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- Andrén, Lennart, 1946, et al.
(författare)
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Circulatory effects of noise.
- 1983
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Ingår i: Acta medica Scandinavica. - : Wiley. - 0001-6101. ; 213:1, s. 31-5
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Tidskriftsartikel (refereegranskat)abstract
- Thirteen patients with mild essential hypertension, mean age 44 years (range 21-59), were studied during "stress" before and after postsynaptic alpha-adrenoceptor blockade and combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade. Loud broad band noise (100 dBA for 10 min) was used as the stress stimulus. Exposure to noise caused a significant increase in systolic (7%, p less than 0.05), diastolic (9%, p less than 0.01) and mean arterial pressure (6%, p less than 0.01). The blood pressure elevation was caused by an increase in total peripheral resistance (12%, p less than 0.05). There was no significant change in heart rate, stroke volume or cardiac output. The blood pressure response during noise stimulation was not affected by postsynaptic alpha-adrenoceptor blockade (prazosin, 2 mg orally). The hemodynamic reaction pattern, however, was totally reversed. Thus, the cardiac output increased significantly (9%, p less than 0.05), while the total peripheral resistance tended to decrease. Combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade (labetalol, 200 mg orally) inhibited the increase in systolic blood pressure caused by noise, while the diastolic and mean arterial pressures still increased significantly (5%, p less than 0.01). Labetalol effectively blocked the stress-induced increase in total peripheral resistance and there was no significant increase in cardiac output after combined alpha- and beta-adrenoceptor blockade. Exposure to noise caused a significant increase in circulating noradrenaline (20%, p less than 0.05). Plasma adrenaline and plasma renin activity were not affected by noise stimulation. These results suggest that blood pressure elevation is essential during "stress" but that the hemodynamic pattern causing blood pressure elevation may vary and may be affected by pharmacological blockade of various parts of the sympathetic nervous system.
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- Andrén, Lennart, 1946, et al.
(författare)
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Ketanserin in hypertension. Early clinical evaluation and dose finding study of a new 5-HT2 receptor antagonist.
- 1983
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Ingår i: Acta medica Scandinavica. - 0001-6101. ; 214:2, s. 125-30
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Tidskriftsartikel (refereegranskat)abstract
- Ketanserin, a new 5-hydroxy-tryptamine antagonist, was given at three different dosage levels (double-blind, randomized) in a dose finding study for 2 months to 31 patients with mild to moderately severe essential hypertension. Treatment with ketanserin was then continued until 9 months had been completed. A significant antihypertensive effect was demonstrated at daily dosages of 20 mg t.i.d. or 40 mg t.i.d. The antihypertensive effect was similar to that of previous multiple drug treatment with conventional drugs. However, 60 mg t.i.d. was not acceptable, at least not as initial dosage. At this dose level, 8 out of 10 patients had to be withdrawn from the study during the initial phase due to unwanted effects. It is conceivable that alpha 1-adrenoceptor blockade may have played a role at this dose level, since postural reactions were observed which was otherwise not the case during this study. Ketanserin is a new and interesting alternative in the treatment of hypertension. At the same time it offers a tool by which the role of 5-hydroxy-tryptamine in the regulation of arterial pressure can be investigated.
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