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Biomedical subjects

R V Jackson

Publications and source records attributed to R V Jackson.

71 records · Page 4Linked to original sources
PubMed1983

Factors affecting the frequency of occurrence of spironolactone bodies in aldosteronomas and non-tumorous cortex.

Histological sections taken from aldosterone-producing-adenomas and from non-tumorous adrenal cortex of 18 patients treated for primary aldosteronism by unilateral adrenalectomy were examined for spironolactone inclusion bodies. Typical inclusions were found in 10 of the 13 patients who received spironolactone up to within 24 h of surgery. They were present in the tumours of 7 patients, and their frequency correlated positively with the percentage of glomerulosa type cells in the tumours. In tumours containing 50% or more glomerulosa-type cells, their frequency correlated negatively with duration of treatment. They were present in the non-tumorous cortex of 4 of these 7 patients, and in the cortex of 3 others whose tumours did not contain them. In the cortex, they were found only in glomerulosa cells, and their presence appeared unrelated to dosage or duration of treatment. No spironolactone inclusion bodies were seen in either the tumour of the non-tumorous cortex of 3 patients who had discontinued spironolactone 19 to 97 d before surgery, or of 2 patients who had never received spironolactone.

Adenoma↗
PubMed1983

Different norepinephrine disappearance rate in venous and arterial plasma in man.

The disappearance of norepinephrine in both arterial (radial) and venous (antecubital) plasma was studied in five patients with mild essential hypertension following isometric exercise and norepinephrine infusion. Arterial levels of epinephrine throughout the study and of norepinephrine during norepinephrine infusion were consistently higher than venous levels, indicating that both amines are removed by passage through the forearm. Following infusion the disappearance rate of norepinephrine from arterial plasma was faster than from venous plasma. After isometric exercise there was a delay in fall of venous levels, consistent with a delayed efflux of norepinephrine from local tissues. Arterial plasma levels probably reflect total body contribution whereas venous plasma levels presumably reflect additional local removal and/or release from the forearm.

Adult↗
PubMed1982

Pituitary microadenomas causing Cushing's disease respond to corticotropin-releasing factor.

Corticotropin-releasing factor (CRF) was administered as an iv bolus to two young women with mild Cushing's disease shortly before and one week after successful transsphenoidal microadenomectomy. The dose of CRF (1 microgram/kg body weight) had previously been shown to stimulate increased plasma ACTH and cortisol in normal subjects. In the first patient, prior to surgery, there were brisk increases in ACTH and cortisol that exceeded those observed in normal subjects. ACTH rose by 2 min and reached a peak between 15-30 min. Cortisol increased by 10 min and peaked between 45-60 min. After surgery, at a time when plasma cortisol was maintained at similar levels with exogenous hydrocortisone, there was no plasma ACTH or LH, TSH and prolactin increased after administration of LRH and TRH, and GH increased in response to insulin-induced hypoglycemia. The second patient had higher basal plasma ACTH and cortisol than the first patient. CRF-induced increments in ACTH and cortisol were much less, but the time course was similar and peak levels attained were still higher than those in normal subjects. After surgery, at a time when plasma cortisol was maintained at a much lower level with exogenous hydrocortisone, there was no plasma ACTH or cortisol response. She had mild, transient diabetes insipidus. Basal levels of all other anterior pituitary hormones were normal. These results demonstrate that two microadenomas causing Cushing's disease were responsive to CRF in situ and suggest that CRF may be involved in the etiology and/or the responses to changes in plasma glucocorticoid concentrations observed in patients with Cushing's disease.

Adenoma↗
PubMed1979

The effects of dietary fibre on glucose tolerance in healthy males.

Previous studies have shown that the addition of non-absorbable carbohydrate (NAC) to test meals decreases the glucose and and insulin response both in normal and diabetic subjects. However, these studies appear to have used brain in the basic test meal without a knowledge of the effect of bran itself or of the added NAC alone. In the present investigation bran alone, pectin alone, guar alone and pectin with guar have been studied. Guar alone added to the test meal significantly lowered blood glucose at 90 minutes. Pectin alone did not have a significant effect. Pectin and guar together resulted in a blood glucose lower at 30 minutes and greater at 120 minutes. No significant changes in insulin response were noted to our study. It appears that NAC alters the glucose response to a given meal, but the extent to which this occurred in the present study was less than in previous studies. The differences may reflect synergism between bran and other NAC's to lower blood glucose response after a meal.

