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Biomedical subjects

H R Keiser

Publications and source records attributed to H R Keiser.

At least 145 records · Page 8Linked to original sources
PubMed1982

Circulatory, plasma catecholamine, cortisol, lipid, and psychological responses to a real-life stress (third molar extractions): effects of diazepam sedation and of inclusion of epinephrine with the local anesthetic.

We studied the circulatory, psychological, plasma catecholamine, cortisol, and lipid responses to a real-life stress--third molar extractions--in 21 patients and the effects of sedation with intravenous diazepam and of inclusion of epinephrine with the local anesthetic. Across all patients, the surgery was associated with significantly increased heart rate (25%), systolic blood pressure (13%) and cardiac output--as indicated using impedance cardiography (34%)--without a significant change in diastolic blood pressure. Plasma norepinephrine increased by 60% during the surgery in nonsedated patients. Diazepam sedation abolished the norepinephrine response to the surgery, without significantly affecting the heart rate or systolic pressure responses. Receipt of epinephrine with the local anesthetic resulted in a fivefold increase in mean plasma epinephrine 5 min after the injection, as well as increased cardiac output. The direct effect of epinephrine accounted for the cardiac output increase observed during the surgery. The results suggest the participation of the sympathetic nervous system in producing the circulatory responses to dental surgery. The elimination of sympathetic recruitment by diazepam-induced sedation, however, without concomitant reductions in heart rate or systolic pressure responses, suggests that other systems besides the sympathetic nervous system influence the circulatory response to this real-life stress.

Adolescent↗
PubMed1982

Localization of functional adrenal tumors by computed tomography and venous sampling.

Fifty-eight patients with functional lesions of the adrenal gland underwent radiographic evaluation. Twenty-eight patients had primary aldosteronism (Conn syndrome), 20 had Cushing syndrome, and 10 had pheochromocytoma. Computed tomography (CT) correctly identified adrenal tumors in 11 (61%) of 18 patients with aldosteronomas, 6 of 6 patients with benign cortisol-producing adrenal tumors, and 5 (83%) of 6 patients with pheochromocytomas. No false-positive diagnoses were encountered among patients with adrenal adenomas. Bilateral adrenal hyperplasia appeared on CT scans as normal or prominent adrenal glands with a normal configuration; however, CT was not able to exclude the presence of small adenomas. Adrenal venous sampling was correct in each case, and reliably distinguished adrenal tumors from hyperplasia. Recurrent pheochromocytomas were the most difficult to localize on CT due to the surgical changes in the region of the adrenals and the frequent extra-adrenal locations.

Adenoma↗
PubMed1982

Effect of bradykinin on renal function in dogs treated with indomethacin or propranolol.

The effect of bradykinin (BK) on renal function was examined in anesthetized dogs with or without treatment with either indomethacin or propranolol. Renal arterial infusion of BK (3 micrograms/min) in control dogs produced a sustained increase in urine flow rate (V), sodium excretion (UNaV), potassium excretion (UKV), and renal plasma flow (RPF) without a consistent change in glomerular filtration rate (GFR) or renin secretion rate (RSR). This increase in salt and water excretion and in RPF could not be blocked with indomethacin (5 mg/kg, followed by 2.1-3.2 mg/kg/h, i.v.). UNaV was 20.8 +/- 7.4 and 123.3 +/- 22.3 muEq/min (mean +/- SEM values) before and after 140 min of infusion of BK (p less than 0.005), respectively. Beta-receptor blockade with propranolol (5 mg/kg, followed by 2.8-3.4 mg/kg/h, i.v.) did not prevent the BK-induced rise in salt and water excretion, or in RPF. UNaV was 26.0 +/- 9.7 and 96.4 +/- 21.5 muEq/min before and after 140 min of infusion of BK (p less than 0.005), respectively. The data suggest that the effects of BK on renal handling of salt and water and on RPF are not mediated by either prostaglandins or beta receptors.

Animals↗
PubMed1982

Comparison of techniques for measuring baroreflex sensitivity in man.

Because discrepancies about baroreflex sensitivity in essential hypertension may have resulted from the use of different measurement techniques, we assessed the extent to which the results of different techniques agree in the same subjects. The eight techniques studied were the change in RR interval per unit change in systolic pressure during the Valsalva maneuver, upon release of the Valsalva maneuver, after injection of phenylephrine and after injection of nitroglycerin; the changes in RR interval and in systolic pressure per mm Hg externally applied neck suction; and the changes in RR interval and systolic pressure per mm Hg externally applied neck pressure. The average intercorrelation among these measures in 30 subjects was statistically significant (r = 0.36, p less than 0.01), but suggests that variance in one measure accounted for an average of about 13% of the variance in other measures. Standard deviations among subjects were often as large as the mean, indicating important interindividual variability as well. These findings demonstrate that baroreflex sensitivity varies widely among subjects and that different techniques for measuring baroreflex sensitivity probably measure different aspects of baroreflex function.

