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Biomedical subjects

I Eide

Publications and source records attributed to I Eide.

At least 91 records · Page 5Linked to original sources
PubMed1986

Platelet volume, platelet release reaction and platelet response to infused adrenaline are increased in essential hypertension.

Hypertensive men aged 42 (n = 35) were compared to normotensive men of similar age (n = 44). Platelet numbers were similar in the two groups, but hypertensive men had larger venous platelets than the normotensive (7.46 versus 7.12 femtoliter, p = 0.01). Plasma concentration of beta-thromboglobulin (BTG), a marker of platelet release reaction, was increased in arterial blood in hypertension (40 versus 21 micrograms/l, p = 0.02). The normotensive subjects had markedly higher BTG concentration in venous compared to arterial blood (p less than 0.01), but this arterio-venous difference was not present in the hypertensive group. Twelve normotensive subjects received infused saline, which did not induce changes in platelet variables. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects, with dose gradually increasing to 0.04 microgram/kg/min. Platelet count increased in both groups, but significantly more in the hypertensive group. Platelet volume and BTG both increased markedly in the hypertensive group, but not in the normotensive men. Thus, young men with hypertension have increased platelet activity and increased sensitivity to exogenous adrenaline.

Adult↗
PubMed1986

Enhanced platelet release reaction related to arterial plasma adrenaline and blood pressure in pre-eclampsia.

The platelet release product beta-thromboglobulin (BTG) in venous plasma, and arterial and venous catecholamines were measured in 13 severe pre-eclamptic and 13 normotensive pregnant women. In the pre-eclamptic group, BTG was significantly higher and the platelet count significantly lower than in the normotensive pregnant group. In the pre-eclamptic group, arterial concentrations were significantly higher for adrenaline, noradrenaline and dopamine, whereas in venous plasma only adrenaline and dopamine were higher. Significant positive correlations appeared in the pre-eclamptic patients between venous BTG and arterial adrenaline (r = 0.82), arterial noradrenaline (r = 0.76) and venous adrenaline (r = 0.55). In the pre-eclamptic group, BTG also highly correlated with systolic (r = 0.84) and diastolic blood pressure (r = 0.77) and heart rate (r = 0.67). These findings indicate that sympathetic nervous tone, as measured by arterial and venous plasma catecholamines, is a good predictor of in-vivo blood platelet activation. In pre-eclampsia, increased sympathetic tone may play a key role in platelet activation and consumption and thus in the activation of the coagulation system.

Adult↗
PubMed1986

Increased arterial catecholamines in pre-eclampsia.

Arterial and venous plasma catecholamines were measured in 13 pre-eclamptic and 13 normotensive pregnant women. In the pre-eclamptic group, arterial concentrations were higher for adrenaline (p less than 0,001), noradrenaline (p less than 0.05) and dopamine (p less than 0.01) than in the normotensive group, whereas in venous plasma only adrenaline (p less than 0.01) and dopamine levels were higher (p less than 0.05). Arterial adrenaline concentrations in the pre-eclamptic group were, on average, three times as high as normotensive arterial adrenaline. The arterial-venous (a-v) differences were higher for adrenaline (p less than 0.001) and dopamine (p less than 0.05) in the pre-eclamptic than in the normotensive group. In the pre-eclamptic group, arterial adrenaline was correlated with mean arterial blood pressure (r = 0.89, p less than 0.001) and with increased heart rate (r = 0.78, p less than 0.01). According to these results, both sympathetic nervous and sympathetic adrenal activities are increased in patients with pre-eclampsia.

Adult↗
PubMed1986

Plasma adrenaline and noradrenaline during orthostasis in man: the importance of arterial sampling.

Plasma adrenaline and noradrenaline were measured in arterial blood and in forearm venous blood during supine rest and after 30 min standing in normotensive, healthy 50-year-old men (n = 16). After 30 min standing, venous noradrenaline had increased from 1.61 +/- 0.11 to 4.22 +/- 0.30 nmol/l and arterial from 1.43 +/- 0.06 to 2.93 +/- 0.15 nmol/l. Orthostasis induced a seven-fold increment in the forearm arterial-venous difference of noradrenaline from -0.18 +/- 0.08 to -1.29 +/- 0.25 nmol/l (p less than 0.001). Orthostasis more than doubled the forearm arterial-venous difference of adrenaline from 0.15 +/- 0.03 to 0.31 +/- 0.05 nmol/l (p less than 0.001) since arterial adrenaline increased from 0.31 +/- 0.03 to 0.53 +/- 0.05 nmol/l and venous from 0.16 +/- 0.02 to 0.22 +/- 0.02 nmol/l. Arterial adrenaline correlated significantly with venous in the supine (r = 0.64, p less than 0.01) but not in the standing position (r = 0.34, NS). The results indicate that arterial concentrations of adrenaline are a much better indicator of sympatho-adrenal activity during orthostasis than peripheral venous concentrations. For noradrenaline, measurements of arterial concentrations during the orthostatic manoeuvre seem to provide information about the total noradrenergic sympathetic reactivity, while the corresponding measurements in peripheral venous blood represent the forearm locally.

