Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 9410526

[Tocolysis].

L Spätling
View original source ↗Export metadata ↓

Abstract

Effectiveness of tocolytic strategies are difficult to prove and should called in question. Tocolysis by betaadrenergic agents inhibit a symptom without eliminating causing pathologies. Initial steps in etiology as well as therapy should be based on the entire organism including the psyche with a special focus on uterus, cervix and feto-placental unit. Magnesium depletion and infection are important causes of preterm labour. Application of betaadrenergic agonists should be pulsatile by bolus tocolysis demonstrating rare side effects.

Explore related subjects

Adrenergic beta-AgonistsDose-Response Relationship, DrugDrug Administration ScheduleFemaleHumansInfant, NewbornObstetric Labor, PrematurePregnancyRisk FactorsTocolysisTocolytic AgentsTreatment OutcomeEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

L Spätling. 1997. [Tocolysis].. https://pubmed.ncbi.nlm.nih.gov/9410526/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Role of cardiac nerves in the cardiovascular response to cocaine in conscious dogs.

BACKGROUND: Although the cardiovascular toxicity of cocaine is well recognized, considerable controversy remains as to the relative contribution of local norepinephrine reuptake inhibition versus central stimulatory effects of cocaine in eliciting its cardiovascular actions. The purpose of the present study was to determine the role of cardiac nerves in mediating the left ventricular (LV) and coronary hemodynamic responses to cocaine. METHODS AND RESULTS: We studied the cardiovascular response to acute cocaine administration (1 mg/kg) in 10 intact, conscious dogs and 6 dogs with ventricular denervation (VD). There were no significant differences in baseline hemodynamic parameters or plasma catecholamines between the 2 groups. In response to acute cocaine, LV and coronary hemodynamic responses were enhanced in the VD dogs. The enhanced systemic pressor and heart rate responses in VD dogs suggest that cardiac nerves mitigate the response to cocaine through ventricular mechanoreceptors rather than mediating the responses. CONCLUSIONS: These data suggest that peripheral blockade of norepinephrine reuptake is not the principal mechanism of the acute cardiac effects of cocaine. Rather, cardiac nerves modulate the effects of cocaine through baroreflex mechanisms. Thus, individual differences in baroreflex sensitivity may explain the hemodynamic variability observed in response to cocaine.

Adrenergic beta-Agonists↗
PubMed2001

Blunted cardiac responses to receptor activation in subjects with Thr164Ile beta(2)-adrenoceptors.

BACKGROUND: Recent evidence indicates that certain genotypes of beta(2)-adrenoceptors (AR) may indicate an increased risk of cardiovascular disease or an increased rate of disease progression. Of particular importance, the Thr164Ile polymorphism, which is found in approximately 4% of humans, shows decreased receptor signaling, blunted cardiac response when expressed in transgenic mice, and is associated with a decreased survival rate in patients with congestive heart failure. METHODS AND RESULTS: In this study, we compared functional activity, ie, chronotropic (heart rate increases) and inotropic (duration of the electromechanical systole) responses to intravenously administered terbutaline, in 6 subjects (4 women and 2 men) who were heterozygous for Thr164Ile with the responses in 12 volunteers (6 women and 6 men) who were homozygous for wild-type (WT) beta(2)-AR (ie, Arg16, Gln27, and Thr164). The beta(2)AR polymorphism significantly affected the dose-response curves for terbutaline-induced inotropic and chronotropic responses: compared with WT individuals, subjects with the Thr164Ile receptor had substantial blunting in maximal increases in heart rate (WT, 29.7+/-3.9 beats/min; Ile164, 20.7+/-1.9 beats/min; P:=0.016) and a shortening of the duration of electromechanical systole (WT, 51.9+/-4.5 ms; Ile164, 37.9+/-4.6 ms; P:=0.02). CONCLUSIONS: These data show that humans with the Ile164 genotype show blunted cardiac beta(2)-AR responsiveness, which may help explain the decreased survival of patients with this genotype in the setting of congestive heart failure.

Adrenergic beta-Agonists↗
PubMed2001

Enhancement of memory consolidation in chicks by beta(3)-adrenoceptor agonists.

The effects of intracranial injection of three beta(3)-adrenoceptor agonists, sodium-4-[-2[-2-hydroxy-2-(-3-chloro-phenyl)ethylamino] propyl]phenoxyacetate (BRL 37344), 2-hydroxy-5(2-((2-hydroxy-3-(4-((1-methyl-4-trifluoromethyl)1H-imidazole-2-yl)-phenoxy)propyl)amino)ethoxy)-benzamide monomethane sulfonate) (+/-)-CGP12177A) and the pro-drug RS-N-(7-carbethoxymethoxyl 1,2,3,4-tetrahydronaphth-2-yl)-2 hydroxy 2-(3-chlorophenyl)ethanamine (SR58611A), were examined on reinforcement of memory in day-old chicks. BRL37344 and CGP12177 facilitated memory, whereas SR58611A had no effect. The dose-response relationships of the beta(3)-adrenoceptor agonists were challenged with the selective beta(3)-adrenoceptor antagonist 3-(2-ethylphenoxy)-1-[(1S)-1,2,3,4-tetrahydronapth-1-ylamino]-2S-2-propanol oxalate (SR59230A) or the beta(2)-adrenoceptor antagonist (-)propranolol. BRL 37344 appeared to act predominantly at beta(3)-adrenoceptors at low doses and at beta(2)-adrenoceptors at higher doses. Facilitation of labile into long-term storage by beta(3)-adrenoceptor agonists appears to be a class action of these drugs.

Adrenergic beta-Agonists↗