[Effect of the combination of the beta-1-blocker metoprolol with the tocolytic fenoterol on uteroplacental hemodynamics and fetal cardiovascular sensitivity with particular consideration of intrauterine fetal malnutrition. Results of animal experiments]. / Zur Auswirkung der Kombination des beta 1-Blockers Metoprolol mit dem Tokolytikum Fenoterol auf die uteroplazentare Hämodynamik und die fetale kardiovaskuläre Reagibilität unter besonderer Berücksichtigung der fetalen intrauterinen Mangelversorgung. Tierexperimentelle Ergebnisse.

7 merino sheep in an advanced state of pregnancy received oxytocin for labour induction under the conditions of control, monotherapy with the beta 2-adrenergic tocolytic fenoterol, combination of the latter with the beta 1-blocking substance metoprolol (Beloc). Likewise, the effect of labour induction was investigated when putting an artificial stenosis around the a. uterina during simultaneous application of fenoterol alone and combined with metoprolol. The following parameters were measured: aortic pressure and heart rate both in dam and fetus, maternal left ventricular pressure rising velocity, intrauterine pressure, uterine blood flow, uterine vascular resistance and regional myometrial contraction patterns by means of an ultrasonic transit time method. Measurement of maternal cardiovascular parameters once more showed, that maternal cardiovascular derangements could excellently be antagonised by metoprolol. Intrauterine pressure measurements as well as regional myometrial contraction patterns proved evidence, that there is no counteraction between the beta 2-mimetic substance and the beta 1-blocking agent concerning the tocolytic effect. When artificially stenosing the a. uterina, a rise in uterine contraction status could be observed; this hypoxic augmentation of myometrial tone could almost completely be reverted when combining fenoterol and metoprolol. Finally, no difference could be observed in the reaction of fetal cardiovascular parameters to reduced uterine blood flow before and after application of the beta 1-blocking substance metoprolol.

[Magnesium aspartate as a cardioprotective agent and adjuvant in tocolysis with betamimetics. Animal experiments on the kinetics and calcium antagonist action of orally administered magnesium aspartate with special reference to simultaneous vitamin B administration]. / Magnesiumaspartat als Kardioprotektivum und Adjuvans bei Tokolyse mit Betamimetika. Tierexperimentelle Untersuchungen zu Kinetik und kalzium-antagonistischer Wirksamkeit oral applizierten Magnesiumaspartats unter besonderer Berücksichtigung von synchroner Vitamin B6-Gabe.

With pregnant Wistar-rats, suffering from alimentary magnesium deficiency, absorption and distributing of Mg28 has been studied, the latter having been applied as aspartate and as chloride, with and without simultaneous substitution of vitamin B6. Absorption and tissue pooling were found to be augmented when using the aspartate and even more when adding vitamin B6. These differences were significant in the blood as well as in fetal and myocardial tissue. Correlation between blood-Mg28 und Mg28-activities in various tissues shows, that blood magnesium levels indicate a magnesium deficiency at least in the tissues of interest: fetus, myocardium, uterus and placenta. Nevertheless blood magnesium levels fail to reflect an additional tissue pooling, that exerts a beneficial action in the respect of cardio protection and of saving beta-mimetic tocolytics. When measuring magnesium and calcium excretion during chronic experiments with and without oral magnesium aspartate substitution, it could be demonstrated, that the amount of substituted magnesium has been pooled almost totally. Oral magnesium substitution furthermore reduces intestinal calcium absorption. Investigation on calcium uptake into the maternal myocardium revealed, that oral magnesium aspartate substitution significantly diminishes myocardial calcium uptake, the latter among others being responsible for cardiac hazards during tocolysis with beta-mimetic substances, while the pharmacologic calcium-antagonist Verapamil failed to do so.