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At least 1,459 records · Page 81Linked to original sources
PubMed1981

Combined use of beta-sympathomimetic drugs and beta-blockers during labour.

None of the betamimetics have a exclusively tocolytic effect. By stimulating the cardiovascular beta-receptor, they also cause a substantial increase in the heart rate and a decrease in blood pressure. We administered 4--5 micrograms/min of Fenoterol to 13 patients during the first stage of labour. This led to complete inhibition of labour. To reduce cardiac side effects, a primarily cardiac beta-blocker (5 mg Atenolol or 20 mg Metoprolol) was also given. The maternal and fetal heart rates were measured by ECG and by fetal scalp-electrode, respectively. The fetal heart rate remained largely unchanged, both during the Fenoterol infusion as well as during the additional administration of the beta-blocker. The maternal heart rate, which increased under the influence of the Fenoterol, fell (p less than or equal to 0.01) but did not return to normal. In all cases the beta-blockade led to a brief increase in uterine activity.

Atenolol↗
PubMed1990

Long-term studies on long-acting sympathomimetics.

Long-term treatment studies with formoterol and salmeterol show that these inhaled long-acting beta 2-agonists compared to available beta 2-agonists produce better bronchodilation, decrease the need for additional doses, decrease asthma symptoms, and are strongly preferred by the patients. Development of tolerance has not been found. One case history indicates that these effective bronchodilators might mask deterioration of asthma.

Administration, Inhalation↗
PubMedDate not supplied

Absolute bioavailability study in the dog with Visacor, a new cardioselective beta blocking drug with intrinsic sympathomimetic activity.

The cardioselective beta-adrenergic blocking drug Visacor (ICI 141,292) was dosed to six beagle dogs in a randomized cross-over manner. Five formulations were examined i.e. a 15 mg/kg intravenous solution, a 50 mg/kg oral solution, and 50, 100 and 200 mg/kg oral powder formulations. Whole blood and urine samples were collected at various times after each dose and analysed for parent drug concentration by a high pressure liquid chromatography procedure. The urine samples were also analysed for parent drug content after hydrolysis with beta-glucuronidase. The normalised intravenous blood levels of ICI 141,292 were found to decay tri-exponentially with a final phase elimination half-life of about 10 h. The computer fitted data showed the drug to possess a high volume of distribution for both the central compartment (54% body weight) and whole body (1384% body weight) indicating the possibility of a high degree of metabolism. The drug clearance following i.v. administration was 196 ml/min and the urinary recovery rate of parent drug was 24% (unhydrolysed) and 40% following hydrolysis with beta-glucuronidase. Following oral dosing at 50 mg/kg (as both powder (C) and solution (B], 100 (D) and 200 (E) mg/kg (as powder) the systemic blood profiles were found to increase with dose. The mean peak blood level attained was 6 +/- 1, 5 +/- 1, 8 +/- 1 and 14 +/- 1 micrograms/ml for formulations, B, C, D and E respectively. The systemic bioavailability of ICI 141,292 was only about 40%. The areas under the curves increased linearly with dose and the elimination phase half-life was unchanged with dose. The calculated half-life (7 h) was apparently shorter after oral administration than after intravenous administration (10 h) but this is probably an artefact dependent on the limit of detection of the assay procedure. At 50 mg/kg there were no significant differences in blood profiles or in the urinary excretion of drug between the solution and powder formulations. However the overall systemic bioavailability was marginally higher with the powder. These observations are consistent for a drug which is cleared by both renal and hepatic elimination processes, which undergoes "first-pass" metabolism on oral dosing and, over the oral dose range studied, obeys linear pharmacokinetics. The significant increase in recovery of parent drug, after hydrolysis of the urine with beta-glucuronidase, indicates that the ICI 141,292 glucuronide conjugate is present to a significant extent. The results also demonstrate that absorption of parent drug from the gastrointestinal tract may not be complete.

Administration, Oral↗
PubMed1978

The effects of hexoprenaline, a beta 2-sympathomimetic drug, on maternal glucose, insulin, glucagon, and free fatty acid levels.

Hexoprenaline, an adrenergic beta 2-receptor agonist, was administered as a 10 microgram intravenous bolus to 9 women in the third trimester of pregnancy. The maternal plasma glucose, serum immunoreactive insulin, plasma immunoreactive glucagon (IRG 30 K), and free fatty acid (FFA) concentrations rose significantly at different times following the bolus injection. Thc serum insulin level increased first and reached a peak at 10 minutes, before the rise in plasma glucose, which reached a maximum at 30 minutes, suggesting that beta 2-receptor stimulation affects insulin secretion directly and not via a rise in the glucose level. Plasma glucagon and FFA levels also rose despite the rise in glucose levels. We therefore conclude that beta 2-receptor stimulation has direct actions on insulin and glucagon release and on glucose and FFA metabolism. The possible fetal sequelae due to these changes in the maternal metabolic milieu are discussed in relation to the use of a 10 microgram intravenous bolus of hexoprenaline as a measure in the treatment of acute fetal distress.

