Drugs
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Randomized Controlled Trial Clinical Trial
The use of roxatidine acetate in fasting patients prior to induction of anaesthesia as prophylaxis against the acid aspiration syndrome.
Aspiration pneumonitis is one of the major causes of anaesthesia related deaths. H2-receptor antagonists are effective drugs for the prevention of the acid aspiration syndrome (Mendelson's syndrome). The new long-acting H2-receptor antagonist roxatidine acetate may be the first H2-receptor antagonist which could effectively reduce acid secretion following a single bedtime premedication on the evening before an operation. ⋯ The mean gastric volume in the placebo group was 23.3 +/- 27.1 ml, compared to 14.5 +/- 9.4 ml for roxatidine acetate. The 5 highest gastric volumes were observed in the placebo group (max 146 ml). A single bedtime oral premedication with roxatidine acetate 150 mg ensures a gastric pH above 2.5 until 11 am the following day.
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Randomized Controlled Trial Comparative Study Clinical Trial
Effects of roxatidine acetate on 24-hour gastric acidity. Early evening versus bedtime administration in healthy subjects.
The gastric antisecretory activity of roxatidine acetate was studied on 24-hour intragastric pH in 12 healthy male volunteers. The study was randomised, double-blind and double-dummy where either roxatidine acetate 150 mg as a slow release granulated formulation or placebo were administered at 7.30 pm or 10 pm. ⋯ There was no significant difference between the median intragastric pH values for early evening and bedtime administration of roxatidine acetate. The present data confirm that roxatidine acetate 150 mg inhibits gastric acid secretion but while a single evening dose is effective in controlling intragastric pH the results suggest there is no clear advantage in an early evening dose compared with a bedtime dose.
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Randomized Controlled Trial Clinical Trial
The pharmacodynamics and pharmacokinetics of multiple doses of the new H2-receptor antagonist, roxatidine acetate, in healthy men.
Roxatidine acetate (HOE 760, TZU 0460) is a new H2-receptor antagonist which is more potent than cimetidine and ranitidine. A randomised, double-blind, placebo-controlled study was conducted in healthy men to determine the effects of multiple oral doses of roxatidine acetate on unstimulated gastric acid secretion, and to assess the preliminary multiple-dose pharmacokinetics of its active desacetyl metabolite. The subjects were randomised to receive either roxatidine acetate 150 mg or placebo daily at 9 pm for 14 days. ⋯ The gastric pH increased with the mean plasma concentrations of the desacetyl metabolite. Mean plasma levels at steady state were attained between the 4th and 7th days after which there was no evidence of appreciable accumulation of the desacetyl metabolite. Roxatidine acetate 150 mg administered orally at 9 pm for 14 days to healthy men was safe, well tolerated, and produced clinically relevant increases in gastric pH, and decreases in gastric acid concentration, without affecting gastric fluid volume.
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Randomized Controlled Trial Clinical Trial
Electrocardiographic and enzymatic infarct size in a randomised study of intracoronary streptokinase and intravenous anisoylated plasminogen streptokinase activator complex in acute myocardial infarction.
The effect of thrombolytic therapy on ECG and enzymatic indices, including estimates of relative infarct size, was studied in 93 patients with acute myocardial infarction randomised to intracoronary streptokinase or intravenous anisoylated plasminogen streptokinase activator complex (APSAC) therapy within 6 hours of the onset of symptoms. 90 minutes after treatment, 49% (19/39) of the evaluable streptokinase patients and 44% (19/43) of the APSAC patients had reperfused (p = NS). The time from treatment to reperfusion was less in the streptokinase patients (30 +/- 18 minutes for streptokinase and 42 +/- 22 minutes for APSAC, p less than or equal to 0.02). Resolution of ST segment elevation, 90 minutes after treatment, was greater in the streptokinase patients (residual ST segment elevation 47 +/- 36% of initial value for streptokinase and 70 +/- 49% for APSAC, p less than or equal to 0.06) and in the patients reperfused by either agent (residual ST segment elevation 46 +/- 34% for reperfused and 68 +/- 52% for non-reperfused, p less than or equal to 0.10). ⋯ However, the time to peak enzyme levels was significantly shorter in the reperfused patients. Early intracoronary streptokinase and intravenous APSAC therapy have similar effects on ECG and enzymatic infarct size. Reperfusion by either agent, given at a mean of 3 hours 25 minutes, may reduce estimates of infarct size modestly.
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Randomized Controlled Trial Comparative Study Clinical Trial
Comparison of intravenous anisoylated plasminogen streptokinase activator complex with intracoronary streptokinase in acute myocardial infarction.
In a randomised trial the efficacy and safety of anisoylated plasminogen streptokinase activator complex (APSAC) administered intravenously and streptokinase administered by intracoronary infusion were compared in patients with proven acute myocardial infarction. Occlusion of the infarct-related vessel, reperfusion and reocclusion were all assessed angiographically. ⋯ These results indicate that APSAC (30U intravenously) is as effective as intracoronary streptokinase (250,000U). The major advantages of APSAC in acute myocardial infarction are its rapid, convenient administration and its low rate of arterial reocclusion.