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PubMed1998

Ocular hypotensive and vasodilative effects of two beta-adrenergic blockers with intrinsic sympathomimetic activity.

PURPOSE: The ocular hypotensive and vasodilative effects of vaninolol and eugenolol, two beta-adrenergic blockers with intrinsic sympathomimetic activity, were tested in rabbits and their pharmacologic mechanisms were also studied in vitro. METHODS: Intraocular pressure was measured in ocular hypertonic rabbits which were induced by infusing 20% NaCl or 5% glucose solution. The rabbit's ocular blood flow was determined using the colored microsphere technique. The concentrations of cAMP were evaluated in porcine ciliary body and cultured A7r5 smooth muscle cells by radioimmunoassay. Ca+2 concentration was measured in A7r5 cells by spectrofluorometry after loading cells with Fura-2-AM. RESULTS: It was found that 0.5% eugenolol and vaninolol could suppress the intraocular pressure in glucose-induced ocular hypertensive rabbits and delay the intraocular pressure recovery in NaCl-induced ocular hypertensive rabbits. In addition, both agents improved the ocular blood flow in the iris, ciliary body, retina and choroid. Vaninolol and eugenolol of 10 microM inhibited the basal cAMP accumulation from 23.9 +/- 2.0 of control to 8.7 +/- 0.4 and 2.4 +/- 0.1 respectively and inhibited the isoproterenol-induced cAMP accumulation from 154.3 +/- 13.6 to 120.6 +/- 8.3 and 74.2 +/- 6.1 respectively in the porcine ciliary body. The cellular cAMP concentration was significantly increased from 10 +/- 1 of control to 96 +/- 5 (vaninolol) and 38 +/- 3 (eugenolol) in cultured A7r5 smooth muscle cells. Both agents also increased the intracellular calcium concentration in A7r5 cells. CONCLUSIONS: These results indicate that the lowering of intraocular pressure by vaninolol and eugenolol may be due to cAMP suppression in the ciliary body by beta-antagonist and/or alpha2-agonist activities. Both agents cause vasodilation via beta2-agonist action that increase the smooth muscle cellular cAMP level more than vasoconstriction via alpha-agonist activity by increasing an influx of extracellular Ca+2.

Adrenergic beta-Antagonists↗
PubMed1976

Sympathomimetic drugs: evaluation for acute central hypotensive activity in alpha-chloralose-anesthetized dogs and cats intravertebral artery administration,.

dl-Amphetamine, phentermine and their para-chloro derivatives were tested for acute central hypotensive activity after intra-vertebral artery (iva) infusions in alpha-chloralose-anesthetized cats and intact and carotid sinus denervated dogs. Iva clonidine (reference standard) caused immediate reductions in blood pressure and heart rate and carotid sinus denervation (CSD) enhanced the clonidine response. dl-Amphetamine and phentermine did not cause acute hypotensive responses in the dog or cat whereas their para-chloro derivatives did. The vasodepressor response to para-chloramphetamine was inconsistent and transient and not modified by CSD. The magnitude and duration of the chlorphentermine vasodepressor response was minimal in the intact and CSD dog compared to clonidine. In contrast, chlorphentermine in the cat (140-300 mug/kg) caused an acute hypotensive response comparable in magnitude to clonidine (0.6-1.0 mug/kg). The bradycardias observed after iva chlorphentermine were much less pronounced than those associated with iva clonidine at comparable vasodepressor doses. By the i.v. route, each drug caused only pressor responses in the dog and cat. Suppression of the pressor response (resulting from "spill-over" of these alpha-stimulants into the systemic circulation after iva dosing) in the dog with small doses of i.v. phenoxybenzamine did not unmask or enhance the vasodepressor or bradycardic actions to iva administration of drugs. Methysergide prevented the hypotensive response to chlorphentermine in the cat and partially suppressed the response to clonidine; the reverse was true after piperoxan. Lilly 110140 and para-chlorophenylalanine reduced or abolished the effects of iva chlorphentermine. In summary, (1) iva chlorphentermine and clonidine were the only alpha-sympathomimetics tested which were effective as hypotensive substances; (2) the cat was considerably more responsive to iva chlorphentermine than the intact or CSD dog; (3) iva clonidine was more bradycardic than iva chlorphentermine; and (4) both adrenergic and serotonergic components appear to be among the mechanisms involved in the acute iva hypotensive response to chlorphentermine in the cat.

