Background: Autologous fat transfer—also referred to as fat grafting—has been reported to provide beneficial effects to overlying scar and skin. Despite procedural frequency, there is a paucity of high-level evidence guiding the surgeon in technique, patient selection, and efficacy. Methods: A multicenter, double-blinded, randomized, internally placebo-controlled trial was performed with an aim to qualitatively and quantitatively evaluate the impact of autologous fat transfer on the quality of overlying scar tissue. Fat-grafted scars were evaluated and compared with paired, saline-injected “control” scars. Subjective and objective metrics were evaluated in treated sites for 12 months after treatment. Results: Blinded qualitative results demonstrated a statistically significant improvement in scar quality over time in fat-grafted scars. However, these improvements were not found to be statistically different from changes noted in scars treated with saline. In addition, objective metrics did not statistically differ between saline-injected and autologous fat-grafted scars. Conclusions: Our results demonstrate that autologous fat grafting can improve the qualitative profile of a scar from both the patient and observer perspectives. However, there was no difference in improvement when compared with scars that were treated with saline in a randomized and blinded fashion. These results demonstrate that any improvements in scar quality related to fat grafting are also achieved using saline and suggest that mechanisms other than cell activity may be at play. Additional randomized, blinded, placebo-controlled trials are required to either corroborate or contest the putative beneficial effect(s) of adipose tissue on scar remodeling.

Introduction: The consequences of low partial pressure of O 2 include low arterial O 2 saturations (SaO 2 ), low blood O 2 content (CaO 2 ), elevated mean pulmonary artery pressure (PAP), and decreased O 2 consumption VO 2 . 5-hydroxymethyl-2-furfural (5-HMF) binds to the N-terminal valine of hemoglobin (HgB) and increases its affinity to O 2 . We used an instrumented, sedated swine model to study the effect of 5-HMF on cardiovascular parameters during exposure to acute normobaric hypoxia (NH). Methods Twenty-three sedated and instrumented swine were randomly assigned to one of three treatment groups and received equal volume of normal saline (VEH), 20 mg/kg 5-HMF (5-HMF-20) or 40 mg/kg 5-HMF (5-HMF-40). Animals then breathed 10% FiO 2 for 120 min. Parameters recorded were Cardiac Output (CO), Mean Arterial Blood Pressure (MAP), Heart Rate (HR), Mean Pulmonary Artery Pressure (PAP), SaO 2 and saturation of mixed venous blood (SvO 2 ). The P 50 was measured at fixed time intervals prior to and during NH. Results 5-HMF decreased P 50 . In the first 30 min of NH, treatment with 5-HMF-20 and 5-HMF-40 resulted in a (1) significantly smaller decrement in SaO 2 and SvO 2 , (2) significantly lower HR and CO, and (3) smaller increase in PAP compared to VEH. In the 120 min of NH there was a trend toward improved mortality with 5-HMF treatment. Conclusion 5-HMF treatment decreased P 50 , improved SaO 2 , and mitigated increases in PAP in this swine model of NH.

Background Significant reductions in ambient pressure subject an individual to risk of decompression illness (DCI); with incidence up to 35 per 10,000 dives. In severe cases, the central nervous system is often compromised (>80%), making DCI among the most morbid of diving related injuries. While hyperbaric specialists suggest initiating recompression therapy with either a Treatment Table 6 (TT6) or 6A (TT6A), the optimal initial recompression treatment for severe DCI is unknown. Methods Swine were exposed to an insult dive breathing air at 7.06 ATA (715.35 kPa) for 24 min followed by rapid decompression at a rate of 1.82 ATA/min (184.41 kPa/min). Swine that developed neurologic DCI within 1 hour of surfacing were block randomized to one of four United States Navy Treatment Tables (USN TT): TT6, TT6A-air (21% oxygen, 79% nitrogen), TT6A-nitrox (50% oxygen, 50% nitrogen), and TT6A-heliox (50% oxygen, 50% helium). The primary outcome was the mean number of spinal cord lesions, which was analyzed following cord harvest 24 hours after successful recompression treatment. Secondary outcomes included spinal cord lesion incidence and gross neurologic outcomes based on a pre- and post- modified Tarlov assessment. We compared outcomes among these four groups and between the two treatment profiles (i.e. TT6 and TT6A). Results One-hundred and forty-one swine underwent the insult dive, with 61 swine meeting inclusion criteria (43%). We found no differences in baseline characteristics among the groups. We found no significant differences in functional neurologic outcomes (p = 0.77 and 0.33), spinal cord lesion incidence (p = 0.09 and 0.07), or spinal cord lesion area (p = 0.51 and 0.17) among the four treatment groups or between the two treatment profiles, respectively. While the trends were not statistically significant, animals treated with TT6 had the lowest rates of functional deficits and the fewest spinal cord lesions. Moreover, across all animals, functional neurologic deficit had strong correlation with lesion area pathology (Logistic Regression, p < 0.01, Somers’ D = 0.74). Conclusions TT6 performed as well as the other treatment tables and is the least resource intensive. TT6 is the most appropriate initial treatment for neurologic DCI in swine, among the tables that we compared.

Exposure to high altitude is associated with a reduction in the partial pressure of oxygen (PO2) that subsequently affects all components of the oxygen transport cascade, from lung to mitochondria. Impaired oxygen transport contributes to decrements in exercise capacity at high altitude. Strategies aimed at improving blood oxygenation are therefore an important focus of study. 5‐hydroxymethyl‐2‐furfural (5‐HMF) may offer prophylaxis at high altitude due to induction of a leftward‐shift in the oxygen‐hemoglobin dissociation curve that results in increased arterial blood oxygen saturation. The objective of this research is to determine whether the benefits afforded by 5‐HMF to blood oxygenation create a measureable attenuation in the decline in physical performance known to occur in hypoxia. Fisher 344male rats (n=40) were implanted with osmotic pumps to continuously deliver either inactive saline or 5‐HMF (40 mg/kg/d), and exposed to either sea level(SL, n=20/group) or a simulated altitude of 18,000 feet (HH, n=20/group) in ahypobaric hypoxic chamber for 24 hours. Muscle function testing was conducted both pre‐ and post‐HH and SL exposures, including peak torque output, force‐frequency analysis, and time to fatigue. Following SL/HH exposure, animals had repeat muscle function testing, then were weighed, had blood collected for determination of blood gases and complete blood counts (CBC), and were humanely euthanized. Muscles were then harvested with wet weights recorded. Rats exposed to HH for 24 hours displayed a 9% decrease in body mass. In 5‐HMF treated animals, increases in erythrocytes (14%), hemoglobin (14%) and hematocrit (16%) were documented. HH led to a 38% reduction in PO2; however 5‐HMF did not attenuate this decline. Posterior crural muscle strength was unaltered in HH‐exposed rats, and although non‐significant, a 9% increase in peak torque output was documented in 5‐HMF treated animals. In spite of 5‐HMFimproving blood oxygen carrying capacity, only modest improvements were observed in muscle function following a 24 hour exposure to a simulated altitude of 18,000 ft. Current studies are underway to assess the benefits of5‐HMF on blood oxygenation with extended HH exposure. In addition, these experiments will determine whether overt alterations in anabolic pathways occur and precede outward functional changes in muscle.Support or Funding InformationThese studies were supported by an Office of Naval Research Grant to NGR.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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