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Biomedical subjects

E Mikkelsen

Publications and source records attributed to E Mikkelsen.

At least 37 records · Page 2Linked to original sources
PubMed1981

The hyperactive child syndrome: peripheral sympathetic nervous system function and the effect of d-amphetamine.

We evaluated sympathetic nervous system function in medication-free hyperactive children by measuring plasma levels of norepinephrine (NE) and dopamine-beta-hydroxylase and then comparing the effects of two therapeutics doses of d-amphetamine to placebo in these patients. The medication-free hyperactive patients and controls had similar plasma NE levels and blood pressures while recumbent, and a similar increase in NE on standing, but the patients had a larger pressor response on standing. In the hyperactive patients d-amphetamine significantly increased blood pressure, pulse rate, and NE levels. The change in NE levels correlated with the change in amphetamine levels. The medication-free patients, when more anxious, had higher plasma NE levels.

Attention Deficit Disorder with Hyperactivity↗
PubMed1981

Effects of 5-hydroxytryptamine and ergotamine on human superficial temporal artery.

Isometric tension was recorded in ring preparations of human superficial temporal arteries contracted by noradrenaline (NA), 5-hydroxytryptamine (5-HT), and ergotamine. In contrast to NA and 5-HT, ergotamine induced long-lasting contractions refractive to additional stimulations and resistant to repeated wash-out. When tested against 5-HT, ergotamine acted as a non-competitive antagonist. When repeating the 5-HT stimulations (4.7 x 10(-5) M) the contractile response decreased indicating tachyphylaxis to this agent. As ergotamine revealed both a vasoconstrictive and a 5-HT-blocking activity, the beneficial effect in migraine may be by an interference during both the vasoconstrictory and vasodilatory phases.

Adult↗
PubMed1981

Comparative studies on the effects of tolmesoxide (Rx71107), a tolmesoxide metabolite (Rx71112) and nifedipine in isolated blood vessels.

1 The effect was studied of tolmesoxide (Rx71107), a tolmesoxide metabolite (Rx71112) and nifedipine on active tension in human isolated crural veins and in rat thoracic aorta. The effects of tolmesoxide and nifedipine on (22)Na and (45)Ca net influx in noradrenaline-induced contractions were investigated in rat thoracic aorta.2 Tolmesoxide, Rx71112 and nifedipine caused a concentration-related inhibition of noradrenaline (NA)- and potassium (K(+))-induced contractions in human veins. Nifedipine was by far the most potent drug in these respects. Tolmesoxide (4.7 muM-4700 muM) and Rx71112 (22 muM-220 muM) inhibited the NA-induced contraction more effectively than the K(+)-induced concentration. The reverse was true for nifedipine (0.0023-3 muM).3 Nifedipine had a similar potency in inhibiting the NA-induced contraction in rat aorta and human veins, whereas the inhibitory effect of tolmesoxide was more pronounced in rat aorta than in human veins.4 Tolmesoxide was a weak antagonist of the contractile effects of the cumulative addition of calcium on human veins. In concentrations up to 470 muM, tolmesoxide was completely devoid of inhibitory effects on (22)Na and (45)Ca net influx in rat aorta. Rx71112 (220 muM) had an inhibitory effect on (22)Na net influx but no significant effect on (45)Ca net influx.5 Nifedipine was an effective antagonist of the contractile effects of cumulative addition of calcium in human veins and had a concentration-related inhibitory effect on both (22)Na and (45)Ca uptake in rat aorta.6 The results indicate that tolmesoxide and Rx71112 cause dilatation of human crural veins in vitro at concentrations that do not interfere with the net transmembranal movements of Ca and are thus clearly different from the effects of nifedipine.

Adult↗
PubMed1981

Effects of ergotamine on isolated human vessels.

In isolated human mesenteric and crural veins, ergotamine induced long-lasting contractions. These contractions were resistant to repeated wash-out and were not affected by alpha-adrenoceptor blockade, but could be abolished by removal of extracellular calcium or by the presence of the calcium-blocker nifedipine. In contrast to its effect on human mesenteric and crural veins, ergotamine had no contractile effect, but a marked relaxant effect on mesenteric arteries mediated via blockade of alpha-receptors. The ergotamine-induced contraction was not affected by indomethacin (0.28--2.8 microM) nor was it influenced by serotonin (5-HT). In both mesenteric and crural veins, the ergotamine-induced contraction was diminished by the 5-HT blocking agent, methysergide. In veins, development of tachyphylaxis to 5-HT was demonstrated. It is concluded that ergotamine has a direct contractile effect on isolated human mesenteric and crural veins. These effects are dependent on unhindered influx of extracellular calcium and are at least partly mediated via 5-HT receptors. In mesenteric arteries, ergotamine acted as an alpha-adrenoceptor blocker, and had no contractant effect.

Adult↗
PubMed1979

Effect of nifedipine on plasma renin, aldosterone and catecholamines in arterial hypertension.

Acute sublingual administration of nifedipine 10--20 mg to 13 hypertensive patients caused a rapid decrease in blood pressure (BP) and a concomitant increase in heart rate (HR), plasma noradrenaline (NA) and plasma renin activity (PRA); there was no significant change in plasma adrenaline (A) or aldosterone (ALDO). Basal PRA was the major determinant of the rise in PRA, as a close correlation was present between the basal value and the increase caused by nifedipine (r = 0.92), p less than 0.001). The rise in PRA was also correlated with the plasma concentration of nifedipine after 60 min (r = 0.80, p less than 0.01), but it was not correlated with the decrease in BP, the rise in HR or the increase in NA. Nifedipine 30--60 mg daily for 6 weeks caused a reduction in mean BP from 133 to 113 mmHg (p less than 0.001). Body weight and serum potassium decreased but no consistent change was noted in NA, PRA, ALDO or 24 h-excretion of catecholamines. A significant correlation was present between the change in NA and that in PRA (r = 0.74, p less than 0.01). The alterations in the various parameters in the acute and chronic studies were not correlated. The findings indicate that different regulatory mechanisms are activated during acute and chronic administration of nifedipine. It is suggested that an initial rise in sympathetic activity gradually decreases during prolonged therapy, but it still remains a determinant of PRA.

