Biomedical subjects
Publications and source records attributed to R A Stone.
A patient receiving polymyxin B sulfate intravenously for Gram-negative "anion gap". Both abnormalities resolved following discontinuation of the drug. In vitro investigation suggested that the electrolyte abnormalities resulted from the polycationic properties of polymyxin B.
We investigated the possibility that variability in classification of patients with essential hypertension into low, normal, or high renin activity subgroups depends on the subject preparation that precedes the measurement of plasma renin activity (PRA). In 47 essential hypertensives, PRA was measured with patients supine and ambulatory who were receiving both an unrestricted dietray sodium intake and a low sodium diet. Additionally, PRA was determined following salt restriction, oral furosemide therapy, and ambulation. These results were compared, using several analytical techniques, to those of a group of age-, race-, and sex-matched normotensive controls. Extreme variability in classification was the rule, with only 28% of patients consistently classified as having normal PRA. No single approach provided maximal detection of both the low and high renin states. We conclude that renin classification of hypertensive patients requires a matched control population and that subtyping appears to be variable depending on diet, posture, and analytical approach.
Changes in hemodynamic variables and plasma renin activity (PRA) induced by short-term alteration of blood pressure and sympathetic nervous system activity were studied in normotensive and hypertensive men on high-sodium and low-sodium intake. Blood pressure and heart rate alterations caused by standard cold pressor tests, amyl nitrite inhalation, phentolamine infusion, and phenylephrine infusion were recorded. PRA was measured at time 0, 5, 15, and 30 min. No change in PRA occurred in either group following cold pressore test and amyl nitrite inhalation. Phenylephrine suppressed PRA in normal but not hypertensive subjects, and phentolamine elevated PRA in normotensive and hypertensive subjects regardless of diet. Short-term stimulation of the sympathetic nervous system does not appear to elevate PRA in man. Suppression of PRA by an alpha agonist was not observed in hypertensives and may reflect barorecptor insensitivity in this group of subjects.
Sixteen patients with increased intraocular pressure (over 20 mm Hg) received 25 and 50 mg of oral methazolamide, twice daily, during consecutive weeks and then 500 mg (Sequels) of acetazolamide. The two methazolamide regimens produced significant decreases in intraocular pressure. Acetazolamide treatment resulted in a greater decrease in intraocular pressure but more systemic acidosis and side effects.
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We investigated the relationship of the kallikrein-kinin system and the renin-angiotensin system in the regulation of blood pressure, salt and water excretion, and renal blood flow. Normotensive and hypertensive black and white men were studied during unresticted sodium intake as well as on a 10-meq/day sodium intake; potassium intake was held constant throughout the study (80 meq/day). During unrestricted sodium intake, urinary kallikrein activity was greater in white normotensives than white hypertensives or black normotensives. There was no difference (P greater than 0.05) between white and black hypertensives or between black normotensives and black hypertensives. All groups had greater urinary kallikrein activity on low sodium vs. unrestricted sodium intake, but the increase in black hypertensives was small, and they excreted significantly less kallikrein than the ogher groups on the low sodium diet. Plasma renin activity showed similar increments after sodium restriction in all groups. Urinary kallikrein activity correlated with renal blood flow in all groups except the black normotensives on low sodium intake. Renal blood flow could be correlated uniformly with log (urinary kallikrein activity/supine plasma renin activity) in all groups on either diet. Urinary sodium and potassium excretion and urine volume were not different among the groups. We conclude: (a) important racial differences exist in urinary kallikrein activity that are unrelated to sodium or potassium excretion or urine volume; (b) dietary sodium restriction further delineates racial differences and suggests alternative pathophysiologic mechanisms for huma hypertension; (c) urinary kallikrein activity correlates with renal blood flow; and (d) our data support the concept that the kallikrein-kinin system and the renin-angiotensin system contribute to the regulation of renal blood flow and may account for racial differences in renal vascular resistance.
Four patients have been studied with maintenance hemodiafiltration. The predominant finding to date has been better control of blood pressure. The mechanism(s) for this improved blood pressure control are under study.