Anesthesia↗
PubMed2002

Anti-cholinergic bronchodilators versus beta2-sympathomimetic agents for acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: Inhaled bronchodilators form the mainstay of treatment for acute exacerbations of COPD. Two types of agent are used routinely, either singly or in combination: anticholinergic agents and beta2-sympathomimetic agonists. OBJECTIVES: To assess the effect of anti-cholinergic agents on lung function and dyspnea in patients with acute exacerbations of COPD, compared with placebo or short-acting beta-2 agonists. SEARCH STRATEGY: A comprehensive search of the literature was carried out on MEDLINE, EMBASE, CINAHL and the Cochrane COPD Trials Register, using the terms: bronchodilator* OR ipratropium OR oxitropium. References listed in each included trial were searched for additional trial reports. SELECTION CRITERIA: Studies were included if the participants were adult patients with a known diagnosis of COPD and had symptoms consistent with criteria for acute exacerbation of COPD. All randomized controlled trials that compared inhaled ipratropium bromide or oxitropium bromide to appropriate controls were considered. Appropriate control treatments included placebo, other bronchodilating agents, or combination therapies. Studies of acute asthma or ventilated patients were excluded. DATA COLLECTION AND ANALYSIS: All trials that appeared to be relevant were assessed by two reviewers who independently selected trials for inclusion. Differences were resolved by consensus. MAIN RESULTS: Four trials compared the short-term effects of ipratropium bromide vs. a beta2-agonist. Short-term changes in FEV1 (up to 90 minutes) showed no significant difference between beta2-agonist and ipratropium bromide treated patients. The differences were similar among the studies and when combined: Weighted Mean Difference (WMD) 0.0 liters (95% Confidence Interval (95% CI) -0.19, 0.19). There was no significant additional increase in change in FEV1 on adding ipratropium to beta2-agonist: WMD 0.02 liter (95% CI -0.08, 0.12). Long-term effects (24 hours) of the ipratropium bromide and beta2-agonist treatment combination were similar: WMD 0.05 liters (95%CI -0.14, 0.05). Neither of two studies found significant changes in PaO2, either short- or long-term, with ipratropium vs. beta-agonist, although one showed an increase in PaO2 in subjects receiving ipratropium bromide at 60 minutes. Adverse drug reactions included dry mouth and tremor. REVIEWER'S CONCLUSIONS: There was no evidence that the degree of bronchodilation achieved with ipratropium bromide was greater than that using a short-acting beta2-agonist. The combination of a beta2-agonist and ipratropium did not appear to increase the effect on FEV1 more than either used alone.

Bronchodilator Agents↗
PubMed1988

Airway obstruction and airway wall instability in cystic fibrosis: the isolated and combined effect of theophylline and sympathomimetics.

Multiple aspects of lung function were measured in 17 cystic fibrosis (CF) patients on four occasions: without therapy (0); with oral theophylline medication (Th); after inhalation of salbutamol (beta 2); and with combined medication (Th + beta 2). In addition to routine measurements, partial and maximum expiratory flow-volume (MEFV) curves were superimposed, and the flow transient equivalent of the MEFV curve was determined. Its volume dimension (volume of airway contribution, VACMEFV) partially reflects airway distensibility. Changes in airway compressibility--the other consequence of airway wall instability--were assessed by observing changes in end-expiratory flow rate. Airway resistance, expired volumes, and early expired flow rates, as well as VACMEFV improved significantly after beta 2 medication. Mean end-expiratory flow also increased after beta 2; in two patients, however, it decreased significantly, indicating that enhanced airway compression dominated over the release of bronchospasm. The alone had only minor effects on lung function. Early expired volume and flow rates as well as VACMEFV showed no significant difference between beta 2 alone and Th + beta 2; airway resistance even decreased significantly with this drug combination. End-expiratory flow rate, however, was significantly lower after Th + beta 2 than after beta 2 alone. Although theophylline does not alter lung function in most patients with CF, sympathomimetics relieve bronchospasm in many, but they enhance airway compressibility and thereby decrease peripheral expiratory airflow in some.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Induction of differential heat shock gene expression in heart, lung, liver, brain and kidney by a sympathomimetic drug, amphetamine.