Adult↗
PubMed1982

Effects of restriction of sodium or administration of fludrocortisone on parotid salivary kallikrein in man.

Urinary kallikrein is increased by restriction of dietary sodium and by administration of fludrocortisone, a sodium-retaining steroid. In order to determine whether salivary kallikrein responds similarly, we studied 16 normal volunteers after 1-week periods of daily intake of 9, 109, and 259 mEQ of sodium; 10 subjects were studied after addition of 0.6 mg/day fludrocortisone for a week to a regimen of 109 mEq/day sodium. During sodium restriction, parotid saliva had a significantly higher mean concentration of kallikrein ad potassium and a significantly lower concentration of sodium than during periods of intake of 109 or 259 mEq/day sodium. Sodium restriction also caused significantly higher urinary excretion of kallikrein and aldosterone. Salivary amylase remained unchanged during the three sodium periods. Administration of fludrocortisone significantly increased the mean concentration of parotid kallikrein and excretion of urinary kallikrein in comparison with control levels, however the concentrations of parotid sodium and potassium did not change significantly. Four patients studied before and after removal of aldosterone-producing adenomas each showed decreased concentrations of parotid kallikrein and potassium and increased concentrations of parotid sodium after surgery. It is concluded that both salivary and urinary kallikrein increased in response to restriction of sodium and that these increases were mediated by levels of sodium-retaining steroid. Increased output of kallikrein in response to increased levels of sodium-retaining steroid may be a generalized response of organs that contain glandular kallikrein and can conserve sodium.

Adenoma↗
PubMed1981

Validity of liquid chromatography with electrochemical detection for measuring dopamine in human plasma.

We tested the validity of liquid chromatography with electrochemical detection (LCEC) for measuring dopamine levels in human plasma, by adding known amounts of dopamine standard to human plasma, and by comparison with levels obtained using the catechol-O-methyltransferase radioenzymatic (COMT-RE) assay technique. The correlation between the obtained dopamine concentrations and picograms of added standard was 1.00 and the correlation between the two assay techniques across 32 plasma samples was 0.97. These results demonstrate that LCEC validly measures human plasma dopamine.

Catechol O-Methyltransferase↗
PubMed1981

Physiologic mechanisms opposing the hemodynamic effects of prazosin.

Prazosin was give for 10 to 14 days to eight hypertensive patients on a fixed intake of dietary salt. Except as limited by side effects, the dose was increased from 2 mg/day to a maximum dose of 24 mg/day. During treatment, when subjects were studied in supine and upright positions, mean arterial pressure (MAP) fell 6% and 12% (p less than 0.025 and p less than 0.005), heart rate rose 3% and 9% (p less than 0.05 and p less than 0.005), and plasma norepinephrine increased 95% and 107% (p less than 0.01 and p less than 0.001) over control. Daily excretion of the norepinephrine metabolites methoxyhydroxyphenyl glycol (MHPG) and vanillylmandelic acid (VMA) increased 42% and 17% (p less than 0.05 for each) during treatment. There were no changes in average body weight or plasma renin for the group, but patients whose body weight increased tended to show less reduction in blood pressure (correlation coefficient, r = 0.72, p less than 0.05) and smaller increases in heart rate (r = -.073, p less than 0.05) during treatment with prazosin. These data suggest that expansion of extracellular fluid and activation of the sympathetic nervous system oppose the hemodynamic effects of prazosin.

Adult↗
PubMed1981

Renal vasoactive hormones in scleroderma (progressive systemic sclerosis).

Plasma renin activity and the urinary excretions of kallikrein, kinin, immunoreactive PGE (iPGE) and aldosterone were determined in 23 patients with progressive systemic sclerosis (PSS) on a fixed sodium and potassium intake who had no clinically apparent renal disease. Urinary excretions of kallikrein and kinin in the PSS patients were not significantly different from those of a group of sex and race-matched normal controls. In the female PSS patients urinary excretion of iPGE was also found to be normal. Upright PRA was appropriate for the urinary sodium excretion in 18 PSS patients (13 normotensive and 5 hypertensives) but was significantly elevated in the remaining 5 (all normotensive). The data suggest that the renal kallikrein-kinin and prostaglandin systems are unaltered in PSS patients without clinical evidence of renal disease.

Adult↗
PubMed1981

Effects of catechol estrogen infusions upon gonadotropin and prolactin concentrations in men.