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We conducted a six-month trial to determine the effect of psychologic relaxation on blood pressure. Alterations of peripheral sympathetic-nervous-system activity, as reflected by changes of dopamine-beta-hydroxylase in plasma, were evaluated, and plasma volume and plasma renin activity were measured. Treated patients exhibited significant (P less than 0.05) reductions of blood pressure when supine and upright, and of plasma dopamine-beta-hydroxylase activity, and furosemide-stimulated renin activity when upright. Blood-pressure changes after six months correlated best with differences in plasma activity of dopamine-beta-hydroxylase with patients supine (r = 0.54; P less than 0.05) and upright (r = 0.62; P less than 0.05). These results suggest that reduction of peripheral adrenergic activity contributes importantly to the improvement of hypertension observed with this form of therapy. Furthermore, the decrease of furosemide-stimulated plasma renin activity suggests that alterations of the renin-angiotensin system may help lower blood pressure in certain patients.
An atypical case of neuroblastoma is described, in which the diagnosis was facilitated by the application of a new biochemical procedure, the assay of plasma dopamine-beta-hydroxylase activity. This laboratory tool is proposed as a useful adjunct to established techniques in the diagnosis of neural crest tumors.
A 14-month-old boy had a microphthalmic left eye. An anterior chamber paracentesis was performed six days after examination under anesthesia. Lactic acid dehydrogenase (LDH) level in the aqueous humor was 1,158 mu and was 202 mu in the serum. The aqueous humor/serum LDH ratio was 5.73. This eye was eventually enucleated and found to have retinal dysplasia and diffuse hemorrhagic necrosis. There was no eividence of retinoblastoma. The elevated LDH level in aqueous humor was probably secondary to the ocular tissue necrosis and hemorrhage. This false-positive result emphasizes the limitation of using the aqueous humor/serum LDH ratio to distinguish eyes with retinoblastoma from those without retinoblastoma.
Plasma dopamine-beta-hydroxylase (DbetaH) activity, a marker of catecholamine secretion that occurs via exocytosis, was determined preoperatively in eight patients with phaeochromocytoma. Despite very elevated urinary catecholamine concentrations, mean plasma DbetaH activity was 32-6 +/- 3 u/l and was not significantly different from apparently healthy subjects. Seven days after surgery, one subject exhibited a 60% postoperative decrease of enzyme activity. These results suggest that diffusion across plasma membranes is the predominant mechanism of catecholamine release from phaeochromocytomas. The postoperative change in one patient suggests tumour heterogeneity and that exocytosis may contribute to the process of catecholamine release in some patients.
Previous investigations have suggested that significant hypotension during hemodialysis may result from abnormalities of sympathetic nervous system activity. To further evaluate these phenomena, plasma dopamine beta-hydroxylase (D beta H) and cold pressor test (proposed indexes of efferent sympathetic nervous system activity) and amyl nitrite inhalation (an index of the entire baroreceptor reflex arc) were studied in two groups of patients: group I, patients exhibiting a mean arterial pressure decrease to less than 70 mm Hg during less than 10% of dialyses; group II (hemodialysis hypotension), patients with a mean arterial pressure decrease to less than 70 mm Hg during more than 90% of dialyses. The groups were similar with respect to plasma renin activity, renin response to ultrafiltration, age, duration of dialysis, nerve conduction velocity, plasma protein concentration, hematocrit, dialysis weight change, resting heart rate, sex, race, blood pressure and heart rate response to cold pressor test, and 125I-albumin plasma volume. Supine mean arterial pressure was higher in patients with hemodialysis hypotension than in patients without hemodialysis hypotension (group I) both before and after dialysis. Plasma D beta H activity was significantly higher in patients with hemodialysis hypotension (group II) than in group I both before and after dialysis. Amyl nitrite inhalation, expressed as change in delta R-R interval/mean arterial pressure decrease, was less in hemodialysis hypotension patients. These results suggest that hemodialysis hypotension may result from a lesion in the baroreceptors, cardiopulmonary receptors, or visceral afferent nerves. Furthermore, elevated mean arterial pressure in patients with hemodialysis hypotension may be neurogenic in origin, as reflected by plasma D beta H activity, and appears similar to the hypertension that follows baroreceptor deafferentation of experimental animals.
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A patient developed a renal venous thrombosis 15 months after renal transplantation. In contrast to other cases described in the literature, the thrombosis was not related to vascular surgical trauma, but was immune-complex mediated. The patient's renal function stabilized and the nephrotic syndrome improved over 18 months follow-up during continuous oral anticoagulant therapy.
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