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Biomedical subjects

T S Harrison

Publications and source records attributed to T S Harrison.

At least 55 records · Page 3Linked to original sources
PubMed1983

HPLC for urinary catecholamines and metanephrines with alpha-methyldopa.

In five healthy selected volunteers with normal blood pressure and one pheochromocytoma patient, high performance liquid chromatography (HPLC) has been evaluated, with electrochemical detection for quantitation of urinary catecholamines and metanephrines during administration of the antihypertensive, alpha-methyldopa. The clinical usefulness of HPLC is compared with that of the conventional assay method--the trihydroxyindole (THI)-fluorometric procedure. The THI fluorometric method is known to suffer from true false-positive interference as a result of its inability to differentiate between alpha-methyldopa, its primary metabolic derivatives, and the structurally similar endogenous catecholamines. It is shown that the HPLC separation methodology yields accurate, reproducible results devoid of interference from the presence of alpha-methyldopa. Free urinary excretion rates of epinephrine, norepinephrine, and dopamine were elevated by alpha-methyldopa, P less than 0.001, for epinephrine, norepinephrine, and dopamine when measured by the trihydroxyindole technique but not with high performance liquid chromatography. With alpha-methyldopa treatment, urinary normetanephrine excretion rates were slightly increased, P less than 0.05, by fluorometric analysis and slightly decreased. P less than 0.05, when measured by HPLC. Of added interest, the formation of the normetanephrine analog of alpha-methyldopa, previously undetected, is suggested. Slightly elevated metanephrine levels are seen by the THI-fluorometric method in the presence of alpha-methyl metanephrines. Establishing that the HPLC assay procedure is suitable for clinical diagnosis of pheochromocytoma, despite the presence of alpha-methyldopa, makes it unnecessary to discontinue use of this antihypertensive in screening for pheochromocytoma.

Adult↗
PubMed1983

Malignant catecholamine-secreting carotid body paraganglioma.

The second known case of a malignant catecholamine-secreting (DA)-secreting carotid body paraganglioma is presented. Dopamine synthesis and secretion can be increased in malignant tumors derived from neural crest cells. Whether this is true, in addition, for extra-adrenal paragangliomas is not yet clear. Malignant paragangliomas of the carotid body and larynx, although rare, frequently have been accompanied by increased catecholamine secretion. Malignant catecholamine-secreting carotid body paragangliomas are best treated by composite resection (internal carotid artery and neck dissection), with special attention being given to measures preventing severe hypertension and arrhythmias in the perioperative period.

Adult↗
PubMed1983

Immunoreactive met-enkephalin in the canine adrenal; response to acute hypovolemic stress.

Immunoreactive met-enkephalin was measured in the adrenal, kidney, liver, and intestine of the dog using radioimmunoassay. Adrenal tissue concentrations were 20 to 200-fold higher than the other tissues studied. In response to acute hypovolemic stress, the concentration of met-enkephalin in the adrenal vein of the dog increased 6-fold over basal peripheral arterial levels. These results suggest that the canine adrenal gland is a rich source of this opioid peptide and that the adrenal releases met-enkephalin in response to acute stress.

Adrenal Glands↗
PubMed1982

Converting enzyme inhibition with captopril in patients with primary hyperaldosteronism.

The humoral and hemodynamic effects of converting enzyme inhibition captopril are presented in two patients with primary hyperaldosteronism (PHA). In all, 20 patients with resistant hypertension were treated with the angiotensin converting enzyme inhibitor captopril. In 18 patients with essential or renovascular hypertension mean (+/- SEM) plasma renin activity (PRA) rose from 5.0 +/- 1.4 to 35.3 +/- 5.3 ng/ml/hr (P less than 0.01) and mean (+/- SEM) plasma aldosterone (PA) declined from 25.8 +/- 2.9 to 15.1 +/- 1.9 ng/ml (P less than 0.01) after captopril. In two patients with PHA the PRA was not stimulated by converting enzyme inhibition, although there was modest decline in PA and a temporary reduction in blood pressure. After surgical removal of aldosterone-producing adenomas, PRA responsed appropriately to captopril. These cases illustrate that a disease process can modify the response to a drug and demonstrate that, in patients with PHA, captopril does not stimulate PRA, induces only minor decrements in PA, and is relatively ineffective as an antihypertensive.

Aldosterone↗
PubMed1981

Effect of prolonged exercise on plasma prostaglandin levels.

The effects of a strenuous marathon run of 42.2 kilometers on the presence of prostaglandins in blood was investigated in 24 healthy males and females. Testosterone, FSH, LH, epinephrine, norepinephrine, dopamine, T4 and T3 were also measured. With the exercise of the marathon run, a significant elevation of plasma PGE2, PGF2 alpha and 6 keto PGF1 alpha was observed in the runners following the race. Significant increases were also noted in blood catecholamine, dopamine and testosterone levels while a significant decline in the gonadotropins, FSH and LH was observed. No changes in thyroxine or tri-iodothyronine were noted.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Primary hyperparathyroidism: four- to eight-year postoperative follow-up demonstrating persistent functional insignificance of microscopic parathyroid hyperplasia and decreased autonomy of parathyroid hormone release.

