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Biomedical subjects

R Fraser

Publications and source records attributed to R Fraser.

At least 307 records · Page 17Linked to original sources
PubMed1981

Pre-operative localization of aldosterone-secreting adrenal adenomas.

Techniques for pro-operative localization of aldosterone-secreting adrenal adenomas were studied in thirty-seven patients, each with hypertension and biochemical evidence of primary hyperaldosteronism and each later having adrenal surgery (thirty-two adenomas, five bilateral hyperplasia). Bilateral adrenal vein catheterization was attempted in all cases; it was successful on the left side in all patients and in 92% of cases on the right. Adrenal vein plasma samples were obtained from the left side in 92% and from the right in 73% of cases. Adrenal vein plasma aldosterone measurements correctly indicated the presence of tumour in twenty-eight cases but falsely predicted unilateral adenoma in two cases of bilateral adrenal hyperplasia. Adrenal venography also correctly predicted unilateral adrenal adenomas in twenty-six cases but falsely suggested the presence of tumour in three cases of bilateral adrenal hyperplasia. Computed tomography (CT) was used in the last eight cases. In seven instances the predictions (six adenomas, one bilateral adrenal hyperplasia) were confirmed at surgery. However, the remaining patient harboured an adenoma 20 mm in diameter which was not detected by CT although diagnosed both by adrenal venography and adrenal vein aldosterone measurements. Ultrasound detected adenoma in only three of twenty-two cases examined. Although further comparative studies of the type described here are required, the results of computed tomography are promising and suggest that this non-invasive technique might well become the first choice procedure in localizing aldosterone-secreting adenomas.

Adenoma↗
PubMed1981

The renin-angiotensin system and aldosterone in hypertension: a brief review of some aspects.

The biochemistry of the renin-angiotensin system has been outlined. The relationship between plasma angiotension II levels, basal or raised as a result of infusion, and blood pressure and aldosterone has been explored in normal human subjects and animals, showing how these relationships can be modified by changes in sodium status and duration of exposure to high circulating levels of the octapeptide. Finally, the relationship has been examined in different categories of hypertensive disease, such as essential hypertension.

Aldosterone↗
PubMed1980

The role of radiation therapy in the management of ocular reticulum cell sarcoma.

Nine patients with ocular lymphomas were seen in the Department of Ophthalmology and the Division of Radiation Oncology at UCSF and Ralph K. Davies Medical Center, San Francisco, from 1978 through 1974. Six of the 9 patients had visual symptoms as the first manifestation of their disease. Eight of the 9 patients developed intracranial lymphoma at some time during the course of the disease. Despite lymphoma work-up including bone marrow biopsies and lymphangiogram, only 1 patient was found to have documented systemic involvement. The diagnosis of ocular lymphoma was based on pathologic material from the eye in 5 cases or from central nervous system biopsy in 4 patients in association with tumor cell infiltrates in the retina and vitreous clouding. Radiation therapy to the eyes improved vision in 10 of 13 eyes treated in 8 patients. The usual dose was in the range of 3500 to 4500 rads given over 4-5 weeks. In addition, 7 patients received central nervous system irradiation. Review of the literature reinforced the findings of this series showing the frequent association of ocular lymphoma with intracranial lymphoma and the rare systemic dissemination. This disease process has previously been referred to as ocular reticulum cell sarcoma.

Adult↗
PubMed1980

Amiloride, spironolactone, and potassium chloride in thiazide-treated hypertensive patients.

Dose-response curves for amiloride and spironolactone were defined in 15 hypertensive patients treated with bendroflumethiazide (bendrofluazide). The relative potency amiloride:spironolactone in correcting hypokalemia was 2.8:1, an estimate significantly lower than the 5:1 potency currently accepted. The relative potency for reduction of plasma sodium was 3.9:1 (amiloride:spironolactone). Amiloride was disproportionately potent in lowering serum bicarbonate, and the data do not suggest that these drugs elevate plasma potassium simply by correcting metabolic alkalosis. Changes in blood pressure were confounded by the presence of carryover effect between treatment phases. Both drugs increased plasma angiotension II and aldosterone, but the rise in aldosterone with spironolactone was smaller than expected from concurrent plasma angiotension II and potassium concentrations. This was consistent with a partial block of aldosterone biosynthesis by spironolactone. The activity of spironolactone did not require the presence of hyperaldosteronism. In a smaller study potassium chloride induced a significant log dose-response on plasma potassium, but the effect was small in absolute terms. At least 64 mmole potassium chloride was needed to match the effect of 20 mg amiloride or 56 mg spironolactone.

Adult↗
PubMed1980

Increased 18-hydroxycorticosterone responses to frusemide in essential hypertension.

