Versatility of Local Fasciocutaneous Island Flaps for Resurfacing Soft Tissue Defects Overlying the Achilles Tendon.

Background: Reconstruction of soft tissue defects overlying the Achilles tendon has always been a challenge. Various modalities of reconstruction have been described to resurface such defects. We aimed to assess the functional and cosmetic outcomes of all patients who had undergone reconstruction of small and medium sized soft tissue defects of the Achilles region using local fasciocutaneous island flaps. Methods: This retrospective study was conducted from January 2020 to June 2022. 15 patients with small (≤ 30 cm2) and medium (30-90 cm2) sized soft tissue defects of the tendo-Achilles region, underwent reconstruction with local fasciocutaneous island flaps and had complete medical records, were included. Results: Thirteen patients were male (86.7%). The mean age was 53.2 years. 5 cases (33.3%) had post-traumatic open AT injuries with skin avulsion, while ten patients (66.7%) had suture line complications after open repair of spontaneous Achilles tendon rupture. Defect sizes ranged from 12 to 63 cm2. Reverse sural flap was used in 5 patients (33.3%) and medial plantar flap in 10 patients (66.7%). All flaps survived completely. Complications were detected in 3 patients (20%); 1 distal superficial necrosis in a sural flap and 2 marginal minimal graft loss. Functional outcome was good in 12 patients (80%), excellent in 1 patient (6.7%) and fair in 2 patients (13.3%). 13 patients (86.7%) were satisfied with the cosmetic results. Conclusion: Local fasciocutenous island flaps are reliable and simple solutions for covering small to moderate soft tissue defects overlying the Achilles Tendon, with acceptable functional and cosmetic outcomes.

Comparison of Nd: YAG Laser and Combined Intense Pulsed Light and Radiofrequency in the Treatment of Hypertrophic Scars: A Prospective Clinico-Histopathological Study.

INTRODUCTION: Hypertrophic scars are fibroproliferative disorders, seen after burn, trauma, and/or surgery. We aimed to compare the clinical and histopathological results of 1064-nm Nd:YAG laser and combined intense pulsed light and radiofrequency in the treatment of hypertrophic scars. METHODS: Fifty patients with hypertrophic scars were included in this prospective, randomized study. Twenty-five patients were treated with Nd:YAG laser and 25 patients with combined intense pulsed light and radiofrequency (E-light). The scars were evaluated at baseline, during and at 3 months after the final treatment session using the Vancouver scar scale. Biopsy specimens from scars were obtained before, during, and 3 months after the final treatment session and were stained with hematoxylin and eosin stain, Masson's trichrome stain, and immunostaining procedures for collagen I, collagen III, and TGF-ß1. RESULTS: Significant improvements in the total Vancouver scar scale scores before and after the treatment in both groups (P < 0.001); however, a significant difference between both groups (P < 0.001), regarding the E-light, which showed better response than Nd:YAG laser. Hematoxylin and eosin and Masson's trichrome staining showed arrangement and thinning of collagen bundles and reduction in collagen density by in both groups, but the collagen bundles thinning and parallelism were more obvious in the E-light group. Significant decrease in the concentration of collagen I, collagen III, and TGF-ß1 in the E-light group as compared with the laser group (P = 0.005, P = 0.003 and P < 0.001, respectively). CONCLUSIONS: Both modalities were successful in the treatment of hypertrophic scars; however, a significant improvement in the clinical and histopathological findings was detected with the E-light method.

Facilitation by the renin-angiotensin system of cyclosporine-evoked hypertension in rats: Role of arterial baroreflexes and vasoreactivity.