Amphetamine, a sympathomimetic drug, can elevate the body temperature by causing enhancement of endogenous lipolysis. This study was designed to examine whether this drug could induce the expression of the genes of heat shock proteins (HSP) in different tissues. Subcutaneous administration of amphetamine (10 mg/kg wt) to the rats increased the rectal temperature of the rats to 42 degrees C within 60 min. After 3 hr rats were sacrificed; and heart, lung, liver, kidney and brain tissue were removed to examine the induction of mRNAs for HSPs by Northern blot analysis using cDNA probes of 27 kDa, 70 kDa and 89 kDa HSPs. The results of this study indicate striking regional and cell type differences in the pattern of induction of the HSP mRNAs by amphetamine suggesting that different organs and cell types respond differently to amphetamine.

Amphetamine↗
PubMed1994

Hyperresponsiveness of the airways following exposure of guinea-pigs to racemic mixtures and distomers of beta 2-selective sympathomimetics.

Allergic bronchospasm in sensitized guinea-pigs was totally suppressed by acute subcutaneous infusion of rac-salbutamol (0.69 microgram/kg per min) for < 1 h. More prolonged infusion of rac-salbutamol induced a progressive susceptibility to inhaled antigen so that, by 48 h, animals collapsed and died following inhalation of antigen. In anaesthetized animals, acute infusion of rac-salbutamol (1.67 micrograms/kg per min) suppressed airway obstruction, an effect that can be attributed to beta 2-adrenoceptor activation by the eutomer (R-salbutamol). Acute intravenous infusion of the distomer (S-salbutamol) (1.67 micrograms/kg per min) induced hyperresponsiveness to histamine without having any effect upon airway calibre. It is suggested therefore that subcutaneous infusion of rac-salbutamol initially abrogates the bronchoconstrictor response to antigen because the bronchodilator action of the eutomer predominates over hyperreactivity attributable to the distomer. Conversion from protection to susceptibility was not determined by reduced beta 2-adrenoceptor activation since animals could be protected from a lethal response to antigen by inhalation of rac-isoprenaline or by subcutaneous injection of rac-salbutamol. The seeming progressive loss of efficacy of R-salbutamol may result from disproportionate accumulation of S-salbutamol if, as in man, there is stereospecific metabolism of R-salbutamol. The capacity of S-salbutamol to evoke hyperresponsiveness is shared by S-isoprenaline and S-terbutaline and, as has been shown previously for rac-isoprenaline, the capacity of S-salbutamol to elicit hyperresponsiveness was not evidenced following section of the vagus nerves. No mechanism has yet been established which might account for this property of S-salbutamol or for other S-enantiomers of sympathomimetics.

Administration, Topical↗
PubMed1977

[The influence of beta-sympathomimetics and so-called Ca++-antagonistic inhibitors on human heart muscle in vitro (author's transl)].

In an in vitro assay on fetal human heart muscle it was demonstrated for the first time that overstimulation by beta-sympathomimetics could cause elective parenchymal necrosis. Fenoterolhydrobromide, which is used for tocolysis on a longterm scale, induces in vitro necroses of individual heart muscle fibers according to a pathogenetic principle postulated by Flekkenstein. The combination of Fenoterolhydrobromide with a Ca++-antagonist prevents elective parenchymal necroses by reducing the Ca++-influx into the heart muscle fibers. These results suggest that elective necroses of heart muscle fibers may be not only of coronarogenic but also of metabolic origin.

Calcium↗
PubMed1982

Plasma insulin levels and beta-adrenoceptor antagonists. The effects of cardioselective and non-cardioselective beta-adrenoceptor antagonists with and without intrinsic sympathomimetic activity on basal insulin level and insulin level after glucose stimulation in normoglycemic dogs.