Arm↗
PubMed1985

Effects of adrenaline infusion on platelet number, volume and release reaction.

At the end of a diagnostic right heart catheterization ten patients received an intravenous infusion of l-adrenaline which gradually increased the arterial plasma adrenaline concentration from resting physiological values to high values as seen during myocardial infarction, pheochromocytoma and hypoglycemia. Blood was sampled from the brachial artery, femoral vein and hepatic vein. During the adrenaline infusion venous beta-thromboglobulin concentrations increased 23% from 61 +/- 5 to 80 +/- 7 micrograms/l (mean +/- SE), arterial platelet counts 20% from 212 +/- 17 to 253 +/- 25 X 10(9)/l and arterial platelet volume 4% from 7.25 +/- 0.20 to 7.56 +/- 0.21 femtoliter. All changes were significant at the 5% level. Thus, acute increments of arterial plasma adrenaline significantly stimulated the blood platelet parameters studied.

Adult↗
PubMed1985

Adrenaline and preeclampsia.

Twenty-one preeclamptic women had increased venous plasma-free adrenaline (45 +/- 5 vs 27 +/- 2 pg/ml, mean +/- SE, P less than 0.01) and plasma-free dopamine (137 +/- 25 vs 55 +/- 6 pg/ml, P less than 0.01) compared with fifteen normotensive pregnant women. Plasma renin activity (P less than 0.001) and aldosterone concentration (P less than 0.02) were depressed in the preeclamptic and serum potassium increased (P less than 0.02). Plasma adrenaline correlated with blood pressure (r=0.80, P less than 0.001) supporting increased sympathetic nervous tone in the development of preeclampsia.

Adult↗
PubMed1985

Evidence of age-related variation in plasma vasopressin of normotensive men.

The influence of age on plasma arginine vasopressin was examined in three groups of healthy men, 25 +/- 1 (n = 12), 40 (n = 23) and 50 years of age (n = 13), respectively. The three groups were comparable in body height, weight, blood pressure, heart rate, serum and urine osmolality, electrolytes and endogenous creatinine clearance. Compared to the 25-year olds, the 50-year old men had more than three times higher basal plasma vasopressin (7.8 +/- 1.4 vs. 2.5 +/- 0.6 ng/l, p less than 0.01), only one-third the plasma renin concentration (0.36 +/- 0.05 vs. 1.10 +/- 0.33 G.U. X 10(-4)/ml, p less than 0.01) and a significantly higher plasma noradrenaline (267 +/- 21 vs. 199 +/- 19 ng/l, p less than 0.05) while plasma adrenaline remained essentially unchanged. The 40-year olds had intermediate plasma vasopressin concentrations (4.2 +/- 0.6 ng/l). Thus, age is a variable with a substantial effect on plasma concentrations of vasopressin in addition to the well-known effect on renin and noradrenaline. Age must be taken into account in further clinical studies on vasopressin.

Adult↗
PubMed1985

Increased arterial adrenaline is highly correlated to blood pressure and in vivo platelet function in pre-eclampsia.

Compared with normotensive pregnant women (n = 13), patients with severe pre-eclampsia (n = 13) had increased arterial plasma adrenaline (P < 0.001), peripheral venous adrenaline (P < 0.01), arterio-venous differences of adrenaline (P < 0.001) and venous concentration of the platelet release product beta-thromboglobulin (P < 0.001). In the pre-eclamptic group, arterial adrenaline correlated with mean blood pressure (r = 0.90, P < 0.001), heart rate (r = 0.78, P < 0.01) and beta-thromboglobulin (r = 0.82, P < 0.001), while in the normotensives adrenaline correlated only with beta-thromboglobulin (r = 0.76, P < 0.01). According to these results, sympathetic adrenal tone is increased in pre-eclampsia and may play a role in the pathogenesis of high blood pressure and platelet activation in this disease.

Adult↗
PubMed1985

Dietary sodium intake increases vasopressin secretion in man.

