Influence of phenformin on gastric emptying rate.
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Biomedical subjects
Publications and source records attributed to J R Ryan.
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Double-blind administration of a single intramuscular dose of 1.5, 2.0, 2.5, or 3.0 mg levonantradol or placebo to 56 patients with moderate to severe postoperative or trauma pain showed significant analgesic effects of each dose of levonantradol as compared to placebo (P less than 0.05). However, no significant dose response was observed. Compared to 2/16 patients on placebo, 23/40 patients (57 per cent) on levonantradol reported one or more side effect. Drowsiness was most frequent. Dry mouth, dizziness, "weird dreams," mild hallucinations, nervousness, apprehension and confusion occurred less frequently. Changes in resting heart rate and blood pressure were minor and general acceptability was good.
The enantiomers of indacrinone (I), an investigational loop diuretic, have different pharmacologic activity. The (-) enantiomer is natriuretic, and the (+) enantiomer is uricosuric. To determine the antihypertensive effects and an isouricemic ratio of indacrinone enantiomers, 37 patients with sitting diastolic blood pressure (BP) between 90 and 104 mm Hg, after a 4-week placebo washout, randomly received one of the ratios of I enantiomers, namely -2.5/+80 mg (A), -5/+80 mg (B), -10/+80 mg (C) or placebo (P), once daily for 12 weeks in a double-blind, parallel study. The mean reductions (baseline-end of treatment) in BP of 23/8, 20/10 and 25/10 mm Hg with treatments A, B and C respectively were greater (p less than 0.01) than that on P (0/3). Initially, serum uric acid decreased with treatments A and B but not with C. Mean changes in serum uric acid were -0.3, -0.4, 0.2 and 0.3 mg/dl respectively with treatments A, B, C and P. The ratio of -10/+80 mg produced least variation in serum uric acid. Reduction in serum K+ and Cl- appeared to be dose related to (-) enantiomer. No serious adverse effects were reported. A 1:9 ratio of I enantiomers intended for wide-scale use as a diuretic also showed good antihypertensive activity, a favorable uric acid profile and absence of hepatic toxicity in 14 patients.
A single-dose, double-blind, randomized, parallel trial was conducted to compare the analgesic efficacy of oral ibuprofen (I) 100, 200, or 400 mg, aspirin (ASA) 650 mg, and placebo in moderate to severe pain after extraction of impacted teeth. Subjective, self-evaluated pain intensity and pain relief reports, hourly for 6 hours, were used as indexes of analgesic response. Data on 227 evaluable patients showed significant differences among the 4 active treatments and placebo (p less than 0.001) by most measurements of analgesia. Although no consistent, significant differences were observed among the active drugs, I 400 mg performed the best, followed by I 200 mg, ASA 650 mg, and I 100 mg. Remedication was required by 59% patients receiving I 400 mg, 67% taking I 200 mg, 73% taking ASA 650 mg, 74% taking I 100 mg, and 96% receiving placebo. Differences between I 400 mg and I 100 mg were significant for remedication data (p less than 0.05). Side effects were minor, infrequent, and not dose related. In this study, I 100 mg was distinctly superior to placebo and probably as effective as ASA 650 mg in relieving pain. Only a shallow dose response of ibuprofen was observed.
The anticholinergic effects of single doses of terfenadine, chlorpheniramine and atropine on salivary flow were compared with those of placebo in a double-blind crossover study in 21 normal adults. Salivary flow was measured immediately before administering study medications and 3 h after dosing, for the evaluation of anticholinergic activity. Mean salivary flow decreased significantly after administration of chlorpheniramine and atropine (P less than 0.01 and P less than 0.001, respectively), and was unchanged by terfenadine and placebo, indicating that terfenadine does not possess detectable anticholinergic activity. Mild drowsiness was reported by 57% and 29% of subjects who received chlorpheniramine and terfenadine, respectively.
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Duodenogastric reflux (DGR) as seen on hepatobiliary scintigraphy has been reported as a useful secondary sign for the diagnosis of acute cholecystitis. We evaluated the association of reflux with cases of acute cholecystitis as compared to those with chronic cholecystitis or other conditions. Thirty-six of 198 patients referred for hepatobiliary imaging showed DGR (18%). Among 26 patients with acute cholecystitis, 6 (23%) had DGR as compared to 9/40 (23%) cases with chronic cholecystitis, 3/12 cases with acute pancreatitis, 4/13 cases with previous cholecystectomy, and 3/8 cases with duodenal ulcer. No statistically significant differences were found between the prevalence of DGR in cases with acute cholecystitis and those with chronic cholecystitis or other nonacute cholecystitis diagnostic categories. Although acute cholecystitis is a condition frequently associated with DGR, such reflux is a nonspecific finding and should not be considered as a secondary sign of acute cholecystitis when interpreting hepatobiliary scans.
To evaluate the response during insulin-induced hypoglycemia, diabetics treated with relatively selective or nonselective beta-adrenergic blocking agents were studied. Placebo, atenolol (100 mg/day), and propranolol (80 mg b.i.d.) were administered to 12 insulin-treated diabetics for 1 week in a double-blind, randomized, crossover fashion with a 2-week washout between treatments. Sufficient intravenous insulin (0.2-0.6 units/kg) was administered to decrease plasma glucose 68% from the basal level or to less than 60 mg/dl within 90 minutes. Blood pressure changes at the nadir of plasma glucose were +15.2/-9.9 mm Hg for placebo, +27.9/0 mm Hg for atenolol, and +38.8/+14.3 mm Hg for propranolol. Diastolic blood pressure changes induced by propranolol were significantly different from those induced by atenolol (p less than 0.01) and placebo (p less than 0.01), and systolic pressure changes were significantly different (p less than 0.02) between propranolol and atenolol. Mild seizures developed in two patients treated with propranolol. Their blood pressure changes at the plasma glucose nadir were +56/+22 and +86/+31 mm Hg. Other symptoms of hypoglycemia were more frequent during beta-blocker than during placebo treatment. Differences in response may be related to the relatively selective adrenergic blocking effect of these drugs.