The effect of beta-adrenoceptor antagonists on the intravenous glucose tolerance test was investigated in conscious dogs. dl-Celiprolol (cardioselective with ISA = intrinsic sympathomimetic activity) 200 and 1000 microgram/kg i.v., dl-metoprolol (cardio-selective without ISA) 200 and 1000 microgram/kg i.v., dl-pindolol (non-selective with ISA) 5 and 25 microgram i.v. and l-bupranolol (non-selective without ISA) 10 and 50 microgram/kg i.v. were used in the study. The influence of beta-adrenoceptor antagonists on the plasma glucose and immunoreactive insulin following intravenous glucose tolerance test were evaluated by calculating the respective areas under the plasma curve. The present investigation clearly demonstrates the marked difference between the various beta-adrenoceptor antagonists on heart rate and, especially on metabolic parameters. dl-Metoprolol, a beta-adrenoceptor antagonist with cardioselectivity and without ISA can be assumed not to alter plasma insulin level and glucose assimilation. l-Bupranolol, a non-selective beta-adrenoceptor antagonist without ISA reduces plasma insulin level and probably enhances peripheral glucose uptake, resulting in an "unchanged" glucose tolerance. dl-Celiprolol or dl-pindolol, beta-adrenoceptor antagonists with ISA, but cardioselective or non-selective enhance both, basal insulin level and insulin level after glucose stimulation but must be assumed to decrease peripheral glucose uptake since here too glucose tolerance was unchanged.

Adrenergic beta-Antagonists↗
PubMed1989

Exercise haemodynamic effects of beta-blockade and intrinsic sympathomimetic activity.

Beta-adrenergic blockade with intrinsic sympathomimetic activity (ISA) causes less depression of resting and submaximal heart rate (HR) than non-ISA beta-blockers. The effects of these drugs on exercise haemodynamics have not been well studied. We evaluated effects of pindolol, propranolol and placebo during rest and steady-state exercise on cardiac output, oxygen consumption, calf blood flow, HR and blood pressure in 18 healthy subjects. Pindolol 5 mg and propranolol 80 mg given twice daily, reduced maximal exercise HR by 50 and 52 beats.min-1 respectively, confirming similarity of beta 1-blockade. Resting cardiac output was unchanged in all three groups after one week of therapy. Cardiac output, measured during steady-state exercise decreased in the propranolol group (18.3 vs 15.6 l.min-1) with no significant changes in pindolol (15.7 vs 16.01.min-1) or placebo (18.6 vs 17.3 l.min-1). The rise in cardiac output, from rest to exercise, was similarly attenuated by propranolol but not by pindolol or placebo. Exercise stroke volume increased 12% on pindolol (123-140 cc) and decreased 7% on propranolol (143-133 cc). Neither drug had a detrimental effect on exercise calf blood flow compared to placebo. Thus, unlike propranolol, pindolol with ISA, maintains a normal cardiac output during submaximal exercise.

Adult↗
PubMed1979

[Hemodynamic and humoral changes during administration of a sympathomimetic and a sympatholytic drug with special notes on the regulation of renin release (author's transl)].

Studies in normal volunteers documented the positive inotropic effects of Etilefrin-HCL, a direct sympathomimetic drug, with increases of systolic blood pressure, renal blood flow and glomerular filtration rate. Sodium and potassium excretion as well as serum potassium decreased. After an additional injection of Metoprolol, a beta 1-sympatholytic drug, blood pressure, renal blood flow and glomerular filtration rate normalized, whereas electrolyte excretion decreased further. Renin release was decreased during administration of Etilefrin as well as during combined Etilefrin and Metoprolol application. Reziprocal to changes of blood pressure, plasma norepinephrine concentration decreased during Etilefrin and increased during combined administration of Etilefrin and Metoprolol. The results lead to the following interpretation: Changes of blood pressure and renal hemodynamics are mediated by beta 1-adrenergic effects of Etilefrin, whereas the electrolyte excretion is influenced by beta 2-adrenergic effects. Renin release seems to be influenced by beta 1 as well as beta 2-adrenergic receptors.

Adult↗
PubMed1990

Transient electrocardiographic changes suggesting myocardial ischaemia in newborn infants following tocolysis with beta-sympathomimetics.

