Solitary rectal ulcer syndrome: findings at barium enema study and defecography

Sixteen cases of histopathologically proved solitary rectal ulcer syndrome were encountered. Fifteen patients underwent barium enema study; in nine cases the findings--including rectal stricture, granularity of the mucosa, and thickened rectal folds-were nonspecific. In six cases the study was normal. All patients had a long history of defecation disorders, and defecography was performed in all. In seven cases, intussusception of the rectal wall was seen; in another case the intussusception was accompanied by a rectocele. One case showed rectal prolapse. In four cases, failed relaxation of the puborectalis occurred and prevented the passage of the bolus; in another case there was abnormal perineal descent. In two patients studies were normal. In patients with defecation disorders, the possibility of this syndrome should be considered. Defecography is the method of choice for establishing the diagnosis.     

Initial lithium augmentation improves the antidepressant effects of standard TCA treatment in non-resistant depressed patients

The hypothesis was tested that an initial lithium-tricyclic antidepressant (TCA) combination has a better antidepressant effect than standard TCA treatment in non-refractory depression at the beginning of an episode. Twenty bipolar melancholic type depressed inpatients under lithium-TCA treatment were compared with 20 patients with the same diagnosis and TCA-placebo treatment for 5 weeks under double-blind conditions. All patients were male. Initial lithium-TCA treatment reduced depressive symptoms significantly more than antidepressant treatment with TCA and placebo after 5 weeks, but not in weeks 1 or 2. It can be concluded that lithium augmentation of TCA treatment should be started even at the beginning of antidepressant TCA treatment to provide a better treatment response in those patients who will profit from long-term lithium prophylaxis, e.g. bipolar patients with melancholic type depression.     

Endocrine pancreatic function during atrophy of the exocrine gland

Serum levels of glucose, insulin, and gastric inhibitory polypeptide (GIP) in response to intraduodenal and intravenous glucose loads have been examined in rats with exocrine pancreatic atrophy induced by feeding them a copper-deficient diet supplemented with D-penicillamine for 10-12 weeks. Whereas pancreatic weight and protein and trypsin content were drastically reduced as compared with pair-fed controls, insulin content was not significantly different between experimental (1.10 U) and control (1.40 U) rats. The intravenous glucose infusion was given in a dose (1.2 g/kg/h) simulating the glucose concentrations observed in response to an intraduodenal glucose load of 2.0 g/kg body weight. Both basal and stimulated insulin concentrations were lower in experimental animals as compared with controls. However, if the relative insulin response is considered, insulin secretion was almost identical in experimental and control animals. Both groups released significantly more insulin after intraduodenal glucose load than after intravenous glucose application. It is concluded that the entero-insular axis is intact in rats with exocrine pancreatic atrophy.     

Ethanol:water mutually enhanced transdermal therapeutic system. I: Nitroglycerin solution properties and membrane transport

The solution properties of aqueous ethanol donor solutions were characterized for the particular case of an increased flux nitroglycerin transdermal system. Permeation through porous and nonporous polymer membranes was investigated and modelled. While the permeation of ethanol through the porous membranes is adequately described by theory, clogging of pores occurs in the presence of lactose. Permeation through ethylene vinyl acetate membranes reflects interactions of the solute and solvent with the polymer.     

Attenuation of hemodynamic responses to rapid sequence induction and intubation in healthy patients with a single bolus of esmolol

The effectiveness of a single preinduction intravenous (IV) bolus of esmolol in blunting hemodynamic responses to rapid sequence induction and tracheal intubation was evaluated. In a randomized double-blind study, 32 ASA I and II healthy patients scheduled for surgery were monitored with electrocardiography (EKG) lead V5, arterial cannulation, and impedance cardiography. After preoxygenation and a priming dose of vecuronium (0.01 mg/kg), patients received either saline (n = 12), esmolol 100 mg (n = 10), or esmolol 200 mg (n = 10) as an IV bolus (20 ml volume). This procedure was immediately followed by a 5 ml IV saline flush, cricoid pressure, thiopental sodium 5 mg/kg, and succinylcholine 1.5 mg/kg. Patients receiving 200 mg of esmolol had a 50% reduction in the usual tachycardia associated with induction and a greater decline in systolic blood pressure (SP) (by 50%) prior to intubation as compared with the placebo group (p less than 0.05). The increase in diastolic blood pressure (DP) and the reduction in stroke volume (SV) produced by induction and intubation were similar in all the groups. Plasma norepinephrine levels at 1.5 minutes after intubation increased in the esmolol groups about 130% above that measured in the placebo group. This finding was associated with a more gradual return of peripheral resistance to baseline following tracheal intubation. However, both doses of esmolol effectively attenuated heart rate (HR), SP, and rate pressure product (RPP) increases (p less than 0.05 vs placebo) produced by laryngoscopy and tracheal intubation.     

Cysteine Conjugate beta-Lyase-Dependent Metabolism of Compound A (2-[fluoromethoxy]-1,1,3,3,3-pentafluoro-1-propene) in Human Subjects Anesthetized with Sevoflurane and in Rats Given Compound A

Background: Sevoflurane undergoes Baralyme- or soda lime-catalyzed degradation in the anesthesia circuit to yield compound A (2-[fluoromethoxy]-1,1,3,3,3-pentafluoro-1-propene), which is nephrotoxic in rats and undergoes metabolism via the cysteine conjugate beta-lyase pathway in those animals. The objective of these experiments was to test the hypothesis that compound A undergoes beta-lyase-dependent metabolism in humans.

Methods: Human volunteers were anesthetized with sevoflurane (1.25 minimum alveolar concentration, 3%, 2 l/min, 8 h) and thereby exposed to compound A. Urine was collected at 24-h intervals for 72 h after anesthesia. Rats, which served as a positive control, were given compound A intraperitoneally, and urine was collected for 24 h afterward. Human and rat urine samples were analyzed by19 F nuclear magnetic resonance spectroscopy and gas chromatography-mass spectrometry for the presence of compound A metabolites.

Results: Analysis of human and rat urine showed the presence of the compound A metabolites [S-[2-(fluoromethoxy)-1,1,3,3,3-pentafluoropropyl]-N-acetyl-L-cysteine, (E)- and (Z)-S-[2-(fluoromethoxy)-1,3,3,3-tetrafluoro-1-propenyl]-N-acetyl-L-cyst eine, 2-(fluoromethoxy)-3,3,3-trifluoropropanoic acid, 3,3,3-trifluorolactic acid, and inorganic fluoride. The presence of 2-(fluoromethoxy)-3,3,3-trifluoropropanoic acid and 3,3,3-trifluorolactic acid in human urine was confirmed by gas chromatography-mass spectrometry.