Surgical Training and Standardised Management Guidelines Improved the 30-Day Complication Rate After Abdominoplasty for Massive Weight Loss.

BACKGROUND: An increasing number of patients need reconstructive surgery after massive weight loss. The hypothesis was that surgical experience together with standardised management guidelines significantly decreases early complication rates after abdominoplasty for massive weight loss. The primary aim was to assess the 30-day complication rate after abdominoplasty following increased surgical training and experience. The secondary aim was to assess whether optimised management guidelines have an impact on the complication rate and patient safety. METHODS: The outcome of 69 consecutive abdominoplasties operated by surgeons in 2011 (Group A) and 70 consecutive patients operated by plastic surgeons in 2010-2012 (Group B) was compared. Another Group of 70 consecutive patients operated by surgeons in 2013-2014 (Group C) was assessed since standardised guidelines for pre- and post-operative treatments and refinement of surgical technique had been introduced. The same surgeons participated in operations of Groups A and C. χ 2-test and Fisher's exact test were applied to dichotomous data. Logistic regression test and ANOVA were used. RESULTS: Group C had more comorbidities and was significantly older. 48 patients in Group A (70%), 31 in Group B (44%) and 13 patients in Group C (19%) had early complications. A significantly decreased rate of complications occurred with improved guidelines and surgical training and experience. (A vs. C p < 0.001 and A vs. B p = 0.008). CONCLUSIONS: Our results indicate that the rate of early complications after abdominoplasty for massive weight loss can be significantly reduced with improved surgical experience and standardised management guidelines. Registered at Clinical Trial.gov (ID: NCT02679391).

Inhibitory effect of exogenous orexin a on gastric emptying, plasma leptin, and the distribution of orexin and orexin receptors in the gut and pancreas in man.

Orexin A (OXA) is a novel peptide that appears to play a role in the regulation of food intake, arousal, and energy balance. The aim of this study was to study the effect of iv infusion of OXA on gastric emptying, appetite, leptin, ghrelin, and glucose metabolism in man (six normal men) and the localization of OXA and orexin receptors (OXRs) 1 and 2 in the human gut. Gastric emptying was studied scintigraphically after ingestion of a 99mTc-labeled omelet and iv infusion of OXA (10 pmol/kg.min). Appetite ratings and blood samples were obtained at regular intervals. The immunohistochemical distribution of OXA and OXRs was examined using antibodies recognizing OXA, OX1R, and OX2R in human gastrointestinal tissue. OXA had no effect on lag phase or gastric half-emptying time. However, the gastric emptying rate was significantly slower without affecting appetite ratings. Plasma concentrations of insulin were increased by OXA, whereas plasma leptin decreased and ghrelin was unchanged. OXA immunoreactivity was observed in a subset of neurons and varicose nerve fibers in the mucosa, ganglia, and circular muscle layer and mucosal endocrine cells in the stomach and small intestine. OXA-immunoreactive cells in the islets of Langerhans contained insulin with a subset expressing OX2R. In conclusion, peripheral OXA seems to slightly affect the regulation of gastric emptying in humans without affecting appetite ratings. OXA decreased plasma levels of leptin, suggesting a possible interaction between leptin and OXA in the regulation of energy homeostasis.

Pharmacokinetic profile of orexin A and effects on plasma insulin and glucagon in the rat.

Orexin A (OXA) is found in the central nervous system (CNS) and in the gut. Peripheral administration of OXA to rats results in an inhibition of fasting motility. Plasma OXA increases during fasting and central administration of OXA increases food intake. The aim of the present study was to assess the pharmacokinetic profile of OXA and the effect of intravenously (i.v.) administered OXA on plasma concentrations of insulin and glucagon concentrations. Rats were given OXA i.v. (100 pmol kg(-1) min(-1)) for time periods of 0, 10, 20, 30 min and for 10, 20, 30 min after ceasing a 30-min infusion. After each time period, rats were then sacrificed and blood obtained. OXA was also administered at increasing doses (0, 100, 300 and 500 pmol kg(-1) min(-1)) for 30 min and blood was obtained. Plasma OXA, insulin and glucagon levels were measured using commercially available radioimmunoassay (RIA) kits. The plasma half-life of OXA was 27.1+/-9.5 min. Stepwise increasing infusion rates of OXA confirmed a linear concentration-time curve and thus first-order kinetics. Its volume of distribution indicated no binding to peripheral tissues. Plasma glucagon decreased during infusion of OXA, while insulin was unaffected. Plasma OXA was raised fourfold after food intake. Thus, OXA has a longer plasma half-life than many other peptides found in the gut. This needs to be taken into account when assessing effects of OXA on biological parameters after peripheral administration.

Physiological regulation and NO-dependent inhibition of migrating myoelectric complex in the rat small bowel by OXA.

