscle anti-inflammatory effects in rats with HF.

Respiratory muscle training improves hemodynamics, autonomic function, baroreceptor sensitivity, and respiratory mechanics in rats with heart failure.

Respiratory muscle training (RMT) improves functional capacity in chronic heart-failure (HF) patients, but the basis for this improvement remains unclear. We evaluate the effects of RMT on the hemodynamic and autonomic function, arterial baroreflex sensitivity (BRS), and respiratory mechanics in rats with HF. Rats were assigned to one of four groups: sedentary sham (n = 8), trained sham (n = 8), sedentary HF (n = 8), or trained HF (n = 8). Trained animals underwent a RMT protocol (30 min/day, 5 day/wk, 6 wk of breathing through a resistor), whereas sedentary animals did not. In HF rats, RMT had significant effects on several parameters. It reduced left ventricular (LV) end-diastolic pressure (P < 0.01), increased LV systolic pressure (P < 0.01), and reduced right ventricular hypertrophy (P < 0.01) and pulmonary (P < 0.001) and hepatic (P < 0.001) congestion. It also decreased resting heart rate (HR; P < 0.05), indicating a decrease in the sympathetic and an increase in the vagal modulation of HR. There was also an increase in baroreflex gain (P < 0.05). The respiratory system resistance was reduced (P < 0.001), which was associated with the reduction in tissue resistance after RMT (P < 0.01). The respiratory system and tissue elastance (Est) were also reduced by RMT (P < 0.01 and P < 0.05, respectively). Additionally, the quasistatic Est was reduced after RMT (P < 0.01). These findings show that a 6-wk RMT protocol in HF rats promotes an improvement in hemodynamic function, sympathetic and vagal heart modulation, arterial BRS, and respiratory mechanics, all of which are benefits associated with improvements in cardiopulmonary interaction.