Plasma concentrations of angiotensin II (AII), aldosterone, 18-hydroxycorticosterone and cortisol were measured in seven patients with benign essential hypertension and in seven age-matched control subjects before, and at frequent intervals for 2 h after the intravenous injection of frusemide (40 mg). In the normal subjects, significant increases in the plasma levels of AII, aldosterone and 18-hydroxycorticosterone were apparent from 15 min after diuretic administration. The integrated responses of each hormone to frusemide administration were calculated. Aldosterone and AII responses to the diuretic were closely related, although three hypertensive patients had normal integrated aldosterone responses despite subnormal increases in the plasma concentrations of AII. The integrated 18-hydroxycorticosterone responses were greater in the hypertensive (median 970 nmol.h h-(1).1-(1)) than in the normal subjects (median 180 nmol.h-(1).1-(1)), P<0.05. Some patients with a raised blood pressure appear to have an enhanced adrenal corticosteroid response to frusemide; this probably reflects an increased sensitivity to angiotensin II.

18-Hydroxycorticosterone↗
PubMed1980

Captopril in clinical hypertension. Changes in components of renin-angiotensin system and in body composition in relation to fall in blood pressure with a note on measurement of angiotensin II during converting enzyme inhibition.

The effect of the converting enzyme inhibitor captopril on arterial pressure, the components of the renin-angiotensin-aldosterone system, and body sodium and potassium content was studied in eight hypertensive patients with renal artery stenosis and, in conjunction with diuretics, in seven patients with hypertension unresponsive to previous treatment. Two hours after the first dose, captopril caused significant falls in systolic and diastolic pressures, plasma angiotensin II, and aldosterone, with converse increases in angiotensin I and both active and total renin; the initial fall in diastolic pressure was significantly related to the drop in plasma angiotensin II. The biochemical changes were sustained during prolonged treatment, even when diuretics were added. One untreated patient with renal artery occlusion had severe secondary aldosterone excess, was sodium and potassium depleted, and severely hyponatraemic and hypokalaemic; captopril restored blood pressure, plasma electrolyte concentrations, and exchangeable sodium and total body potassium to normal. In one man with renal artery stenosis and overall renal impairment captopril led to sodium retention, and blood pressure did not fall until a diuretic was added. In the remaining patients with renal artery stenosis, pretreatment renin, angio tensin II, and aldosterone concentrations were either normal or only modestly raised, and plasma electrolyte concentrations and body content of sodium and potassium were normal. Captopril alone controlled arterial pressure in all, three cases showing a gradual fall of pressure over the first six weeks of treatment; no significant changes in exchangeable sodium or total body potassium were seen. The group of patients with previously intractable hypertension were all controlled with a combination of captopril and diuretic.

Aldosterone↗
PubMed1980

Severe hypokalaemia with paralysis induced by small doses of liquorice.

A patient, who presented with a flaccid quadriplegia due to profound hypokalaemia, is described. Hypokalaemia and myoglobinuria were caused by the ingestion of small amounts of liquorice contained in a laxative preparation. Subsequent controlled administration of small amounts of this preparation induced marked hypokalaemia. This was associated with sodium retention and potassium loss confirming a mineralocorticoid-like action. The sodium retention was associated with suppression of plasma levels of renin and aldosterone.

Aged↗
PubMed1980

Influence of sodium balance on ACTH/adrenal corticosteroid dose-response curves in the dog.

In order to define short-term ACTH/corticosteroid dose-respone characteristics, we infused ACTH for 1 h at each of five incremental rates into pedigreed male beagle dogs in four different states of sodium balance. Progressive sodium depletion was associated with progressive increased in basal (pre-ACTH) plasma levels of renin, angiotensin II, aldosterone, 18-hydroxycorticosterone (18-OH-B), and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC). Administration of dexamethasone significantly reduced the preinfusion levels of cortisol, aldosterone, 18-OH-B, and 18-OH-DOC. The threshold dose of ACTH required to elicit an aldosterone response during low-sodium intake was similar to that for cortisol, but was higher during normal or high-sodium intake. Steepest portions of the dose-response curves were at lower rates of ACTH infusion for cortisol than for aldosterone, and maximum increment was much greater for cortisol (60-fold) than for aldosterone (12-fold). Whereas the slopes of ACTH/aldosterone and ACTH/18-OH-B dose-response curves were steepened by lower sodium diets, the ACTH/cortisol response was significantly flattened by severe sodium depletion. We conclude that ACTH is a potent and direct-acting short-term regulator of aldosterone secretion, subject to modification by altered sodium balance.

Adrenal Cortex Hormones↗
PubMed1980

Damage of rat liver sinusoidal endothelium by ethanol.

Hepatic blood in normal rats is separated from the space of Disse and hepatocytes by an ultrastructural sieve formed by pores in the sinusoidal endothelium. This sieve has previously been shown to shield hepatocytes from circulating chylomicrons, the largest of the lipoproteins, which transport most triglycerides of dietary origin. In the present paper it has been shown that the chronic ingestion of ethanol leads to a significant enlargement of pores within the sieve, increasing them from a normal median diameter of 100 nm to 120 nm. A decrease in the normal sieving of perfused labelled large and small chylomicrons has also been noted. It is postulated that the decreased shielding of hepatocytes from large chylomicrons may be a factor in the pathogenesis of alcoholic fatty liver.

