J Leyba | PubMed Health

PubMed2001

Colostomy closure using local anesthesia.

The feasibility of performing colostomy closures using local anesthesia was evaluated. The subjects comprised 14 patients: 2 with colostomies involving a mucous fistula and 12 with loop colostomies. Patients who had colostomies with mucous fistulas separated by 10cm or more were excluded from this study. All patients were graded as ASA 1 (according to the American Society of Anesthesiologists). The bowel was evaluated by colonoscopy in 6 patients and by barium enema in 8 patients. Bowel preparation was performed with Colayte and all patients were given prophylactic antibiotics. Closure of the colostomy was extraperitoneal and the time taken to perform the operation ranged from 40 to 120min. Tolerance was regarded as excellent in 9 patients, good in 3, and average in 2. There were 3 anastomotic leaks that resolved without further surgical treatment, 2 wound infections, and 1 bowel obstruction that was successfully treated with medication. Patients were discharged 2-22 days postoperatively, after a mean period of 9 days. Local anesthesia offers a safe and effective alternative to general or regional anesthesia for surgical closure of colostomies.

Adolescent↗

PubMed1992

Characterization of proteolipid protein fatty acylesterase from rat brain myelin.

A protein fatty acylesterase activity that catalyzes the removal of fatty acid from exogenous proteolipid protein (PLP) has been demonstrated in isolated rat brain myelin. Optimum enzyme activity for the deacylation of PLP was obtained in 0.5% Triton X-100, 1 mM dithiothreitol at pH 7.0 and at 37 degrees C. Other detergents (octyl beta-D-glucoside, Nonidet P-40, and Tween 20) have little or no effect, whereas deacylation was completely abolished by 0.1% sodium dodecyl sulfate or boiling the membrane fraction for 5 min prior to incubation. Under optimal conditions, the rate of deacylation was linear up to 20 min, and the apparent Km for bovine [3H]palmitoyl-PLP was 18 microM. The myelin-associated PLP fatty acylesterase has no apparent requirements for divalent cations (Ca2+, Mg2+, Mn2+), and chelators such as EDTA, [ethylenebis(oxyethylenenitrilo)] tetraacetic acid, and 1,10-phenantroline have little or no effect on enzyme activity. Sulfhydryl and histidine residues are needed for full enzyme activity, whereas the "active serine"-directed inhibitor phenylmethylsulfonyl fluoride has no effect. The myelin-associated protein fatty acylesterase was present throughout brain development and in all myelin subfractions, in agreement with the dynamic metabolism of PLP-bound fatty acids. Enzyme activity was also present in sciatic nerve, brain cortex, and heart whereas liver was devoid of activity. Several esterases, including phospholipase A2, glyoxalase II, and acetylcholinesterase, did not remove fatty acid from PLP. Myelin basic protein, palmitoyl-CoA hydrolase, and myelin-associated nonspecific esterase were also ruled out as the PLP fatty acylesterase. Thus, all data seem to indicate that this enzyme is different from esterases of the lipid metabolism. Finally, stimulation of protein phosphorylation with Ca2+, but not with cyclic-AMP, inhibited PLP deacylation, suggesting that the myelin-associated protein fatty acylesterase activity is regulated by endogenous Ca(2+)-dependent protein kinases.

Acylation↗