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Biomedical subjects

E Enger

Publications and source records attributed to E Enger.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Treatment of hypertension in Norway. Indications, therapeutic intensity and economic aspects].

The Norwegian Society of Hypertension held its third scientific meeting in February 1991. One of the issues discussed was when to initiate drug treatment of uncomplicated essential hypertension and what level of blood pressure should be the goal of treatment. The American guidelines suggest that a blood pressure of 140/90 mm Hg or higher should be treated pharmacologically, whereas WHO suggests 160/95 mm Hg. The consensus at the meeting was that, in otherwise healthy subjects without end organ damage, a diastolic blood pressure of 100 mm Hg or more over three to six months should be treated with drugs, and that a safe goal would be around 135-140/85-90 mm Hg.

Drug Costs↗
PubMed1992

Long term morbidity and mortality after kidney transplantation.

A cohort of 69 patients received a kidney transplant in the period 1963-1977. The mean observation time was 9.5 years. Accumulated follow-up time was 661.4 patients year. The mean (SE) 10-year survival was 55(5.9)%. Univariate analysis showed that female patients had poorer survival than male. Patients with a cadaveric donor had lower survival than those with a living donor. Also survival with different HLA-A,B match differed significantly. A multivariate analysis pinpointed nature of donor, cadaveric vs. living, as the sole independent predictor of mortality. Patients receiving a cadaveric kidney were on double (2.2) relative risk of mortality as compared to patients with a living donor. The major causes of death were infections during rejection treatment, and cardiovascular disease. Patients had low rates of morbidity. Our results showed satisfactory outcome of kidney transplantation.

Adolescent↗
PubMed1990

Effects of beta 1- and beta 2-blockade on blood pressure and sympathetic responses to flight phobia stress.

Cardiovascular and sympathoadrenal effects of short-term oral treatment with beta 1-blockade (atenolol, 50 mg, administered two times) and beta 2-blockade (ICI 118,551, 50 mg, administered three times) were compared with placebo during actual flying in subjects with flight phobia (n = 34). beta 1-Blockade lowered resting blood pressure and heart rate and prevented a heart rate response but not a blood pressure response to this psychologic stress. beta 2-Blockade minimally lowered resting heart rate and prevented a heart rate response, but it failed to lower resting blood pressure or blood pressure response to the stress. Plasma epinephrine increased with all three treatments and more with beta 1-blockade than with placebo. Plasma norepinephrine decreased with administration of beta 2-blockade. Thus neither beta 1- nor beta 2-blockade prevents an increase in blood pressure during acute flight phobia stress. Increased plasma epinephrine seems to be the sympathetic variable that is closest related to this increase in blood pressure. Norepinephrine may be less consistently related to the blood pressure rise during flight phobia stress as shown by the decrease in plasma norepinephrine with administration of beta 2-blockade.

Administration, Oral↗
PubMed1990

Correlations between psychological and physiological responses to acute flight phobia stress.

Exposure of phobic subjects to real-life psychological stress may induce a high level of anxiety and be better than laboratory experiments for studies of physiological responses to psychological stress in human research. Therefore, by introducing natural psychological stress, i.e. actual flying in subjects with flight phobia (n = 23), the present study aimed at testing the hypothesis that there is, during mental stress, a direct relationship between the level of anxiety and the responses in the physiological variables blood pressure, heart rate and plasma catecholamines. Plasma adrenaline, heart rate, blood pressure and perceived anxiety measured by three different scales increased highly significantly during flight whereas plasma noradrenaline did not change. No direct relationship was found between the physiological and psychological variables. Thus, the physiological responses to natural psychological stress in terms of phobic anxiety may be definite, but the way the responses are related is less clear.

Adult↗
PubMed1988

Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

The catecholamine content in blood platelets is considerably higher than that in plasma, and platelet catecholamines must be taken up from plasma, since blood platelets lack enzymes for catecholamine synthesis. However, it is unknown whether platelets take up and store catecholamines during physiological in vivo increments in plasma catecholamines. Previously untreated 50-year-old men (n = 17) with mild to moderate essential hypertension were given a low sodium diet for 2 weeks. Urinary excretion of sodium decreased from 201 +/- 11 (SE) to 24 +/- 5 and 19 +/- 4 mmol/24 hr after 1 and 2 weeks, respectively. During the first week, the blood platelet concentration of norepinephrine increased from 27.2 +/- 2.9 to 39.6 +/- 4.7 pg/mg (p less than 0.005) and venous plasma norepinephrine increased from 3.7 +/- 0.4 to 5.6 +/- 0.5 pg/ml (p less than 0.005), and venous plasma dopamine increased from 26 +/- 4 to 41 +/- 5 pg/ml (p less than 0.05). During the second week, both plasma and platelet norepinephrine and dopamine remained elevated. Platelet epinephrine showed a small increase from baseline to the second week (p less than 0.05), but no concomitant increase in plasma epinephrine occurred. Thus, sodium depletion increases both platelet and plasma catecholamines and blood platelets may take up catecholamines in vivo. Platelet catecholamine content may be an integrated measure of plasma catecholamine concentrations during variations caused by sodium depletion.

Blood Platelets↗
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↗