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Biomedical subjects

H Iven

Publications and source records attributed to H Iven.

At least 55 records · Page 3Linked to original sources

Failure of peptides (angiotensin, bradykinin, substance P, physalaemin, Met-enkephalin) to influence the cardiac action potential.

Angiotensin, bradykinin, substance P, physalaemin, and Met-enkephalin were tested for their ability to affect the action potential (AP) of the isolated guinea pig papillary muscle driven at 1/sec and 3/sec. Variables studied were height and duration of AP, dV/dtmax, half-life of recovery of dV/dtmax, and refractory period. At relevant concentrations the peptides were not effective.

Action Potentials↗

Effects of the local anesthetics brufacain and lidocaine on transmembrane action potentials, refractory period, and reactivation of the sodium system in guinea pig heart muscle.

Lidocaine (3-10(-5) and 10(-4) M) and equimolar concentrations of brufacain dose-dependently reduced the depolarization velocity (dV/dtmax) and the force of contraction of guinea pig atria and papillary muscles. Repolarization time was increased in atria but reduced in papillary muscles. The maximum effects on action potential parameters were identical but developed with brufacain more slowly than with lidocaine. In papillary muscles lidocaine (3-10(-5) M) prolonged the functional refractory period. No such effect but even a shortening was observed with brufacain. As brufacain reduced the duration of the action potential (AP) more than the functional refractory period, the "relative refractory period" (in percent of AP duration) was slightly prolonged. The half-time of the recovery of the Na+ system was increased three to five times the control value after lidocaine but only doubled after brufacain.

Action Potentials↗

The pharmacokinetics and organ distribution of ajmaline and quindine in the mouse.

After i.v. infusion into mice (lasting 10 s) the time courses of ajmaline and quinidine concentrations in blood, heart, lung, liver, and brain were studied. The drugs were assayed by a spectrofluorophotometric procedure. Blood concentration data obtained were fitted graphically and calculations were performed in accordance with an open two compartment model. Blood kinetic data were very similar for both alkaloids. A rapid distribution phase with a t0.5alpha of 3.0 min for ajmaline and 2.5 min for quindine was followed by a disposition phase with a t0.5beta of 16 min for ajmaline and 20 min for quinidine. High tissue accumulation of both alkaloids was found in lung, liver, and heart and this is also reflected by the volume of distribution Vdbeta, which was 136 ml for ajmaline and 116 ml for quinidine (body weight of the mice = 31 g). With equilibrium dialysis a 62% binding of ajmaline and a 77% binding of quinidine to mouse blood constituents was found. Both drugs were highly metabolized since only 5% of a given dose was excreted unchanged in the urine.

Ajmaline↗

[Plasma concentrations and renal excretion of vincamine after oral administration in man (author's transl)].

Plasma concentrations and renal excretion of 14,15-dihydro-14beta-hydroxy-(3alpha,16alpha)-eburnamenine-14-carbonic acid methylester (vincamine, Vincapront) were studied in 5 healthy volunteers following the oral intake of 30 or 60 mg vincamine, respectively. After the higher dose (60 mg vincamine), the treatment was continued by the daily intake of 3 X 20 mg vincamine for 5 days. Plasma vincamine levels were determined in the morning prior to the ingestion of the first 20-mg dose and in the evening 2 h after the intake of the third 20-mg dose. Our results prove that vincamine is rapidly liberated and absorbed from the tablet formulation used, the maximum plasma levels being reached 90 min after ingestion and amounting to a mean value of 139 ng/ml after 30 mg and to a mean of 252 ng/ml after 60 mg of vincamine. There was a biphasic elimination of vincamine after both doses indicating a process of distribution influencing also the elimination phase. In the 24-h urine, unchanged vincamine amounted to 5.8% of the applied dose after 30 mg and to 7.3% after 60 mg vincamine. Vincamine did not accumulate during the daily intake of 60 mg for 6 days. Side-effects were not observed in any volunteer during the period of observation.

Administration, Oral↗

Fluorescence data and studies on the lipid solubility and chemical structure of N-propyl-ajmaline as compared to ajmaline.

The quaternary N-propyl-ajmaline was found to have a higher lipid solubility than ajmaline. Lipid solubility was pH dependent. From chemical, fluorescence and IR-spectroscopic studies it is concluded that the existence of N-propyl-ajmaline in a tautomeric state between a carbinol-ammonium and an aldehyde-amine structure is responsible for the high lipid solubility.

Ajmaline↗

[A comparative study about the therapeutic effect of theophylline and doxapram in apnoeic disorders].

The objective of this study was to prove the superiority of doxapram compared to theophylline therapy in apneas of prematurity in very low birth weight infants. Therefore all VLBW infants (gestational age < 35 weeks) were randomized if they had in a 2 hours-interval more than 2 apneas, 4 bradycardias or 4 oxygen desaturations. They received either theophylline (loading dose 5 mg/kg b. w., 3 mg/kg b. w. bid) or doxapram by continuous infusion of 0.5 mg/kg/h. Apneas, bradycardias and desaturations were recorded from the trend analysis of our monitoring system over the first 3-days and a 7 days period and compared statistically (Mann-Whitney U-test). Plasma levels of both drugs and a polysomnographic recording were obtained during steady state conditions in parallel to a behavioral observation according to Prechtl. The recorded events were again compared using the Mann-Whitney U-test. Twenty patients were treated with theophylline, 14 with doxapram. In 9 patients of each group we could perform a polysomnography and behavioral observation. The incidence of apneas, bradycardias and desaturations in a 7 days-interval was not significantly different between both groups. Analyzing the first 3 days of treatment, however, we could detect a significantly lower rate of apneas in the doxapram group (2.5 apneas compared to 7 in the theophylline group, p < 0.037). In the polysomnographic recording and in our behavioral observations we could not record any significant differences between both groups. Therefore we can conclude that theophylline and doxapram are comparable in the treatment of apneas of prematurity, however, doxapram is superior to theophylline in reducing the rate of apneas in the first 3 days of treatment.

Apgar Score↗