Sensitive high-performance liquid chromatographic determination of pseudoephedrine in plasma and urine.
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Biomedical subjects
Publications and source records attributed to C De Mey.
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The present publication reviews actual knowledge of the electrophysiological properties of low doses of digitalis in perspective of its use in patients with ventricular dysrhythmia. Both animal experiments and observations in humans have demonstrated that increased adrenergic and decreased cholinergic tone predispose to ventricular arrhythmia. An increased cholinergic tone on the other hand has been shown to protect against increased ventricular vulnerability, especially in situations of increased adrenergic tone. Therefore the combination of the cholinergic and anti-adrenergic actions of digitalis may help to control situations of increased ventricular vulnerability. This principle is especially attractive because digitalis, in contrast to classical anti-arrhythmics is devoid of any cardiodepressive effects. The clinical experience with digitalis in ventricular dysrhythmia as documented by the group of Lown is discussed in detail. The studies presently available do not yet allow digitalis to be accepted as a drug of first choice in this indication, but its careful use is not longer to be rejected for patients with non-digitalis induced ventricular dysrhythmia.
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Intermittent claudication is a non-pathognomic symptom elicited by an inbalance between the metabolic demands of the exercising skeletal muscle and its blood supply. In normal conditions hyperemia to the working muscles will be impaired during the exercise by mechanical compression of the microvessels. The resulting anaerobic metabolism will cause further vasodilatation. Both phenomena (exercise and reactive hyperemia) contribute to a maximal increase in local blood flow as soon as the exercise is stopped. If the local circulation is impaired by occluding arterial disease (eventually complicated by aggravating factors) the tolerance to skeletal work is lowered and the circulatory reserves are entirely exhausted as demonstrated by the ischemic exercise-test. In the case of a major obstruction and poor collateralisation, a "steel phenomenon" may occur. The pharmacotherapeutic possibilities to cope with in this situation are briefly discussed.
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The isolated and perfused kidney of the mature spontaneously hypertensive rat (SHR) exhibits an increased vascular reactivity and a delayed tachyphylaxis to 5-hydroxytryptamine, when compared to weight-matched normotensive animals. To evaluate the influence of the duration of the hypertensive state on these differences, the vascular reactivity to 5-hydroxytryptamine was determined in isolated kidneys from age-matched normotensive and spontaneously hypertensive rats of 3.5, 6 and 12 months of age. Responses to increasing doses of 5-hydroxytryptamine were compared. At all ages the responses to the agonist were greater in the SHR than in the control rats. In the normotensive rats, the sensitivity to the monoamine decreased, while the maximal response increased with aging. The vascular reactivity to increasing doses of 5-hydroxytryptamine was not altered by aging in the SHR. There was a significant correlation between the maximal vasoconstrictor response to 5-hydroxytryptamine in the isolated kidneys and the systolic arterial blood pressure (SBP) of the donor rats. Maximal constrictor responses to 5-hydroxytryptamine were repeated at given intervals. The degree of tachyphylaxis was decreased in hypertensive rats compared with normotensive rats at 3.5, and 6 months age. Tachyphylaxis to 5-hydroxytryptamine was depressed by aging in both normotensive and hypertensive rats. By contrast, tachyphylaxis to angiotensin II (AII) was not effected by either age or hypertension. There was no cross-tachyphylaxis between 5-hydroxytryptamine and AII. Lowering the Ca2+-concentration of the perfusate did not affect tachyphylaxis to either 5-hydroxytryptamine or AII. The present experiments indicate that the delayed tachyphylaxis to 5-hydroxytryptamine in the kidneys of SHR is due to a specific alteration of th vascular smooth muscle cells, which may be the consequence of premature aging.
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