Comparison of postoperative complications following conventional latissimus dorsi flap versus muscle-sparing latissimus dorsi flap breast reconstruction.

INTRODUCTION: Breast reconstruction is becoming increasingly important in the management of breast cancer. Among breast reconstruction with flap, latissimus dorsi flap is the most frequent technique used in France. Lipofilling's emergence led to changes for using latissimus dorsi flap in breast reconstruction. The aim of this study was to compare postoperative complications following conventional latissimus dorsi (CLD) flap versus muscle-sparing latissimus dorsi (MSLD) flap breast reconstruction. MATERIALS AND METHODS: Data from 96 patients, who underwent CLD flap or MSLD flap breast reconstruction, were retrospectively collected from January 2018 to December 2019 in Georges-Francois Leclerc Cancer Center in France. Uni- and multivariate analyses, using a logistic regression, were performed to define operative factors and postoperative morbidity associated with surgical technique and evaluate whether MSLD flap could be associated with less postoperative outcome. RESULTS: After univariate analysis, factors significantly associated with MSLD flap were reduced surgical time (p<0.001), reducing seroma and punctures (p<0.001), postoperative complications of donor site (p=0.09), and a shorter length hospital stay (p<0.001). After multivariate analysis, a shorter length hospital stay was significantly associated with the muscle-sparing group (OR=0.47, 95% CI (0.30-0.73), p<0.001). DISCUSSION: This is the first French study comparing postoperative complications following the two techniques of latissimus dorsi flap breast reconstruction. In this study, the hospital stay was significantly decreased with MSLD flap compared with the CLD flap breast reconstruction. Both seem to be reliable methods with few complications.

SL25.1131 [3(S),3a(S)-3-methoxymethyl-7-[4,4,4-trifluorobutoxy]-3,3a,4,5-tetrahydro-1,3-oxazolo[3,4-a]quinolin-1-one], a new, reversible, and mixed inhibitor of monoamine oxidase-A and monoamine oxidase-B: biochemical and behavioral profile.

SL25.1131 [3(S),3a(S)-3-methoxymethyl-7-[4,4,4-trifluorobutoxy]-3,3a,4,5-tetrahydro-1,3-oxazolo[3,4-a]quinolin-1-one] is a new, nonselective, and reversible monoamine oxidase (MAO) inhibitor, belonging to a oxazoloquinolinone series. In vitro studies showed that SL25.1131 inhibits rat brain MAO-A and MAO-B with IC50 values of 6.7 and 16.8 nM and substrate-dependent Ki values of 3.3 and 4.2 nM, respectively. In ex vivo conditions, the oral administration of SL25.1131 induced a dose-dependent inhibition of MAO-A and MAO-B activities in the rat brain with ED50 values of 0.67 and 0.52 mg/kg, respectively. In the rat brain, duodenum, and liver, the inhibition of MAO-A and MAO-B by SL25.1131 (3.5 mg/kg p.o.) was reversible, and the recovery of MAO-A and MAO-B activities was complete 16 h after administration. SL25.1131 (3.5 mg/kg p.o.) increased tissue levels of dopamine (DA), norepinephrine, and 5-hydroxytryptamine and decreased levels of their deaminated metabolites 3,4-dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxyindolacetic acid. In mice, SL25.1131 induced a dose-dependent potentiation of 5-hydroxytryptophan-induced tremors and phenylethylamine-induced stereotypies with ED50 values of 0.60 and 2.8 mg/kg p.o., respectively. SL25.1131 was able to reestablish normal striatal dopaminergic tone and locomotor activity in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mice. In addition, when coadministered with L-DOPA, SL25.1131 increased the available DA in the striatum and the duration of L-DOPA-induced hyperactivity. The duration of the effect of L-DOPA on circling behavior in 6-hydroxydopamine-lesioned rats was also increased. The neurochemical profile of SL25.1131 demonstrates that this compound is a mixed, potent, and reversible MAO-A/B inhibitor in vitro, in vivo, and ex vivo. SL25.1131 has therapeutic potential as a symptomatic treatment during the early phase of Parkinson's disease and as an adjunct to L-DOPA therapy during the early and late phases of the disease.

Effects of infused sodium acetate, sodium lactate, and sodium beta-hydroxybutyrate on energy expenditure and substrate oxidation rates in lean humans.

Infusion of sodium acetate in lean humans results in a decrease in respiratory exchange ratio, which may be advantageous in patients with respiratory failure. However, this potential decrease in respiratory work was observed to be offset by significant thermogenesis. The metabolic effects of sodium acetate, sodium lactate, and sodium beta-hydroxybutyrate, infused at a rate of 20 mumol.kg-1.min-1 for 3 h, was monitored in six healthy human volunteers. Respiratory exchange ratio decreased from 0.85 +/- 0.02 at baseline to 0.75 +/- 0.02, 0.75 +/- 0.02, and 0.80 +/- 0.02, after acetate, lactate, or beta-hydroxybutyrate, respectively (P < 0.05 for each). Acetate produced a larger thermic effect (22.7% of energy infused) than did lactate (16.3%) or beta-hydroxybutyrate (13.6%). Thus, sodium salts of organic acids may potentially decrease the respiratory requirements by decreasing the respiratory exchange ratio. However, this effect is partially offset by the thermic effect of these substrates. The maximal doses and safety of these anions during larger infusion periods remain to be determined.

Metabolic and respiratory effects of infused sodium acetate in healthy human subjects.

The metabolic and respiratory effects of intravenous 0.5 M sodium acetate (at a rate of 2.5 mmol/min during 120 min) were studied in nine normal human subjects. O2 consumption (VO2) and CO2 production (VCO2) were measured continuously by open-circuit indirect calorimetry. VO2 increased from 251 +/- 9 to 281 +/- 9 ml/min (P < 0.001), energy expenditure increased from 4.95 +/- 0.17 kJ/min baseline to 5.58 +/- 0.16 kJ/min (P < 0.001), and VCO2 decreased nonsignificantly (211 +/- 7 ml/min vs. 202 +/- 7 ml/min, NS). The extrapulmonary CO2 loss (i.e., bicarbonate generation and excretion) was estimated at 48 +/- 5 ml/min. This observation is consistent with 1 mol of bicarbonate generated from 1 mol of acetate metabolized. Alveolar ventilation decreased from 3.5 +/- 0.2 l/min basal to 3.1 +/- 0.2 l/min (P < 0.001). The minute ventilation (VE) to VO2 ratio decreased from 22.9 +/- 1.3 to 17.6 +/- 0.9 l/l (P < 0.005), arterial PO2 decreased from 93.2 +/- 1.9 to 78.7 +/- 1.6 mmHg (P < 0.0001), arterial PCO2 increased from 39.2 +/- 0.7 to 42.1 +/- 1.1 mmHg (P < 0.0001), pH from 7.40 +/- 0.005 to 7.50 +/- 0.007 (P < 0.005), and arterial bicarbonate concentration from 24.2 +/- 0.7 to 32.9 +/- 1.1 (P < 0.0001). These observations indicate that sodium acetate infusion results in substantial extrapulmonary CO2 loss, which leads to a relative decrease of total and alveolar ventilation.