Thirty-nine patients with primary hyperparathyroidism were studied four to eight years after their initial operation. In six patients, both the pathologist and surgeon agreed on the diagnosis of solitary adenoma; in 16 patients, the surgeon diagnosed solitary adenoma and the pathologist parathyroid hyperplasia (microscopic hyperplasia). In 16 patients, primary chief cell hyperplasia was agreed upon by the pathologist and surgeon. In the 16 patients with microscopic hyperplasia, there have been no long-term recurrences of hypercalcemia, but, in two patients, plasma parathyroid hormone levels are high. Parathyroid hormone--total calcium regression curves demonstrate significant preoperative correlation in solitary adenoma, p less than 0.01, and primary chief cell hyperplasia, p less than 0.05. After operation, significant correlations were not found between parathyroid hormone and total calcium. T-testing slope differences of pre- and postoperative parathyroid hormone--total calcium regression curves demonstrates a significant (p less than 0.01) shift to the right of the microscopic hyperplasia patients after operation, moving them to a broader range of total calcium per picogram parathyroid hormone. We conclude that 1) in primary hyperparathyroidism, positive regulation of total calcium by autonomously released parathyroid hormone exists in patients with solitary adenoma and chief cell hyperplasia; 2) autonomously functioning parathyroid tissue has been removed by operation for solitary adenoma with coexistent microscopic parathyroid hyperplasia. In this four- to eight-year follow-up period, it is clear that microscopic parathyroid hyperplasia is not associated with recurrent hypercalcemia. Two functionally distinct forms of parathyroid suppression are suggested; positively regulated microscopic hyperplasia and negatively regulated pathologically suppressed glands.

Adenoma↗
PubMed1980

Beta-2-Adrenergic stimulation of ornithine decarboxylase activity in porcine granulosa cells in vitro.

Epinephrine, norepinephrine, and isoproterenol produced dose-dependent stimulation of ornithine decarboxylase (EC 4.1.1.17) activity in isolated porcine granulosa cells maintained under defined conditions in vitro. beta- but not alpha-receptor-blocking agents prevented enzyme stimulation by catecholamines. Application of preferential beta-1 and beta-2-receptor antagonists and agonists localized the epinephrine effect to beta-2-adrenergic mediation. Epinephrine action was enhanced by the phosphodiesterase inhibitor, 1-methyl-3-isobutyl-xanthine, but not by saturating concentrations of the cyclic AMP analogue, 8-bromocyclic AMP, of follicle-stimulating hormone, or of prostaglandin E2. However, stimulation by epinephrine was additive to that of luteinizing hormone. Follicular fluid obtained from immature Graafian follicles contained concentrations of norepinephrine and epinephrine active in vitro. Thus, catecholamines may participate in the regulation of ornithine decarboxylase activity in the ovary. Catecholamine effects may be mediated by beta-2-receptors linked to the adenylate cyclase system.

1-Methyl-3-isobutylxanthine↗
PubMed1980

Pheochromocytoma. A persistently problematic and still potentially lethal disease.

Fifty patients with pheochromocytomas have had their conditions diagnosed and have been treated by these authors during a 13-year peneod. Three patients died in the postoperative period, for an overall mortality of 6%. Thirty-two patients underwent primary excision without fatality. Eighteen patients had more complicated illnesses associated with recurrences, notable other disease, acute catecholamine crisis, and/or pregnancy. All three postoperative deaths occurred in this group. Diagnosis was made by urinary catecholamine analysis of epinephrine, norepinephrine, metanephrine, and normetanephrine. Localization was done by plain films, ultrasonograms, computerized tomograms, radioactive isotope scans, intravenous pyelograms, caval samples, venograms, and arteriograms. Management of these complicated cases requires prompt and accurate diagnosis, availability of sophisticated methods of tumor localization, and thoughtful awareness of the potential outcome by an experienced team of surgeons and anesthesiologists.

Acute Disease↗
PubMed1980

Plasma norepinephrine, epinephrine, and thyroid hormone interactions in severely burned patients.

In this prospective study of thyroid catecholamine interactions, 15 severely burned patients were divided into two groups. Nine patients receiving 200 micrograms/day of triiodothyronine constituted the T3-treated group. Eight additional patients constituted the untreated group. Mean serum concentrations of T3 were significantly lower in the untreated group than in the treated group. Mean serum thyroxine (T4) concentrations were significantly higher in the untreated group than in the treated group. The mean plasma norepinephrine concentration in the untreated group was significantly greater than that of the treated group. In the untreated group, log plasma norepinephrine correlated inversely with serum T3. Similarly, in the untreated group, log plasma epinephrine correlated inversely with serum T3. Metabolic rates were not different between groups. These data suggest that a reciprocal relationship exists between plasma concentration of T3 and both norepinephrine and epinephrine in untreated burn patients and that treatment with the metabolically active hormone, triiodothyronine, does not alter the level of hypermetabolism accompanying thermal injury.