Serial electrocardiograms (ECGs) were studied prospectively in 80 apparently healthy newborn infants; 30 infants exposed in utero to prolonged tocolytic therapy (21 to ritodrine and 9 to isoxsuprine) and 50 infants non-exposed in utero to drugs (control group) matched for gestational age, Apgar score, and birth weight. Duration of exposure to tocolysis was at least 30 days (30-180 days) with an oral dosage of 10 mg 3 times daily. ECGs were graded for changes suggestive of ischaemia using the arbitrary grading system described by Jedeikin et al. In all infants with ECG features of myocardial ischaemia, serum creatine-phosphokinase iso-enzyme (CK-MB) activity was measured. Six out of 21 infants to ritodrine and six out of nine infants exposed to isoxsuprine showed a degree of ECG ischaemia which persisted for several weeks. No control infant presented grade 2 or 3 ECG changes after the 5th day of life. The results of this study seem to show that prolonged tocolytic therapy with beta-sympathomimetics has side-effects on the fetal myocardium and suggest that this treatment be reserved only for selective cases and/or for short periods of time.

Adrenergic beta-Agonists↗
PubMed1981

Pirbuterol: a new oral sympathomimetic amine for the treatment of congestive heart failure.

Fourteen patients with refractory congestive heart failure (CHF) were given a single oral dose ranging from 5 to 30 mg of the new sympathomimetic drug pirbuterol. Hemodynamic measurements and plasma pirbuterol levels were obtained at control and then serially for 6 hours following drug administration. The optimal pirbuterol dose range was determined to be 20 to 30 mg. Ten patients received 20 to 30 mg pirbuterol. In this group cardiac index was significantly increased (1.9 to 2.6 L/min/m2, p less than 0.001). Pulmonary artery wedge pressures fell significantly (24 to 20 mm Hg, p less than 0.02). Decreases were also noted in mean pulmonary artery pressure (36 to 31 mm Hg, p less than 0.02), aortic diastolic pressure (71 to 65 mm Hg, p less than 0.05), systemic vascular resistance (1782 to 1201 dynes. sec. cm-5, p less than 0.001), and pulmonary vascular resistance (265 to 175 dynes.sec.cm-5, less than 0.001). Systolic and mean aortic pressure and heart rate showed no significant change from control. Hemodynamic effects persisted for 5 hours. Pirbuterol was clinically well tolerated. The mechanism of action is unclear at this time, but both inotropic and vasodilator effects are possible. Pirbuterol orally has a marked and prolonged salutary hemodynamic effect and offers promise in CHF treatment.

Administration, Oral↗
PubMed1985

The role of beta blockade, with and without intrinsic sympathomimetic activity, in preserving compromised left ventricular function in patients with ischemic heart disease.

To determine if intrinsic sympathomimetic activity (ISA) is associated with a hemodynamic advantage over non-ISA beta blockade, 17 patients with ischemic heart disease underwent resting echocardiography and symptom-limited stress radionuclide angiography on three occasions: control, pindolol (with ISA), 10 mg twice a day, and propranolol, 40 mg four times a day, in a nonrandomized design. In six patients with normal resting ejection fraction (EF) (mean = 57 +/- 4%), neither drug was associated with a significant hemodynamic improvement over control. In 11 patients with reduced resting EF (mean = 37 +/- 9%), pindolol was associated with a higher EF and peak velocity of circumferential fiber shortening at rest compared with propranolol but not control. On maximal exertion, pindolol was associated with a higher EF than that during control but was similar to propranolol. These observed beneficial effects on pindolol appear primarily to be related to the partial beta agonist activity which this agent possesses.

Adrenergic beta-Antagonists↗
PubMed1988

Acute hemodynamic effects of pindolol and propranolol in patients with dilated cardiomyopathy: relevance of intrinsic sympathomimetic activity.

The administration of beta-blocking agents to patients with poor left ventricular (LV) function may result in clinical and hemodynamic deterioration. The beta antagonist pindolol has intrinsic sympathomimetic activity (ISA) and therefore may be better tolerated. To test this hypothesis 30 patients with a precatheterization diagnosis of dilated cardiomyopathy were randomly assigned to three groups to receive intravenous injections of placebo, propranolol, or pindolol. The baseline ejection fraction and hemodynamics were similar for all groups. For propranolol 1 mg, 2 mg, 3 mg, and 4 mg doses were given 5 minutes apart until a maximum dose of 10 mg was reached, until a 25% reduction in the heart rate or mean arterial pressure occurred, or until clinical deterioration developed. For pindolol, 0.1 mg, 0.2 mg, 0.3 mg, and 0.4 mg boluses were used with the same end points. Baseline hemodynamics were measured and repeated 15 minutes after the last dose of each drug was administered. The mean number of doses given was similar for both groups: 3.3 doses for the propranolol group and 3.4 for the pindolol group. Compared to propranolol, pindolol caused less of a reduction in heart rate, cardiac output, cardiac index, stroke volume index, and stroke work index and less of an increase in the mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure, left ventricular end-diastolic pressure, and pulmonary vascular resistance; there was a decrease in systemic vascular resistance. These differences were statistically significant for changes in heart rate, right atrial pressure, cardiac index, and systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Influence of beta blockade and intrinsic sympathomimetic activity on hemodynamics, inotropy and respiration at rest and during exercise.