Adult↗
PubMed1977

Use of a microprocessor in the control of malignant hypertension with sodium nitroprusside.

In a malignant hypertensive, steady control of blood pressure at a pre-determined level has been achieved with the continuous intravenous infusion of sodium nitroprusside. A microprocessor was programmed to assess the patient's blood pressure and adjust the rate of nitroprusside infusion so that a mean pressure of 106 mmHg was achieved. Brief interruption of the nitroprusside infusion allowed the effectiveness of changes in oral therapy to be evaluated. Thiocyanate concentrations were measured throughout as an index of potential nitroprusside toxicity. After six days, blood pressure control was maintained with oral therapy alone and papilloedema had almost resolved.

Adult↗
PubMedDate not supplied

Hypersensitivity of the hypothalamic-pituitary-adrenal axis to naloxone in post-traumatic stress disorder.

Naloxone, which increases endogenous corticotropin-releasing hormone (CRH) release by blocking an inhibitory opioidergic tone on the hypothalamic-pituitary-adrenal (HPA) axis, was administered in a dose-response protocol to seven healthy volunteers and 13 patients with treated posttraumatic stress disorder (PTSD). Six of the PTSD patients showed an increased hormonal response to the lowest naloxone dose (6 micrograms/kg) compared to both the control subjects and the other PTSD patients. This difference persisted on detailed subgroup analysis, although it was less marked at the highest naloxone dose (125 micrograms/kg). The responses of the other seven PTSD patients were indistinguishable from those of the control group. The greater responses of the six PTSD patients could not be explained on the basis of associated psychiatric illnesses or psychotropic drug therapy, and did not correlate with standard psychological testing or severity of PTSD. The results of this preliminary study therefore suggest that a hypersensitivity of the HPA axis to endogenous CRH stimulation may occur in PTSD.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Polyneuropathy in Australian outpatients with type II diabetes mellitus.

In order to determine the local prevalence of polyneuropathy among adult outpatients with type II (non-insulin-dependent) diabetes mellitus, we applied a series of standardised measures to patients attending a multidisciplinary diabetes clinic. The study group comprised 94 men and 15 women; mean age, 70.6+/-7.8 years; mean duration of diabetes, 11.7+/-10.1 years; and mean HbA1c 8.3%+/-1.7%. Neuropathy Symptom Scores > or = 1 were present in 97% of patients (mean, 3+/-2; range, 0-12), and 95% had Neuropathy Disability Scores > or = 2 (mean, 27+/-19; range, 0-87). 52% of men reported impotence. Autonomic dysfunction on cardiovascular reflex testing was present in 46% of patients (39/84). Finger and toe vibration perception thresholds were greater than 3SD higher than mean thresholds measured in control subjects without diabetes in 43% and 58% of patients, respectively. Polyneuropathy, defined as lower limb sensory and motor nerve conduction velocity or latency outside mean +/-2 SD of that measured in age-matched controls, was present in 49% of patients (53/109). These results suggest that there is a high prevalence of polyneuropathy in Australian out-patients with type II diabetes mellitus. In this study, clinical assessment using Neuropathy Disability Scores was not diagnostically useful since only five patients had a normal score. Using nerve-conduction studies as the "gold standard" diagnostic criteria, the best alternative test for the presence of polyneuropathy was toe vibration perception threshold (sensitivity 74%, specificity 56%). In view of the emerging evidence that intensive glycaemic control reduces the rate of progression of polyneuropathy, we recommend that patients with type II diabetes mellitus have nerve-conduction studies performed for early detection of this important complication.

Adult↗
PubMedDate not supplied

Relationship of renal hemodynamic and functional changes following intravascular contrast to the renin-angiotensin system and renal prostacyclin in the dog.