Orexin A (OXA)-positive neurons are found in the lateral hypothalamic area and the enteric nervous system. The aim of this study was to investigate the mechanism of OXA action on small bowel motility. Electrodes were implanted in the serosa of the rat small intestine for recordings of myoelectric activity during infusion of saline or OXA in naive rats, vagotomized rats, rats pretreated with guanethidine (3 mg/kg) or N(omega)-nitro-L-arginine (L-NNA; 1 mg/kg). Naive rats were given a bolus of the orexin receptor-1 (OX1R) antagonist (SB-334867-A; 10 mg/kg), and the effect of both OXA and SB-334867-A on fasting motility was studied. Double-label immunocytochemistry with primary antibodies against OXA, neuronal nitric oxide synthase (nNOS), and OX1R was performed. OXA induced a dose-dependent prolongation of the cycle length of the migrating myoelectric complex (MMC) and, in the higher doses, replaced the activity fronts with an irregular spiking pattern. Vagotomy or pretreatment with guanethidine failed to prevent the response to OXA. The OXA-induced effect on the MMC cycle length was completely inhibited by pretreatment with L-NNA (P < 0.05), as did SB-334867-A. The OX1R antagonist shortened the MMC cycle length from 14.1 (12.0-23.5) to 11.0 (9.5-14.7) min (P < 0.05) during control and treatment periods, respectively. Colocalization of OXA and nNOS was observed in myenteric neurons of the duodenum and nerve fibers in the circular muscle. Our results indicate that OXA inhibition of the MMC involves the OX1R and that activation of a L-arginine/NO pathway possibly originating from OX1R/nNOS-containing neurons in the myenteric plexus may mediate this effect. Endogenous OXA may have a physiological role in regulating the MMC.

Localization and effects of orexin on fasting motility in the rat duodenum.

The orexins [orexin A (OXA) and orexin B (OXB)] are novel neuropeptides that increase food intake in rodents. The aim of this study was to determine the distribution of orexin and orexin receptors (OX1R and OX2R) in the rat duodenum and examine the effects of intravenous orexin on fasting gut motility. OXA-like immunoreactivity was found in varicose nerve fibers in myenteric and submucosal ganglia, the circular muscle, the mucosa, submucosal and myenteric neurons, and numerous endocrine cells of the mucosa. OXA neurons displayed choline acetyltransferase immunoreactivity, and a subset contained vasoactive intestinal peptide. OXA-containing endocrine cells were identified as enterochromaffin (EC) cells based on the presence of 5-hydroxytryptamine immunoreactivity. OX1R was expressed by neural elements of the gut, and EC cells expressed OX2R. OXA at 100 and 500 pmol x kg(-1) x min(-1) significantly increased the myoelectric motor complex (MMC) cycle length compared with saline. Similarly, OXB increased the MMC cycle length at 100 pmol x kg(-1) x min(-1), but there was no further effect at 500 pmol x kg(-1) x min(-1). We postulate that orexins may affect the MMC through actions on enteric neurotransmission after being released from EC cells and/or enteric neurons.

Cooling and asphyxia differentially affect augmented noradrenaline turnover in the brain of the externalized rat foetus.

The object was to investigate the effect of various perinatal conditions particularly cooling and asphyxia on the noradrenaline (NA) turnover in the foetal rat brain. The ratios between the noradrenergic metabolite 3-methoxy-4-hydroxy phenyl-ethylene glycol-sulphate (MHPG) and noradrenaline were determined as indexes of NA-turnover in the cortex and the pons-medulla of the foetal rat brain using high pressure liquid chromatography (HPLC). Rat foetuses were externalized by caesarean section performed on a spinally anaesthesized highly pregnant rat mother. One uterine horn was used as control while the other was exposed to externalization, simulated uterine contractions, cooling or asphyxia. Externalization per se and simulated uterine contractions did not cause any significant change in the NA-turnover. Cooling at 25 degrees C for 20 min caused a significant increase in NA-turnover in the cortex while a significant decrease was observed after 10 min of asphyxia in both the cortex and the pons-medulla and after 15 min in the cortex. We conclude that externalization and simulated uterine contractions per se do not seem to affect the augmented NA-turnover at birth. Cooling caused an increase suggesting a potentiating role on NA-turnover in conjunction with the externalization. On the other hand NA-turnover was depressed by asphyxia, suggesting that the level of oxygen is important for NA neuron activity.

Osmotic fragility and fluidity of erythrocyte membranes from rats raised on an essential fatty acid deficient diet.

Erythrocyte membranes from rats raised on a diet with low content of essential fatty acids were studied by osmotic sensitivity tests and spin labeling techniques. This diet induced significant modifications in acylglycerophosphocholine fatty acid composition with regard to 16 : 1, 18 : 1, 18 : 2 (n-6), 20 : 3 (n-9), and 20 : 4 (n-6). No changes in membrane fluidity as monitored by spin label motion were found but the diet caused an increased osmotic sensitivity in essential fatty acid deficient erythrocytes. 50% hemolysis was obtained at a 51.0% dilution of saline with H2O as compared to a 57.0% dilution for the control material. Membrane fluidity was unaffected by gamma-irradiation up to 80 krad.

ESR spectral analysis of the molecular motion of spin labels in lipid bilayers and membranes based on a model in terms of two angular motional parameters and rotational correlation times.

Electron spin resonance (ESR) spectral line shapes are calculated for a nitroxide spin-labeled molecule undergoing rapid restricted rotations (twisting) about its long molecular axis while simultaneously tumbling within a cone. Explicit expressions are derived for the hyperfine splittings and g-values, as well as for the secular contributions to the motionally modulated linewidths. The present model is useful for analyzing the restricted twisting and tumbling motions, and rotational correlation times, of spin-labeled molecules in bilayers. Simulated spectra compare well with experimental spectra of lecithin bilayers marked with cholestane spin label, over a wide temperature range.