Adult↗
PubMed1979

Abrupt withdrawal of beta-blocking agents in patients with arterial hypertension. Effect on blood pressure, heart rate and plasma catecholamines and prolactin.

Chronic treatment with beta-blockers was interrupted abruptly in six patients with arterial hypertension. Three patients, who had experienced symptoms during a previous withdrawal, again complained of transient palpitations, tremor, sweating, headache and general malaise. A significant increase in standing blood pressure (BP) and heart rate (HR) was noted after 24 h. The standing HR reached a maximum after 48 h and had decreased significantly on the 7th day (p less than 0.005). There was a strong tendency to greater increase in standing BP and HR in the patients who experienced symptoms than in those who did not. Plasma concentrations of noradrenaline, adrenaline and prolactin did not change significantly. Thus, beta-blocker withdrawal symptoms are reproducible and are indicative of a transient sympathetic hyperresponse. The increased activity is not likely to be caused by increased production of circulating catecholamines, but rather by increased sensitivity of the beta-receptor.

Adrenergic beta-Antagonists↗
PubMed1979

Serum potassium and uric acid changes during treatment with timolol alone and in combination with a diuretic.

Timolol, 10 to 40 mg daily, given to 103 patients with uncomplicated arterial hypertension induced significant increments of serum potassium at all dose levels (p less than 0.05). The magnitude of the increments was dependent on daily timolol dosage. When hydrochlorothiazide and amiloride were added, serum potassium decreased (p less than 0.001), but a major determinant of the magnitude of the decrease was the dosage change of the timolol. Serum uric acid was influenced in a paradoxical way during timolol monotherapy; there was a rise in all 3 dosage groups (p less than 0.02) but the lowest group showed the largest increase and vice versa. On addition of hydrochlorothiazide and amiloride, there was a further increase in serum uric acid, the magnitude of which depended on the concomitant reduction in the dose of timolol, with reductions in dose causing a larger rise in serum uric acid and increments, a smaller rise. The increments of serum uric acid were greater in females than in males during both treatment periods. The results indicate that beta blockers induce dose-dependent rises in serum potassium and may counteract undesirable effects of diuretics on serum potassium. Beta blockers seem to have a paradoxical effect on serum uric acid and may aggravate the hyperuricemia induced by diuretics.

Amiloride↗
PubMed1979

Individual factors influencing the response to a beta-adrenergic blocking agent given alone and in combination with a diuretic on arterial hypertension.

103 patients with arterial hypertension were treated with timolol + placebo for 7 weeks in a multicentre trial, and with timolol + hydrochlorothiazide and amiloride for a further 7-week period. The decrease in blood pressure (BP) produced by timolol alone was influenced neither by the dose of timolol, initial heart rate, magnitude of pretreatment BP nor by age. 64% of the patients less than 40 years of ages, and 48% of the older patients, were well regulated on beta-blocker monotherapy. When the diuretic was given in addition, the BP response in the older age group improved, whereas younger patients showed no change. A significant correlation was found between age or magnitude of untreated BP and the decrease in BP caused by the diuretic. The cardiothoracic ratio increased significantly on timolol alone, whereas no change was found on the combined therapy. Weight changes in the two different treatment periods showed a significant correlation, but they were not related to the observed reduction in BP. The results suggest that in younger patients, beta-blocker therapy is just as effective as a combined treatment with a diuretic, whereas in older patients considerably better regulation is achieved by combined therapy.

Adult↗
PubMed1979

Verapamil and nifedipine inhibition of contractions induced by potassium and noradrenaline in human mesenteric arteries and veins.

Ring preparations of human mesenteric arteries and veins were contracted by noradrenaline (1.8 x 10(-5)M) or potassium (127mM). Isometric tension was recorded. In the arterial preparations, the maximum response to noradrenaline was 97 +/- 8% (mean +/- S.E.M.) of that to potassium. In the veins, the corresponding figure was 38 +/- 4%. The calcium antagonists verapamil (2.2 x 10(-7)-2.2 x 10(-5)M) and nifedipine (2.9 x 10(-8)-2.9 x 10(-6)M) relaxed both arteries and veins contracted by noradrenaline or potassium, and reduced the responses to these agents when added 15 min. before stimulation. The time course of relaxation of potassium contracted preparations, induced by verapamil and nifedipine, was more rapid and complete than that produced by a calcium-free, high potassium solution. In contrast to verapamil, nifedipine caused a more pronounced inhibition of the potassium than of the noradrenaline evoked contractions in both arteries and veins. After exposure to a calcium-free medium for 30 min., the arterial response to noradrenaline was significantly (P less than 0.05) greater than that to potassium. However, the reverse was found in the veins. In both types of vessel, verapamil (2.2 x 10(-6)M) and nifedipine (2.9--10(-7)M) were equi-effective in reducing the noradrenaline reactivity, not only between mesenteric arteries and veins, but also between, e.g. peripheral and mesenteric vessels. The calcium antagonists nifedipine and verapamil do not have an identical mode of action. However, both agents seem to inhibit influx of extracellular calcium, and might also have an inhibitory effect on the release of intracellular calcium.

Aged↗