Deterioration in renal function has been observed after the use of intravascular contrast media. In an attempt to identify factors responsible for this phenomenon, meglumine iothalamate (Conray 60), in a dosage range of 2.5-3.3 ml/kg, was injected as a bolus into the aorta of dogs. Serial measurements were made of parameters of renal function as well as of changes in aortic and renal venous levels of angiotensin II, renin activity, and 6-keto-PGF1 alpha, the stable metabolite of prostacyclin. The major findings were (1) an initial, brief increase followed by approximately a 20% sustained decrease in renal blood flow and creatinine clearance, (2) no significant changes in angiotensin II and renin levels, and (3) a significant decline in the renal secretory rate of 6-keto-PGF1 alpha. These observations suggest that the suppression of prostacyclin, rather than the activation of the renin-angiotensin system, may contribute to the renal function changes attending the use of intravascular contrast media.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Renal venous renin ratio as a predictor of improvement in hypertension following nephrectomy for unilateral renal disease.

Renal venous renin ratio (RVRR) was measured in twenty hypertensive patients before removal of a kidney for unilateral, parenchymal renal disease. They were then followed for 1.3-9 y. Hypertension was cured or improved in six of eight patients with positive unstimulated and stimulated ratios, in none of five whose ratios became positive only on stimulation, and in one of seven with all ratios negative. Patients improved or cured by surgery had a significantly shorter duration of hypertension and a significantly lower serum creatinine after nephrectomy. Unstimulated RVRR was a reliable predictor of the effect of unilateral nephrectomy on blood pressure level.

Female↗
PubMedDate not supplied

Increased plasma noradrenaline during low dose adrenaline infusion in resting man and during sympathetic stimulation.

Both resting and stimulated (straight-leg raising and head-up tilt) levels of arterial and venous plasma noradrenaline were significantly higher during low-dose adrenaline infusion in five mild hypertensive and four normotensive patients with one adrenal. Repeat adrenaline infusions in the five hypertensive patients while measuring noradrenaline clearance (3H-noradrenaline constant infusion) achieved similar levels of plasma adrenaline, and similar increases in plasma noradrenaline, within five min of achieving target infusion rate. Increased plasma noradrenaline was not explained by reduced clearance. These results are consistent with the hypothesis that physiological concentrations of adrenaline are capable of facilitating noradrenaline release in man.

Epinephrine↗
PubMedDate not supplied

Effect of sodium valproate on naloxone-stimulated ACTH and cortisol release in humans.

1. Gamma-aminobutyric acid (GABA) and endogenous opioids each inhibit hypothalamic CRH secretion. In humans, the opioid antagonist, naloxone, stimulates the release of CRH, and so of ACTH and cortisol, while alprazolam, an indirect GABAA agonist, blocks naloxone-induced ACTH and cortisol secretion. Sodium valproate (SV) inhibits ACTH release in response to CRH, metyrapone and substance P. We hypothesized that, if this action is GABAA-mediated, SV should also inhibit naloxone-stimulated ACTH release. 2. We studied five healthy volunteers in randomized, double-blind, placebo-controlled afternoon studies with SV 400 mg, given 180 min before i.v. naloxone 125 micrograms/kg bodyweight. Plasma concentrations of ACTH, cortisol and SV were measured at intervals during the experiments. 3. SV had no effect on the mean integrated ACTH and cortisol responses to naloxone; ACTH: 165 +/- 21 versus 284 +/- 40 pmol.min per L, P = 0.08; cortisol: 10.5 +/- 1.9 versus 12.8 +/- 1.2 nmol.min per L-3, P = 0.14, placebo/nal versus SV/nal respectively. Basal ACTH and cortisol levels were also not significantly altered by SV (P > 0.30). Mean SV levels were not significantly different between SV/nal and SV/placebo studies (P > 0.50). 4. In conclusion, SV had no effect on naloxone-induced ACTH and cortisol release in normal humans at the dose and plasma drug concentrations studied. This contrasts with the potent inhibitory effect of alprazolam, and suggests that the effect of SV on the human hypothalamic-pituitary-adrenal axis may not be through a GABAA-mediated mechanism. Alternatively, higher plasma SV levels or more sustained exposure to SV may be necessary to inhibit hypothalamic secretion of CRH.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

New diagnostic tests for Cushing's syndrome: uses of naloxone, vasopressin and alprazolam.