AIMS: Cyclosporine (CSA) elevates blood pressure (BP) and alters arterial baroreflex sensitivity (BRS) and vasoreactivity. In this study we determined whether the renin-angiotensin system (RAS) interplays with other vasopressor pathways in mediating the CSA actions. MATERIALS AND METHODS: Whole animal and isolated vascular preparations were employed to determine the effects of pharmacologic interruption of angiotensin II (Ang II), endothelin (ET), or thromboxane (TXA2) signaling on the adverse cardiovascular effects of CSA. KEY FINDINGS: CSA (25mg/kg/day i.p. for 7days) caused significant increases in BP that were paralleled with (i) reduced BRS measured by phenylephrine (BRSPE) or sodium nitroprusside (BRSSNP), (ii) enhanced aortic contractile responses to Ang II and U-46619 (thromboxane analogue), and (iii) reduced aortic eNOS expression and acetylcholine, but not SNP, vasorelaxations. Except for the reduced BRSSNP, the CSA effects disappeared upon concurrent administration of losartan (angiotensin AT1 receptor antagonist), captopril (angiotensin converting enzyme inhibitor), or their combination. Moreover, CSA augmentation of Ang II contractions was abolished after cyclooxygenase inhibition (indomethacin) or endothelin ETA/ETB receptor blockade (atrasentan/BQ788). By contrast, the blockade of thromboxane receptors (terutroban) failed to alter the CSA-evoked facilitation of Ang II responsiveness. SIGNIFICANCE: The facilitation of baroreflex control and inhibition of vascular responsiveness to Ang II and thromboxane contribute to the BP lowering effect of RAS inhibitors in CSA-treated rats. Further, endothelin receptors and vasoconstrictor prostanoids contribute to the CSA-evoked exaggeration of Ang II vascular responsiveness and hypertension.

Blockade of endothelin ET(A), but not thromboxane, receptors offsets the cyclosporine-evoked hypertension and interrelated baroreflex and vascular dysfunctions.

The impairment of arterial baroreceptor and vasodilator functions are two major contributors to the hypertensive action of cyclosporine (CSA). In this study, in vivo and in vitro pharmacological studies were performed to investigate whether these effects of CSA are differentially modulated by endothelin and thromboxane signaling. The treatment of rats with CSA (25mg/kg/day i.p.) for 7 consecutive days caused significant increases in blood pressure (BP), attenuated reflex heart rate (HR) responses to vasopressor (phenylephrine, PE) and vasodepressor (sodium nitroprusside, SNP) agents, and reduced cumulative vasorelaxant responses elicited by acetylcholine (Ach, 1×10(-9)-1×10(-5)M) in PE-precontracted isolated aortas. These effects of CSA were blunted after concurrent i.p. administration of atrasentan (selective ETA blocker, 10mg/kg/day), but not terutroban (thromboxane receptor blocker, 10mg/kg/day). Moreover, atrasentan reversed the reductions in aortic protein expression of eNOS caused by CSA whereas terutroban was without effect. We also report that the favorable effect of atrasentan on CSA-evoked impairment in aortic Ach responsiveness disappeared in rats treated simultaneously with L-NAME (NOS inhibitor, 10mg/kg/day) but not BQ 788 (ETB receptor blocker, 0.1mg/kg/day) or indomethacin (cycloxygenase inhibitor, 5mg/kg/day). Together, the data implicate endothelin ETA receptors in baroreflex and vascular derangements which predispose to the hypertensive effect of CSA. Moreover, the facilitation of NOS, but not ETB receptors or cycloxygenase-derived prostanoids, signaling is pivotal for advantageous effect of atrasentan on the aortic CSA-Ach interaction.

The involvement of K(ATP) channels in morphine-induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats.

This study investigated the role of K(ATP) channels in morphine-induced antinociception and hepatic oxidative stress in acute and inflammatory pain. The K(ATP) channel modulators (K(ATP) channel opener, diazoxide 100 mg/kg, p.o, and K(ATP) channel blocker, glibenclamide, 3 mg/kg i.p.) were administered with morphine (80 mg/kg, i.p.). Antinociception was assessed by the tail-flick and formalin tests in rats and measured by the area under the curve values and the maximum percent effect for 3 h. The indices of hepatic oxidative stress: glutathione, glutathione peroxidase, and malondialdehyde were then determined in the liver homogenates obtained from the treated animals. In both tests, glibenclamide antagonized morphine-induced antinociception, whereas diazoxide augmented it in the tail-flick test only. In the formalin test, glibenclamide alone has a significant hyperalgesic effect, whereas diazoxide decreased the number of flinches. Coadministration of glibenclamide with morphine antagonized the hepatotoxic effect of morphine in both animal models. In the tail-flick test, glibenclamide administered alone significantly increased malondialdehyde's level. Coadministration of diazoxide with morphine increased glutathione level in the formalin test. Diazoxide administered alone exacerbated the hepatic oxidative stress in both animal models. These findings suggest a role of K(ATP) channel modulators on morphine-induced antinociception and hepatic oxidative stress. The administration of glibenclamide may prevent morphine-induced hepatotoxicity. The effectiveness of diazoxide in the management of pain is limited due to its deleterious effect on the liver. However, the interaction of the K(ATP) channel modulators with morphine depends on the differential sensitivity to the pain stimulus.