Biomedical subjects
Publications and source records attributed to E H Prosnitz.
Green urine, a well described condition, can be caused by a variety of agents. Here we describe a case of green urine caused by blue food colouring during tube feeding. In the article, we list more than 20 drugs, chemical agents and microorganisms which have been associated with green urine.
A 31-y-old epileptic man developed coma and shock after suicidally ingesting large amounts of valproic acid and gabapentin. His peak valproic acid, level was 1306.9 micrograms/mL (therapeutic range = 30-100 micrograms/mL). His peak gabapentin level was 60.0 micrograms/mL (therapeutic range = 2.0-8.0 micrograms/mL). His hypotension was refractory to crystalloid and pressor infusions, but resolved during concurrent hemoperfusion and hemodialysis to enhance elimination of valproic acid. Concurrent hemoperfusion and hemodialysis, in series, produced a maximum valproic acid plasma clearance of 55.4 mL/min versus a maximum reported intrinsic valproic acid plasma clearance of 10.6 mL/min. concurrent hemoperfusion and hemodialysis, in series, should be considered in hemodynamically unstable patients with valproic acid poisoning whose clinical condition is worsening in spite of aggressive supportive care.
The success of digital video subtraction angiography (DVSA) in screening hypertensive patients for renal artery stenosis and the apparent value of percutaneous transluminal angioplasty (PTA) prompted re-evaluation of the philosophy of indiscriminate medical therapy for newly discovered cases of hypertension. DVSA was diagnostic in 87% of cases. The cost of screening for renovascular hypertension by DVSA and treatment by PTA when feasible is about the same as that of medical therapy. Considering the problems of noncompliance and drug side effects associated with medical antihypertensive therapy, DVSA screening for renovascular hypertension in a broader population seems both medically and economically sound.
The effects of theophylline upon cardiovascular function were studied in 8 male subjects, aged 22-33 years, before and during concomitant administration of metoprolol (50 mg every 6 h) and propranolol (40 mg every 6 h). Theophylline, as aminophylline (6.7-7.3 mg/kg) was given over 30 min. The theophylline level five minutes after completion of the aminophylline infusion was 15.9 +/- 1.8 micrograms/ml in the absence of beta blockade, 16.1 +/- 1.7 micrograms/ml during metoprolol, and 15.1 +/- 1.6 micrograms/ml during propranolol. Theophylline produced a 7% increase in mean arterial pressure which was not attenuated by either metoprolol or propranolol. Heart rate was not changed by theophylline. The QS2 Index (QS2I), a sensitive indicator of inotropism, was shortened from 488 +/- 16 to 476 +/- 16 msec (p less than 0.01) by theophylline alone. After administration of metoprolol or propranolol, theophylline produced no shortening of the QS2I. Theophylline has a mild inotropic effect in healthy subjects. This effect is prevented by pretreatment with beta-adrenergic antagonists.
Hypertension in the elderly may be of the classical or isolated systolic type. The former is amenable to therapy, and reduction in blood pressure clearly decreases morbidity and mortality. Isolated systolic hypertension is an undesirable risk factor, but the effectiveness of antihypertensive therapy for the problem is as yet unknown. Although various physiologic parameters change with age, diuretics, methyldopa, and beta-adrenergic blockers are generally safe in the elderly and are recommended.
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The effect of decreases in renal sympathetic nerve activity on renal tubular sodium reabsorption was examined in anesthetized dogs. Reflex decreases in renal sympathetic nerve activity were produced by left atrial distention and stellate ganglion stimulation. Both interventions produced significant decreases in directly recorded efferent renal sympathetic nerve activity of 42 and 36%, respectively. With renal perfusion pressure held constant, neither glomerular filtration rate nor renal blood flow were significantly altered, but significant and reversible increases in urine flow and sodium excretion occurred. These studies demonstrate that reflex decreases in efferent renal sympathetic nerve activity result in decreases in renal tubular sodium reabsorption without changes in renal hemodynamics.
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Bilateral carotid artery occlusion results in an increase in mean arterial pressure, an increase in renal sympathetic nerve activity, and a redistribution of renal blood flow from inner to outer cortex. To elucidate the mechanism of the renal blood flow redistribution, carotid artery occlusion was performed in anesthetized dogs with the left kidney either having renal perfusion pressure maintained constant (aortic constriction) or having alpha-adrenergic receptor blockade (phenoxybenzamine); the right kidney of the same dog served to document the normal response. When renal perfusion pressure was maintained constant, renal blood flow distribution (microspheres) was unchanged by carotid artery occlusion. In the presence of renal alpha-adrenergic receptor blockade, carotid artery occlusion elicited the usual redistribution of renal blood flow from inner to outer cortex. The redistribution of renal blood flow observed after carotid artery occlusion is mediated by the increase in renal perfusion pressure rather than the increase in renal sympathetic nerve activity.
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