1. We set out to investigate whether the administration of naloxone alone, naloxone plus vasopressin (AVP) or naloxone plus alprazolam to patients with Cushing's syndrome would result in a blunted dynamic response of the pituitary-adrenal axis compared with normal volunteers. Cushing's syndrome is often difficult to diagnose. It would be helpful if new tests were available to help in the biochemical distinction between Cushing's syndrome and non-Cushing's syndrome patients. 2. Naloxone testing correctly distinguished all seven patients with Cushing's syndrome (four pituitary Cushing's, two adrenal adenomas, one ectopic ACTH) from normal. Six patients were distinguished by the per cent change of plasma ACTH from basal being less than the normal range of 10 volunteers. The seventh patient (a pituitary Cushing's) was distinguished by the per cent change from basal of plasma cortisol being less than the normal range. 3. Naloxone plus AVP testing of two of four patients with pituitary Cushing's showed a smaller per cent change for both ACTH and cortisol compared with five normal volunteers, correctly distinguishing Cushing's from the normals. 4. Naloxone plus alprazolam did not distinguish Cushing's from normal. 5. Naloxone testing and naloxone plus AVP testing appear to be promising methods of distinguishing Cushing's syndrome from normal. Further experience with these tests, especially with obese and pseudo-Cushing's individuals, will be necessary to determine their place in the diagnosis and differential diagnosis of the cause of Cushing's syndrome.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Pituitary-adrenal responses to combined oral D-fenfluramine and intravenous naloxone in humans.

1. 1. Fenfluramine is an optically active 5-hydroxytryptamine (5-HT) releaser and re-uptake inhibitor. Increased brain 5-HT mediates appetite suppression, the D enantiomer being more active than L- or DL-fenfluramine. Fenfluramine also stimulates the hypothalamic-pituitary-adrenal (HPA) axis, leading to suggestions that this could act as a marker for its biological actions. However, the D enantiomer appears less active than a comparable DL racemate dose in animals, while effects of D-fenfluramine on the human HPA axis remain unproven. The aim of the present study was to clarify this. 2. Seven healthy human volunteers (three male, four female; 18-58 years) received 30 mg oral D-fenfluramine or placebo, followed by 125 micrograms/kg, i.v. naloxone or placebo, in randomized, double-blinded, placebo-controlled afternoon studies. We measured plasma adrenocorticotropic hormone (ACTH) and cortisol levels in samples taken at intervals throughout the study period. 3. In contrast to previous results with DL-fenfluramine, we found no dynamic responses to D-fenfluramine alone and no augmentation of responses to naloxone. 4. Central pathways to HPA axis activation are apparently not stimulated by D-fenfluramine at this dose in humans, in contrast with DL-fenfluramine, where the L enantiomer may be more selective for proposed corticotropin-releasing hormone-mediated, post-synaptic 5-HT2 or noradrenergic mechanisms. As previously reported, D-fenfluramine significantly blunted the circadian fall in basal plasma cortisol, providing in vivo evidence for serotonergic involvement in circadian regulation.

Adolescent↗
PubMedDate not supplied

Increased sympathetic activity in renovascular hypertension in man.

1. Concentrations in venous plasma of adrenaline, noradrenaline and dopamine were measured in samples collected simultaneously from three different sites in three varieties of hypertension. 2. In adrenal venous plasma, levels of catecholamines were increased in renovascular hypertension (n = 8) and decreased in primary aldosteronism (n = 8) when compared with essential hypertension (n = 9). 3. Concentrations were similar in antecubital and low inferior vena caval plasma, where noradrenaline was higher in renovascular hypertension. 4. Altered adrenal venous in renovascular hypertension and in primary aldosteronism. 5. Adrenal venous catecholamines deserve further study as an index of sympathetic activity.

Adrenal Glands↗