Plasma vasopressin concentration and urinary vasopressin excretion were measured in a control situation, during sodium depletion and on days 1, 2, and 7 during high sodium intake in twelve 23-26-year-old men on a free-water intake. Urinary vasopressin excretion decreased from 6.7 +/- 1.0 ng/hr (control) to 3.9 +/- 0.3 ng/hr (p less than 0.01) when sodium excretion decreased from 188 +/ 18 to 16 +/- 2 mmol/24 hr. During the first day of high sodium intake, the urinary vasopressin excretion increased to 10.0 +/- 1.2 ng/hr (p less than 0.01) compared with control and remained high throughout the sodium repletion. Through all collection periods at low, normal, and high sodium intake, vasopressin excretion increased concomitantly with serum sodium concentration and osmolality. After low sodium intake for 7 days, the serum vasopressin concentration averaged 2.7 +/- 0.6 ng/l, and this level was maintained throughout the sodium repletion period. These results are compatible with a stimulatory effect of dietary sodium intake on pituitary vasopressin secretion in man. Dietary sodium may stimulate vasopressin secretion through extracellular osmolality or even by a direct effect of extracellular sodium on periventricular receptors. Plasma renin concentrations or sympathetic nervous activity offered no further explanations. Urinary vasopressin excretion provides more useful information than do plasma concentrations, as the latter can fluctuate rapidly.

Adult↗
PubMed1984

Ouabain inhibits renin release by a direct renal haemodynamic effect.

The effect of intrarenal infusion of ouabain (90 micrograms/kg) on renin release was examined in the anaesthetized dog. Ouabain reduced cortical Na-K-ATPase activity to 23% and outer medullary activity to 18% of the control level. During renal arterial constriction to a perfusion pressure below the autoregulatory range, renin release rose from 1.2 +/- 0.4 to 47.4 +/- 6.9 micrograms/min (P less than 0.001). This response was abolished by ouabain. When superimposed on renal arterial constriction, beta-adrenergic stimulation enhanced renin release from 25.6 +/- 10.7 to 56.9 +/- 9.5 micrograms/min (P = 0.02) at a urinary sodium excretion of 2 +/- 1 mumol/min. After ouabain, the corresponding increment substantially decreased since release rose from 5.6 +/- 2.0 to 19.9 +/- 5.3 micrograms/min only (P = 0.02), at a urinary sodium excretion of 140 +/- 67 mumol/min. When glomerular filtration was reduced to zero by ureteral occlusion in one series, renin release increased to 22.6 +/- 5.1 but was reduced (P less than 0.05) by ouabain to 13.5 +/- 5.5 micrograms/min and superimposed isoproterenol had no effect. According to these observations, ouabain inhibits renin release by a direct effect on the afferent arteriole through constriction of the autoregulating renin-secreting segment.

Adrenergic beta-Agonists↗
PubMed1984

Increased plasma vasopressin and serum uric acid in the low renin type of essential hypertension.

In 22 50-year-old men with long-standing, untreated essential hypertension of the low renin type, venous plasma vasopressin concentrations were about three times those of 15 matched normotensive control subjects (p less than 0.005). These patients also had increased arterial concentrations of noradrenaline and adrenaline (p less than 0.05) but there was no direct association between these two catecholamines and vasopressin. On the other hand, adrenergic beta-receptor blockade with oxprenolol reduced both blood pressure and plasma vasopressin (p less than 0.01) while venous plasma dopamine concentrations significantly increased. In addition, the hypertensives had highly significantly increased serum uric acid (p less than 0.001) that correlated positively with venous vasopressin concentrations (p less than 0.05). According to these data, patients with the volume-sustained low renin type of essential hypertension have increased plasma vasopressin concentrations that probably are inversely related to dopaminergic nervous activity. The data also indicate that increased plasma vasopressin correlates with serum uric acid, most probably through increased tubular reabsorption of this acid.

Atenolol↗
PubMed1984

Changes in the lipoprotein profile during antihypertensive therapy.

In the Oslo study serum lipids have been studied during treatment with some of the most frequently used antihypertensive drugs. Hydrochlorothiazide induced no significant changes. However, those patients with the most marked increase in uric acid showed an increase of serum triglycerides. Total cholesterol was unchanged in these men. The beta-adrenoceptorblocking drugs propranolol, atenolol and oxprenolol caused a reduction of HDL cholesterol and an increase of total triglycerides. Total cholesterol remained unchanged. Pindolol induced no significant lipoprotein changes. Prazosin reduced total cholesterol and total triglycerides. HDL cholesterol remained unchanged. LDL + VLDL cholesterol was reduced.