To study the effects of catechol estrogens upon gonadotropin secretion, 2-hydroxyestrone (2-OHE1) and 2-hydroxyestradiol (2-OHE2) were administered iv to young adult men in a range of doses for 4 days. Blood samples were obtained for plasma LH, FSH, and PRL at 20-min intervals for 6 h before and at the end of the infusion period. 2-OHE1 had no effect upon gonadotropins or PRL in doses up to 1.6 mg/day; at 3.2 and 6.6 mg/day, it produced a slight suppression of LH and FSH, with no change in PRL. 2-OHE2 was generally ineffective at 100 micrograms/day, but doses from 200-800 micrograms/day suppressed gonadotropins, without changes in PRL. These infusions elevated 2-OHE1 and 2-OHE2 plasma levels to values comparable to those measured in late pregnancy. There were no associated effects upon blood pressure and only minimal changes in urinary catecholamine excretion. No effects that could be interpreted as antiestrogenic were observed. These results are consistent with the hypothesis that circulating catechol estrogens behave as weak estrogens in men.

Adult↗
PubMed1980

Prostaglandin F-2 alpha functions as a local hormone on human airways.

Vasoactive hormones may be classified either as 'local' or as 'circulating', depending on whether they are or are not removed by the pulmonary circulation. Prostaglandin F-2 alpha is partially removed by the human pulmonary circulation. We examined the hypothesis that, with respect to the human lung, PGF-2 alpha functions as a local mediator. Prostaglandin F-2 alpha was given to normal and asthmatic subjects via both intravenous and aerosolized routes, and we measured specific airway conductance, spirometry, functional residual capacity, and closing volume. Aerosolized PGF-2 alpha induced significant changes of all measured parameters in both normals and asthmatics, while intravenous PGF-2 alpha-induced changes were limited to the FVC in both normals and asthmatics. The data suggest that intravenous PGF-2 alpha induced constriction of peripheral lung units. The greater sensitivity of the peripheral lung units of asthmatics versus normals to PGF-2 alpha, suggest that the increased sensitivity of airway smooth muscle of asthmatics versus normals to PGF-2 alpha is not restricted to the conducting airways, but extends to the smooth muscle of the peripheral lung units. The data is consistent with the hypothesis that, with respect to the lung, PGF-2 alpha functions as a local hormone, but, furthermore, suggest that, possibly of greater importance than the definition of a hormone as 'local' or 'circulating', is the definition of the intrinsic properties of the muscles on which the hormone is exerting its effects.

Adolescent↗
PubMed1980

Regulation of prostaglandin E2 synthesis by angiotensin II, potassium, osmolality, and dexamethasone.

We investigated the regulation of cellular prostaglandin E2 (PGE2) biosynthesis in rabbit renomedullary interstitial cells in tissue culture. Arachidonic acid markedly stimulated PGE2 biosynthesis by these cells. Repeated exposure to arachidonic acid, resulted in progressively less stimulation of PGE2 biosynthesis. Potassium and dexamethasone diminished PGE2 biosynthesis by decreasing the rate of arachidonic acid release from the endogenous arachidonic acid storage pool. Hyperosmolality, like angiotensin II, bradykinin, and arginine vasopressin, stimulated PGE2 biosynthesis by increasing the rate of arachidonic acid release. Inhibitors of protein synthesis diminished angiotensin II-, bradykinin-, and arginine-vasopressin-stimulated PGE2 biosynthesis by decreasing hormone-stimulated arachidonic acid release. The effects of potassium, dexamethasone, arachidonic acid, and hyperosmolality on PGE2 biosynthesis were unaffected by protein synthesis inhibitors. Hormone-stimulated phospholipase activation is dependent on protein synthesis, whereas potassium, hyperosmolality, and dexamethasone alter the release of arachidonic acid from cellular lipids via a mechanism that is independent of protein synthesis.

Angiotensin II↗
PubMed1980

The kallikrein-kinin system in essential hypertension.

The kallikrein-kinin system is a potent vasodilator system with components in plasma and in exocrine glands, including the kidney. Kinins function as local hormones and exert effects on blood vessels and on water and electrolyte balance. The most frequently studied component of this system, urinary kallikrein, has been shown to respond to changes in sodium-retaining steroid activity and in renal blood flow. Urinary kallikrein is subnormal in patients with either essential or renovascular hypertension and supranormal in patients with primary aldosteronism or Bartter's Syndrome. The changes in the kallikrein-kinin system appear to be secondary to changes in blood pressure or in other vasoactive systems: i.e., kinins appear to attenuate the vasoconstrictor effects of angiotensin and stimulate the vasodilator actions of the prostaglandins. The kallikrein-kinin system is altered in hypertension, however, its role in this disease remains unclear.

Adult↗