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Biomedical subjects

F Bühler

Publications and source records attributed to F Bühler.

At least 19 recordsLinked to original sources
PubMed1988

Serotoninergic mechanisms in hypertension. Focus on the effects of ketanserin.

Aggregating platelets release serotonin, which induces contraction of most vascular smooth muscle by activation of S2-serotoninergic receptors. Serotonin released in the circulation may contribute to the increase in peripheral resistance of hypertension as the responsiveness of blood vessels from hypertensive animals and humans to the vasoconstrictor action of the monoamine is augmented. The data obtained with the new antihypertensive agent ketanserin may favor that interpretation. Ketanserin is a selective S2-serotoninergic antagonist with additional alpha 1-adrenergic blocking properties. In humans, it has a terminal half-life of 12 to 25 hours and is eliminated predominantly by the liver. The hemodynamic profile of ketanserin is that of a vasodilator drug with actions on both resistance and capacitance vessels. On short-term intravenous administration, it lowers blood pressure in hypertensive patients with minimal reflex changes in cardiovascular function. When given orally long term to hypertensive patients, ketanserin causes a sustained reduction in arterial blood pressure, comparable to that obtained with either beta-adrenergic blockers or diuretics. Several studies have shown a greater efficacy in older (greater than 60 years of age) than in younger patients independent of starting pressure. Side effects mainly consist of dizziness, somnolence, and dry mouth, but they are usually not severe. The mechanism underlying the antihypertensive effect of ketanserin is unclear. It cannot be attributed to either S2-serotoninergic or alpha 1-adrenergic blockade alone, but an interaction between the two effects appears to be required.

Humans↗
PubMed1986

Acute and chronic sympathetic reflex activation and antihypertensive response to nifedipine.

The importance of counterregulatory mechanisms triggered by arterial vasodilation for the antihypertensive response to the calcium entry blocking agent nifedipine was investigated in 13 men with mild to moderate essential hypertension. Blood pressure and systemic vascular resistance were significantly reduced 30 minutes after sublingual administration of 10 mg of nifedipine while heart rate, cardiac index and plasma norepinephrine concentrations increased (all p less than 0.01). Also, changes in mean blood pressure correlated inversely with arterial baroreflex sensitivity (r = -0.74, p less than 0.01), suggesting that arterial baroreflex mechanisms by means of sympathetic activation tend to limit the acute antihypertensive response. Blood pressure, but not systemic vascular resistance, decreased further (p less than 0.01) after 6 weeks of therapy with nifedipine 20 mg three times daily, while average heart rate, cardiac index and plasma norepinephrine concentrations had returned toward pretreatment values. Thus, a reduction of acutely increased sympathetic activity toward pretreatment values during long-term nifedipine therapy was associated with further decreases in blood pressure. The importance of sympathetic activity was also stressed by the finding of an inverse relation between chronic changes in heart rate and blood pressure (percent of control, r = -0.76, p less than 0.01). Blood volume did not change during long-term nifedipine therapy. The results suggest that the degree of sympathetic reflex activation in part determines the antihypertensive response to nifedipine monotherapy.

Adult↗
PubMed1986

Pharmacokinetics of conventional and slow-release verapamil.

Verapamil is a racemic mixture of two optical isomers, the (-)-form being the more active component. Recent studies indicate a rapid hepatic transformation of (-)-verapamil, which results in different concentration-effect relationships after oral and intravenous administration. In practice the important pharmacokinetic properties of verapamil are low bioavailability (20%), predominant elimination by metabolism (greater than 95%) and a relatively short half-life (t1/2, beta is 3-5 h). After repeated dosing, the rate of hepatic drug clearance seems to decrease. Slow release (SR) formulations of verapamil may offer certain therapeutic advantages during long-term treatment. A comparison of conventional (C) and SR tablets in a 1-week treatment of eight cardiac patients showed a relative bioavailability (AUCSR/AUCC) of 90 +/- 30%. More stable serum drug levels were maintained by 12-hourly administration of SR verapamil. A further study using a new 240 mg SR preparation in patients with arterial hypertension showed that even a single daily dose can be sufficient for adequate blood pressure control over 24 h.

Adult↗
PubMed1975

Light and electron microscopic examinations of experimentally produced heart muscle necroses following normobaric hyperoxia.

Heart muscle necroses following normobaric hyperoxia as examined under a light microscope occur after 40 hours exposure in the rabbit and increase in intensity with prolongation of the exposition time. Simultaneous arterial blood gas analysis excludes a hypoxemis as the cause, In addition electron microscopic examination of the necroses demonstrate the primary changes in the myofibrils but not in the mitochondria. The ultramorphological picture is however, quite similar to the myocardial necroses after epinephrine application in the rabbit. A pathogenetic relationship between heart muscle necroses after normobaric hyperoxia and after epinephrine should be considered.

Cardiomyopathies↗
PubMed1969

"Normal central venous pressure," significance of reference point and normal range.

The principal methods for determining the central venous pressure have been compared in 26 patients undergoing cardiac catheterization. The method in which the reference point is taken to be 10 cm. above the surface supporting a horizontal patient gave false high-pressure values. All the other methods, however, gave pressure values which corresponded to those obtained in the catheter studies.

Adult↗