Animals↗
PubMed1980

Angiotensin II and renal hypertension in dog, rat and man: effect of converting enzyme inhibition.

The role of the renin-angiotensin system in the pathogenesis of one-clip, two-kidney hypertension has been studied in man, dog and rat. Particular attention has been paid to peripheral plasma concentrations of angiotensin II in different circumstances; angiotensin II infusion has been combined with radioimmunoassay to construct angiotensin II/blood pressure dose-response curves. The effect of converting enzyme inhibitors has been studied, precautions being taken to avoid obtaining falsely high values for plasma angiotensin II because of cross-reaction with angiotensin I in these circumstances. The initial phase of one-clip, two-kidney hypertension is attributable to the direct pressor effect of the immediate rise in plasma angiotensin II. Subsequently, plasma angiotensin II is relatively lower, although blood pressure remains high. This upward resetting of the plasma angiotensin II/blood pressure relationship can be mimicked by infusing angiotensin II chronically at low dose. After reconstruction of a stenosed renal artery, or excision of a post-stenotic kidney, the angiotensin II/blood pressure relationship returns slowly to normal. In this second phase of one-clip, two-kidney hypertension, the long-term administration of saralasin, or of converting enzyme inhibitor, can also return arterial pressure to normal; brief administration of these drugs is less effective or ineffective. The results are compatible with, although they do not conclusively establish, an important slow pressor action of the renin-angiotensin system in the second phase of one-clip, two-kidney hypertension. This provides a rational basis for the use of captopril clinically in this condition.

Adult↗
PubMed1980

The acute effect of angiotensin II on adrenal and anterior pituitary function in normal subjects and subjects with primary hyperaldosteronism.

Previous studies have shown that infused angiotensin II acutely suppresses ACTH release. In normal human subjects, the response to angiotensin II infused alone is specific to aldosterone and 18-hydroxycorticosterone. Other compounds such as cortisol, corticosterone and DOC do not respond. This is transformed into a general adrenocortical response by infusing small, constant quantities of ACTH. In patients with primary hyperaldosteronism, a poor response of plasma aldosterone to angiotensin II infused alone was altered to a response comparable with that in normal subjects by supplying ACTH during the infusion. Aldosterone secretion is more sensitive to ACTH in cases of primary hyperaldosteronism than in normal subjects. The poor response to angiotensin infusion may have been caused by inhibition of ACTH release, a phenomenon shown to occur in normal human subjects.

Adrenal Glands↗
PubMed1980

High perfusion pressure damages the sieving ability of sinusoidal endothelium in rat livers.

Fenestrated endothelium lining liver sinusoids forms an ultrastructural sieve between blood and hepatocytes which at physiological perfusion pressures has previously been shown to shield hepatocytes from large triglyceride-rich chylomicrons. In the study reported in this paper, enlargement of endothelial fenestrae at high perfusion pressures has been confirmed and a concurrent increase in trapping of large chylomicrons by the liver noted. These findings suggest the importance of employing physiological perfusion pressures in studies designed to examine hepatic lipoprotein metabolism and also suggest a possible mechanism in the pathogenesis of fatty change seen in the "nutmeg" liver of chronic venous congestion.

Animals↗
PubMed1979

T and B lymphocytes in patients with acute anterior uveitis and ankylosing spondylitis, and in their household contacts.

During episodes of acute anterior uveitis, patients had a T-lymphopenia and a temporary increase in B-lymphocytes. The T-lymphopenia was not present in patients investigated early in their first attacks, and it persisted after the patients recovered clinically. In household contacts of patients with uveitis, there was a temporary T-lymphopenia. A similar degree of T-lymphopenia was present in patients with ankylosing spondylitis who had not had uveitis, but not in their household contacts. In patients with spondylitis, there was no greater reduction of T-cells when they had episodes of uveitis. In all groups of subjects studied, T-lymphopenia could be abolished, in vitro, with thymosin, a bovine thymic-hormone estract. The finding of T-lymphocyte depletion in the contacts of uveitis patients, as well as in the patients themselves, suggests that there may be lateral transmission of an infective agent (or agents) in the households during (or before) attacks of uveitis.

Acute Disease↗
PubMed1979

Hyponatraemic hypertensive syndrome with renal-artery occlusion corrected by captopril.

Malignant hypertension with severe hyponatraemia, hypokalaemia, depletion of sodium and potassium, and elevated blood levels of renin, angiotensin I, angiotensin II, aldosterone, and arginine vasopressin developed in a woman with renal-artery occlusion. Plasma angiotensin II was disproportionately high in relation to exchangeable sodium. Captopril, by inhibiting conversion of angiotensin I to angiotensin II, further elevated the blood levels of renin and angiotensin I but corrected all other abnormalities. Unilateral nephrectomy was subsequently curative.

Aldosterone↗