Antigens↗
PubMed1986

Effect of long-term administration of beta 2-sympathomimetic drug in the diet-restricted pregnant rat model.

To assess whether the maternal-fetal balance could be altered in favor of the fetus during malnutrition by increasing uteroplacental blood flow, 0.5 mg of hexoprenaline per day was added to the diet of one group of diet-restricted rats, while another group served as controls. The radionuclide-labeled microsphere method was used to determine blood flow to the maternal placentas and other organs. Maternal carcass weight but not fetal or placental weights were increased in the hexoprenaline-fed rats. Blood flow to the ileum, jejunum, hepatic artery, kidneys, and placentas was significantly greater in the hexoprenaline group compared with those rats fed the restricted diet alone. Although the placental blood flow was increased in the hexoprenaline-fed rats, the supply of nutrients remained restricted, and in the mother the inherent maternal-fetal balance was maintained by an increase in the blood flow to the liver and small intestine.

Animals↗
PubMed1991

The effects of indomethacin and a beta-sympathomimetic agent on the fetal ductus arteriosus during treatment of premature labor: a randomized double-blind study.

To study the effect of maternal indomethacin or nylidrine hydrochloride treatment on the fetus ductus arteriosus and the pulmonary artery, 27 women with threatened preterm labor between 24 and 34 weeks' gestation were studied by echocardiography. Fourteen women were treated with indomethacin and 13 with nylidrin. Both systolic and diastolic velocities in the ductus increased after administration of indomethacin indicating constriction in nine fetuses, and exceeded the corresponding velocities in the fetuses of the nylidrin group (p = 0.001). However, there were no changes in pulmonary artery flow velocities (p greater than 0.5). In the indomethacin group, there was a significant linear positive relationship between the gestational age and the change in ductal flow velocity. Three of the nine patients with ductal constriction also had tricuspid regurgitation. These findings indicate that indomethacin, not nylidrin, causes transient constriction of the ductus arteriosus and the constrictive response increases with the gestational age. We recommend echocardiographic surveillance of fetal hemodynamics when prostaglandin synthesis inhibitors are used in the treatment of spontaneous preterm labor.

Blood Flow Velocity↗
PubMed1989

The effect of beta-sympathomimetic stimulation on parotid salivation in the red kangaroo (Macropus rufus).

Salivation was stimulated by intracarotid isoprenaline infusion given alone or combined with acetylcholine. By itself, isoprenaline (0.12-1.2 nmol kg-1 min-1) stimulated flow rates of 0.037-0.233 ml min-1 (2.77-10.5 microliters/g gland per min). Salivary Na, Cl, PO4 and total solute concentrations were positively correlated with flow; K, Mg and urea were negatively correlated with flow; and Ca, H+, HCO3, protein and amylase activity were not correlated with flow. Relative to cholinergic saliva, isoprenaline-evoked saliva had higher levels of amylase activity, urea, protein, K, Mg, H+, PO4 and Cl but lower osmolality, Na, Ca and HCO3. At a steady flow (1 ml min-1), isoprenaline infusion (0.3 nmol kg-1 min-1) superimposed on a pre-existing acetylcholine infusion increased salivary amylase activity, protein, urea, K, Mg, Cl and PO4, reduced HCO3 and did not alter Na, Ca, H+ and osmolality. Superimposition of isoprenaline infusion (0.5 nmol kg-1 min-1) on a low-level acetylcholine infusion increased flow rate by 400-900%. Excretion rates of K, Mg, Cl and PO4 were higher and Ca lower than predicted for saliva secreted at equivalent flows during acetylcholine stimulation. Na, H+ and HCO3 were as predicted for the same flow rate under cholinergic stimulation. The simplest coherent interpretation of these data is that isoprenaline affects transport of protein and ions at the end organs, but has little effect on the resting transport characteristics of the striated and excretory ducts of the kangaroo parotid, in accord with the known nerve distribution of this gland.

Acetylcholine↗
PubMed1981

The effects of intrathecal sympathomimetic agents on neural activity in the lumbar sympathetic chain of rats.

Intrathecal injections of norepinephrine (0.30 mumol) and clonidine (0.035 mumol) produced decreases in neural activity recorded from the lumbar sympathetic chain and caused changes in rat thermoregulation consistent with a reduction in efferent sympathetic activity. These results support the conclusion that bulbospinal noradrenergic pathways inhibit sympathetic outflow. The data also indicate that the spinal cord is a potential site of action for clonidine.

Animals↗