We determined the effects of helium-neon (He-Ne) laser irradiation on wound healing dynamics in mice treated with steroidal and nonsteroidal anti-inflammatory agents. Male albino mice, 28-32 g, were randomized into 6 groups of 6 animals each: control (C), He-Ne laser (L), dexamethasone (D), D + L, celecoxib (X), and X + L. D and X were injected im at doses of 5 and 22 mg/kg, respectively, 24 h before the experiment. A 1-cm long surgical wound was made with a scalpel on the abdomens of the mice. Animals from groups L, D + L and X + L were exposed to 4 J (cm 2 ) -1 day -1 of He-Ne laser for 12 s and were sacrificed on days 1, 2, or 3 after the procedure, when skin samples were taken for histological examination. A significant increase of collagen synthesis was observed in group L compared with C (168 ± 20 vs 63 ± 8 mm 2 ). The basal cellularity values on day 1 were: C = 763 ± 47, L = 1116 ± 85, D = 376 ± 24, D + L = 698 ± 31, X = 453 ± 29, X + L = 639 ± 32 U/mm 2 . These data show that application of L increases while D and X decrease the inflammatory cellularity compared with C. They also show that L restores the diminished cellularity induced by the anti-inflammatory drugs. We suggest that He-Ne laser promotes collagen formation and restores the baseline cellularity after pharmacological inhibition, indicating new perspectives for laser therapy aiming to increase the healing process when anti-inflammatory drugs are used.

The investigation of resistance vessels is generally costly and difficult to execute. The present study investigated the diameters and the vascular reactivity of different segments of the rat tail artery (base, middle, and tail end) of 30 male Wister rats (EPM strain) to characterize a conductance or resistance vessel, using a low-cost simple technique. The diameters (mean ± SEM) of the base and middle segments were 471 ± 4.97 and 540 ± 8.39 µm, respectively, the tail end was 253 ± 2.58 µm. To test reactivity, the whole tail arteries or segments were perfused under constant flow and the reactivity to phenylephrine (PHE; 0.01-300 µg) was evaluated before and after removal of the endothelium or drug administration. The maximal response (E max ) and sensitivity (pED 50 ) to PHE of the whole tail and the base segment increased after endothelium removal or treatment with 100 µM L-NAME, which suggests modulation by nitric oxide. Indomethacin (10 µM) and tetraethylammonium (5 mM) did not change the E max or pED 50 of these segments. PHE and L-NAME increased the pED 50 of the middle and the tail end only and indomethacin did not change pED 50 or E max . Tetraethylammonium increased the sensitivity only at the tail end, which suggests a blockade of vasodilator release. Results indicate that the proximal segment of the tail artery possesses a diameter compatible with a conductance vessel, while the tail end has the diameter of a resistance vessel. In addition, the vascular reactivity to PHE in the proximal segment is nitric oxide-dependent, while the tail end is dependent on endothelium-derived hyperpolarizing factor.

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Coronary artery (CA) remodeling may lead to increased arterial stiffness and decreased coronary flow reserve. The molecular mechanisms that dictate diabetes‐induced CA remodeling are undefined. This study established a link between oxidative stress, angiotensin II (Ang II), CA remodeling and stiffness in Type 2 diabetic mice. CA (<100 μ) were isolated from 16 wk heterozygous (Db/db) and diabetic (db/db) mice ± treatment with the NADPH‐oxidase inhibitor apocynin (5mM) or the AT1R blocker candesartan (1mg/kg/day). Mean arterial pressure, measured by telemetry, was similar between groups. CA were mounted on a pressure myograph for measurement of structural and passive mechanical properties. Significant inward remodeling was detected in db/db vs. Db/db, defined by increased wall thickness, media:lumen ratio, remodeling index and decreased compliance. This inward remodeling in db/db CA was associated with increased oxidative stress and collagen accumulation as measured by DHE and picrosirius red staining respectively. Immunoblot analysis indicted that basal JNK, ERK, and AKT phosphorylation were increased in db/db CA tissue lysates vs. Db/db. In vivo treatment with apocynin or candesartan reduced inward CA remodeling. These data suggest that increased oxidative stress and Ang II is critical for altered structural and functional remodeling of CA in Type 2 diabetes. Supported by HL056046 and P20RR18766 (PAL).