Antihypertensive Agents↗
PubMed1984

Renal venous and urinary PGE2 output during intrarenal arachidonic acid infusion in dogs.

Inferences about total renal (venous and urinary) PGE2 output from determinations of urinary excretion rates (U PGE2 V) cannot be made unless the distribution of PGE2 between renal venous plasma and urine is known. Therefore, in the present study on intact kidneys of anesthetized dogs both urinary excretion of PGE2 and the renal venous output (the product of plasma flow and venous concentration of PGE2) was determined during low and high rates of renal PGE2 synthesis. PGE2 was measured in urine and arterial and renal venous plasma by radioimmunoassay during the following conditions: (1) Hydropenia. In the control condition U PGE2 V averaged 0.041 +/- 0.012 pmol/g . min and varied between 4 and 70% of the total PGE2 output. With infusion of arachidonic acid (AA, 160 micrograms/kg . min) into the renal artery total PGE2 output increased from 0.18 +/- 0.03 to 3.23 +/- 0.51 pmol/g . min, whereas arterial concentrations of PGE2 were unchanged. The urinary fraction still varied between 6 and 46% of total renal PGE2 output. (2) High urine flows caused by mannitol, saline or saline and ethacrynic acid (ECA) infusion. These procedures did not stimulate total renal PGE2 output and the urinary fraction varied between 4 and 49%. ECA combined with saline infusion increased the urinary fraction significantly to 34.7 +/- 4.0%. AA increased the total PGE2 output as during hydropenia, but the urinary fraction fell to 13% in 13 dogs and was unchanged at about 8% in six dogs. On average the urinary fraction of total PGE2 output was significantly lower than in hydropenia. Thus, the urinary fraction of total renal PGE2 output is not constant, and urinary excretion of PGE2 does not give reliable information about renal synthetic rates of prostaglandins.

Animals↗
PubMed1984

Arteriovenous difference of plasma vasopressin in normal man and effect of posture.

In 13 normotensive 50-year-old men arterial plasma vasopressin (11.3 +/- 2.1 ng/l, mean +/- SE) was significantly increased over venous (7.8 +/- 1.4 ng/l) in the supine position with an arteriovenous difference of 3.5 +/- 1.2 ng/l (p less than 0.05). After 30 min in the upright position, an average increment of 45% to 11.3 +/- 1.8 ng/l was observed for venous vasopressin. Since a similar increase was not found for arterial vasopressin, the arteriovenous difference decreased with 29% to 2.5 +/- 2.1 ng/l and was no longer statistically significant. The correlation between supine and standing vasopressin was statistically significant both for arterial (p less than 0.001) and venous plasma (p less than 0.05). These data indicate a substantial removal of plasma vasopressin by receptors even in the peripheral vascular beds (forearm) and not only in the liver and the kidneys as previous literature claims. The arteriovenous difference decreases in the upright position, most likely because of reduced plasma vasopressin clearance.

Arginine Vasopressin↗
PubMed1984

Dietary sodium intake and vasopressin excretion in man.

The present study was undertaken to examine the possible relationship between dietary sodium intake and arginine vasopressin (AVP). In 12 normotensive men (aged 23-26 years) urinary AVP excretion decreased from 6.7 +/- 1.0 to 3.9 +/- 0.3 ng/h (P less than 0.01) when sodium excretion by dietary intervention for one week was reduced from 188 +/- 18 to 16 +/- 2 mmol/24 h. At a high sodium intake (300 mmol/day), AVP excretion increased to 10.0 +/- 1.2 ng/h during the first day (P less than 0.01) and remained high throughout one week of sodium load. These results are compatible with a major physiological role of sodium in AVP secretion in man. A sodium-AVP relationship may play a role in the pathogenesis of essential hypertension since recent reports suggest elevated plasma AVP in essential hypertensive states.

Adult↗
PubMed1983

Uptake of elemental mercury by brain in relation to concentration of glutathione and activity of glutathione peroxidase.

Uptake of mercury by brain after i.v. injection of elemental mercury was investigated in the rat, after depletion of glutathione or inhibition of glutathione peroxidase in brain tissue. When glutathione in brain was depleted 76% by an intraventricular injection of diethylmaleate, a 13% increase in mercury uptake by brain was observed. After an intraventricular injection of iodoacetate, activity of glutathione peroxidase in brain was inhibited 19% and the content of reduced glutathione was decreased 20%. In these animals mercury uptake by brain increased 66% relative to controls.

Animals↗