The role of the family nurse practitioner.
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Biomedical subjects
Publications and source records attributed to E Doyle.
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An oral dose of 14C-bupranolol hydrochloride was well absorbed by humans (100 mg), dogs (1 mg/kg), and rhesus monkeys (1 mg/kg). These species excreted 87.8 and 3.5%, 81.1 and 13.6%, and 92.9 ad 5.0% of the 14C-dose in urine and feces, respectively, mainly in 12 or 24 hr. Mean plasma levels of 14C, which appeared to be almost entirely associated with a single metabolite, peaked at 1 hr in humans (1.6 micrograms-equiv./ml) and dogs (1.6 micrograms-/ml) and at 2 hr in monkeys (0.8 micrograms-equiv./ml). Concentrations initially declined with similar half-lives (about 1.5 hr) in all three species. Biliary excretion of 14C occurred in the animal species in which also peak plasma 14C levels exceeded those in most tissues. Unchanged bupranolol was not detected in plasma; the peak plasma and urinary 14C was mainly associated (greater than 90% in humans) with a metabolite produced by oxidation of the aromatic ring methyl group of bupranolol to a carboxyl group.
A 15 month old black male who developed near fatal intravascular hemolysis two days after repair of an ostium primum septal defect with a teflon patch is presented. One month after initial operation, reoperation was required for control of hemolysis. At that time a piece of pericardium was placed over the underendothelialized left atrial side of the patch and the mitral cleft was repaired. He initially did well but within several days developed mitral regurgitation. Hemolysis recurred two months postoperatively, but then spontaneously subsided. We propose that the recurrent mitral insufficiency created a defect in the pericardial patch and that caused recurrent hemolysis. Normal endothelial ingrowth probably covered this small defect and hemolysis subsided. Following the second hemolytic episode six months ago, the patient continues to do well.
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