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Biomedical subjects

E Enger

Publications and source records attributed to E Enger.

At least 55 records · Page 3Linked to original sources
PubMed1987

Decreased central dopaminergic activity in essential hypertension.

Baseline serum prolactin (PRL) was found to be similar in 35 men with untreated essential hypertension (149 +/- 2/98 +/- 1 mmHg; means +/- s.e.) and 44 healthy normotensive men (126 +/- 1/80 +/- 1 mmHg), all 40 years old. A correlation between baseline PRL and aldosterone was found in the normotensive (r = 0.534, P less than 0.001), but not in the hypertensive group (r = -0.011, NS). Ten subjects from each group received intravenous metoclopramide, a competitive dopamine antagonist, while another 12 normotensive subjects were given saline only, and the effect on PRL, vasopressin (AVP) and catecholamines was followed. An exaggerated PRL response to metoclopramide was observed in the hypertensive group compared with the normotensive (P less than 0.05), and the mean normotensive peak value never exceeded the hypertensive. Plasma noradrenaline increased significantly compared with baseline (P less than 0.05) and the control group (P less than 0.001), concomitant with increased heart rate (P less than 0.05), after the administration of metoclopramide both in the hypertensive and normotensive group. After intravenous injection of metoclopramide, forearm blood flow increased significantly by 50% in the hypertensive (P less than 0.001), and 80% in the normotensive group (P less than 0.001) compared with the control group. Mean blood pressure remained unchanged as did plasma AVP, dopamine and adrenaline. The present study indicates an altered central dopaminergic activity in essential hypertension. Even at rest, endogenous dopamine exerts a modulating effect on noradrenaline release in both hypertensive and normotensive men.

Adult↗
PubMed1985

Plasma vasopressin in hereditary cranial diabetes insipidus.

A family comprising 46 members of 4 generations is described; 21 members suffered from incomplete diabetes insipidus (DI) of central origin. The pedigree showed a dominantly transmitted condition. The onset is gradual and starts in early infancy. The clinical symptoms are highly variable and decline in the sixth decade. Plasma vasopressin (AVP) during water deprivation was significantly lower in the DI group than in the controls (4.2 +/- 0.5 vs. 10.6 +/- 1.7 ng/l) (p less than 0.01), the difference being more pronounced in the high osmolality range (4.8 +/- 0.7 vs. 14.4 +/- 3.1 ng/l) (p less than 0.01). Urine osmolality was lower (241 +/- 36 vs. 928 +/- 46 mOsm/kg H2O) (p less than 0.01) despite higher serum osmolality during water deprivation, rendering the ratio between urine and serum osmolality less than unity compared with greater than 3:1 in the control group (p less than 0.001). In two affected females, addition of a non-osmotic stimulus caused no increase in plasma AVP. The findings are consistent with a partial defect in the production or release of AVP and not with a dysfunction of the intracranial osmoreceptors. The variable features of incomplete DI indicate that to define the condition by excessive urinary output alone is insufficient. The ratio between urine and serum osmolalities after an appropriate osmotic stimulus together with plasma AVP measurements may be necessary to confirm the diagnosis.

Adolescent↗
PubMed1984

Pharmacokinetic evaluation of haemoperfusion in phenobarbital poisoning.

Charcoal haemoperfusion was performed for 5-12 h in three patients with maximal plasma phenobarbital concentrations of 600, 946 and 1044 mumol/l (138, 217 and 240 micrograms/ml). During haemoperfusion with constant blood flow phenobarbital elimination followed first order kinetics with half-lives of 11.1, 10.0 and 7.2 h, respectively. After termination of the haemoperfusion there was no rebound effect in plasma phenobarbital concentration and the elimination was first order with half-lives of 51, 82 and 48 h, respectively. Thus, the plasma phenobarbital half-life was reduced by 78-88% during haemoperfusion. In the same period 76-86% of the total body clearance of phenobarbital was due to the haemoperfusion column at a calculated volume of distribution of phenobarbital of 1.1-1.21/kg. This is clear evidence for recommending haemoperfusion in cases of serious poisoning with phenobarbital.

Adult↗
PubMed1983

The in vivo metabolism of C3 in human glomerulonephritis and after renal transplantation.

Metabolic investigations of complement component C3 have been performed to study pathogenetic mechanisms in patients with glomerulonephritis and after renal transplantation. Purified and biologically active 125I-labelled C3 was given intravenously together with 131I-albumin to nine patients with different forms of glomerulonephritis and nine allograft recipients at different stages after renal transplantation. Control studies were performed in 16 normal individuals. The fractional catabolic rate (FCR) of the proteins was calculated with the metabolic clearance method (U/P ratio) and/or by analysis of the plasma radioactivity disappearance curve. An increased FCR of C3 was found in three patients with glomerulonephritis. A modestly elevated FCR of C3 was found in all but one of the transplant patients as calculated by the U/P ratio, while the FCR was high in only two when calculated from plasma radioactivity disappearance. Slight increases of C3 catabolism were found during two suspected rejection episodes, but may have been due to a general increase in protein turnover. The serum level of C3 was reduced in two recipients and in one of these the FCR of the protein was elevated. The remaining patients had normal or increased C3 levels. Judged from these results, activation of complement was only of modest importance in the patients studied.

Adolescent↗
PubMed1981

Effects of hydroflumethiazide in congestive heart failure: renal electrolyte excretion related to urinary thiazide excretion and aldosterone.

The effect of hydroflumethiazide (HFT) on renal excretion of sodium, chloride, and potassium was studied in congestive heart failure and related to urinary excretion of thiazide and aldosterone. HFT 75 or 150 mg was administered orally once daily for 4 days to 8 male patients with roentgenological evidence of enlarged heart and slight or no peripheral oedema receiving digitalis and controlled diet. Urinary excretion of HFT did not change after repeated doses, whereas urinary excretion of a metabolite increased significantly. Initially, HFT induced a significant increase in the urinary excretion of sodium and potassium. After repeated doses, the natriuretic effect declined gradually in 6 of the patients. There was consistently a small natriuretic effect and a large kaliuretic effect at high serum aldosterone concentrations and high urine aldosterone excretion rates, whereas at low aldosterone levels, there was a wide range in magnitude of these effects. Relationships of the log urinary excretion rate of HFT to the increase in urinary excretion rate of sodium, chloride, and potassium showed positive and significant correlations. It was concluded that reduced natriuretic effect of HFT in congestive heart failure is not due to reduced delivery of thiazide to renal tubular cells but to compensatory adjustments of the kidney in part induced by aldosterone.

Aged↗