Adult↗
PubMed1980

Adrenal medullary epinephrine secretion: effects of cortisol alone and combined with aminoglutethimide.

Adrenal E synthesis is thought to require locally high glucocorticoid concentrations to induce the enzyme PNMT for methylation of NE. By suppressing ACTH secretion, exogenous glucocorticoids may limit secondarily adrenal medullary E production. AG, a competitive inhibitor of adrenal steroidogenesis, also may limit adrenal medullary E synthesis. In the present study, three groups of male beagles (mean wt. 9.45 kg) were studied with controlled endotracheal ventilation (98% O2/2% CO2) under Na pentobarbital anesthesia after a 2-week period during which group 1 (N = 4) received no drug, group 2 (N = 5) received C (0.5 mg/kg b.i.d.), and group 3 (N = 4) received C (0.5 mg/kg b.i.d.) and AG (20 mg/kg b.i.d.). Adrenal medullary secretions of E and NE were determined (single isotope radioenzymatic assay) at 15 min intervals over 1 hr basal period and 15 and 30 min following rapid hemorrhage to 50 mm Hg mean arterial pressure. Mean resting adrenal medullary E secretion of group 1 (0.576 +/- 0.181 (1 S.D.) micrograms/min) exceeded that of group 2 (C) (0.150 +/- 0.026 micrograms/min, p < 0.01) and group 3 (C and AG, (0.144 +/- 0.071 micrograms/min, p < 0.01). Maximum E secretion after hemorrhage was higher in group 1 (3.450 +/- 1.990 micrograms/min) than in group 2 (0.649 +/- 0.300 micrograms/min, p < 0.05) and group 3 (0.717 +/- 0.129 micrograms/min, p < 0.05). Highest measured E concentration after hemorrhage was also lower in treated groups (C, p < 0.01) (C and PG p < 0.01). C recipients also had suppressed resting and early reflex (p < 0.01) NE secretion. These results are consistent with the functional importance of the intimate anatomic relationship between the adrenal cortex and medulla. A defect in E-related adrenergic reflexes may occur in patients treated similarly to these experimental groups.

Adrenal Medulla↗
PubMed1979

Cage size and exercise affects infarct size in rat after coronary artery cauterization.

Left coronary occlusion in the rat was performed by cornary artery cauterization. A small amount of myocardial damage at the site of occlusion was noted, and myocardial infarction occurred in the distal distribution of the obstructed coronary. The effects of cage size and level of physical activity on estimated infarct size (as measured by creatine kinase depletion) 48 h after occlusion were determined. Isolation in small cages and moderate treadmill exercise resulted in an approximate doubling of the amount of infarction when compared to grouping of rats in large cages. Mild exercise did not increase infarct size. Total urinary catecholamines in normal rats placed in small cages for 48 h were elevated when compared to unconfined rats in larger cages. Cornary artery occlusion by cauterization is an easily performed technique. Cage size and level of activity (and their effects on sympathoadrenal function) are important independent determinations of infarct extent after coronary occlusion in the rat.

Animals↗
PubMed1978

Converting enzyme inhibition augments and competitive inhibition of angiotensin II partially restores reflex adrenal catecholamine release in anephric dogs.

Adrenal epinephrine (E) release after hemorrhage in anesthetized dogs is blunted by acute nephrectomy and restored by angiotensin II infusion. In the present study, we report the effect of converting enzyme inhibition by SQ 20881, a decapeptide, and of competition inhibition of angiotensin II by saralasin (1-Sar-8-Ala-Ang-II) on reflexly stimulated adrenal release of E and norepinephrine (NE) in three groups of acutely anephric dogs. Aortic catheters and adrenal vein to femoral vein Silastic shunts were placed in dogs anesthetized with pentobarbital and mechanically ventilated. Adrenal secretion rates were calculated from adrenal vein to aorta catecholamine concentration differences divided by measured adrenal venous flow. Catecholamine concentrations were determined with trihydroxyindole technique. Blood samples were obtained before and 15, 30, and 60 min after rapid hemorrhage to a stable mean arterial pressure of 50 mm Hg. Saralasin infusion (10 microgram/kg/min) supported adrenal E release in anephric hemorrhaged dogs toward secretion rates comparable to those seen in intact dogs. Anephric SQ 20881 (approximately 0.5 microgram/kg) recipients had delayed (60 min) augmented adrenal E and NE release after hemorrhage. In resting animals not reflexly stimulated by hypovolemia, neither drug provoked adrenal E or NE release. These results suggest an agonist effect of saralasin on reflex adrenal E release and increased responsiveness of the stimulated adrenal medulla under the influence of converting enzyme inhibition.

Adrenal Medulla↗