ABSTRACT
Intrathoracic gastric herniation after laparoscopic antireflux surgery is a rare but well known phenomenon. It may occur during the early and late postoperative period. We report on a patient with early onset of dysphagia after surgery due to a tight wrap. Subsequent vomiting and dysphagia increased due to a gastric herniation. After gastroscopy and bougienage, tension pneumothorax developed. The context and relationships are illustrated and discussed referring to the current literature.
Subject(s)
Deglutition Disorders/etiology , Dyspnea/etiology , Fundoplication , Hernia, Hiatal/diagnostic imaging , Hernia, Hiatal/surgery , Laparoscopy , Pneumothorax/diagnostic imaging , Postoperative Complications/etiology , Stomach Diseases/diagnostic imaging , Deglutition Disorders/diagnostic imaging , Deglutition Disorders/surgery , Dilatation , Dyspnea/diagnostic imaging , Dyspnea/surgery , Esophageal Perforation/diagnostic imaging , Esophageal Perforation/surgery , Esophageal Stenosis/diagnostic imaging , Esophageal Stenosis/etiology , Esophageal Stenosis/surgery , Esophagoscopy , Hernia , Humans , Male , Middle Aged , Pneumothorax/surgery , Postoperative Complications/diagnostic imaging , Postoperative Complications/surgery , Radiography , Reoperation , Stomach Diseases/surgery , Surgical Wound Dehiscence/diagnostic imaging , Surgical Wound Dehiscence/surgeryABSTRACT
Inhibitory effects of the class III antiarrhythmic compound D/L-sotalol on acetylcholinesterase (AChE; EC 3.1.1.7) isoenzymes of both erythrocytes and the human caudate nucleus and on serum cholinesterase (ChE; EC 3.1.1.8) were studied in vitro using a spectrophotometric kinetic assay with acetylthiocholine (ASCh) as substrate. Sotalol concentrations in the assays varied from 0.32 to 3.2 mM. All isoenzymes studied were inhibited by D/L-sotalol in a reversible and concentration-dependent manner. Double reciprocal plots of the reaction velocity against varying ASCh concentrations revealed that D/L-sotalol reduced substrate affinity (apparent Michaelis constant, KM, increased) of serum ChE, but did not change the enzyme's maximal rate of ASCh hydrolysis (Vmax). Thus, D/L-sotalol inhibition of serum ChE was of the competitive type (rate constant for reversible competitive inhibition: Ki = 0.51 mM). In contrast, D/L sotalol reduced the maximal reaction velocity of the AChE isoenzyme from the central nervous system (caudate nucleus), but had no influence on substrate affinity of the enzyme (KM with ASCh unchanged) indicating purely non-competitive inhibition kinetics (rate constant of reversible non-competitive inhibition: Ki = 0.44 mM). D/L-sotalol inhibition of erythrocyte AChE was of mixed competitive/non-competitive type (Ki = 0.31 mM, Ki = 0.49 mM). Non-competitive D/L-sotalol inhibition of caudate nucleus AChE and the non-competitive component of erythrocyte AChE inhibition cannot be overcome by increased concentrations of the cholinergic transmitter acetylcholine (ACh). Peak D/L-sotalol plasma levels as described in the literature for both humans (15 microM) and experimental animals (dogs: 18 microM; rats: 260 microM) as well as maximal myocardial concentrations of the substance (dogs: 46 microM; rats: 478 microM) are in the range of about 2% to 100% of the sotalol inhibition rate constants determined in the present paper for cholinesterase isoenzymes in vitro. Thus, D/L-sotalol inhibition of ACh hydrolysis in vivo may contribute to both the well known antiarrhythmic potential and proarrhythmic side effects of the compound.