The degree of intrinsic sympathomimetic activity (ISA) is reported to influence the effects of beta blockade at rest, but the effects during exercise are not well documented. Heart rate, blood pressure and left ventricular (LV) function (as assessed by systolic time intervals) were measured at rest and during upright bicycle exercise as well as with flow-volume spirometry at rest in 13 healthy volunteers. The measurements were performed before and 4 and 24 hours after a single oral dose of pindolol (10 mg), nadolol (80 mg) and acebutolol (400 mg) in a double-blind, randomized, crossover manner. All drugs reduced heart rate, but nadolol had the most pronounced and longest bradycardic effect at rest. Diastolic blood pressure was only slightly influenced by the drugs, whereas systolic pressure was significantly lower compared with control values, especially during exercise (p less than 0.001). Neither preejection period (PEP) nor LV ejection time (LVETc) was changed at rest after pindolol, but PEP increased and LVETc decreased significantly after nadolol (p less than 0.05 for PEP and p less than 0.01 for LVETc) and acebutolol (p less than 0.05 for both). During exercise, PEP and LVET were significantly longer after all 3 drugs compared with control values. Only nadolol, which lacks ISA, significantly decreased expiratory flow values (p less than 0.05). Thus, unlike the other beta blockers, pindolol (with strong ISA) did not depress LV function at rest, while during exercise all 3 beta blockers had equal adverse effects. The degree of ISA appears to be important in determining the hemodynamic effects of beta-blocking drugs.

Acebutolol↗
PubMed1990

Relevance of intrinsic sympathomimetic activity for beta blockers.

Intrinsic sympathomimetic activity (ISA) characterizes a group of beta blockers that are able to stimulate beta-adrenergic receptors (agonist effect) and to oppose the stimulating effects of catecholamines (antagonist effect) in a competitive way. Partial agonists are ligands that elicit a submaximal response when bound to beta receptors at maximal occupancy. In the isolated rat atrium, acebutolol produces a maximal stimulatory effect that is only 17 +/- 8% of the maximal effect induced by the full beta agonist isoproterenol. The presence of ISA results in less resting bradycardia and less of a reduction in cardiac output than is observed with beta blockers without ISA. In the long term, partial beta agonists may produce arterial vasodilation and increase arterial compliance, possibly leading to additional beneficial effects in the treatment of hypertension. beta blockers with ISA do not have adverse effects on plasma lipoproteins during long-term treatment; in addition, the presence of ISA could counteract the up-regulation of beta adrenoceptors often observed with beta blockers without ISA. Finally, the presence of ISA has been a conflicting issue for the use of such beta blockers in secondary prevention after myocardial infarction. However, the impressive results of the Acebutolol Prevention of Secondary Infarction trial in high-risk patients after myocardial infarction show that acebutolol, a beta blocker with moderate partial agonist activity, can be effective in decreasing the postinfarction mortality rate. By exhibiting a strikingly different hemodynamic profile from that of beta blockers without ISA, the partial beta agonists form an intriguing pharmacologic class of drugs for which prospective clinical trials should be extensively pursued.

Acebutolol↗
PubMed1977

Use of a beta 2-sympathomimetic drug as a temporizing measure in the treatment of acute fetal distress.

Severe fetal distress in labor is an obstetric emergency which may result in the delivery of a severely asphyxiated baby or even death of the fetus. This problem may be compounded by a hurried mechanical vaginal delivery or by delay before a cesarean section can be performed. The rationale for using a beta sympathomimetric drug as a temporizing measure in the treatment of fetal distress to prevent deterioration in and even to improve the condition of the fetus before delivery is discussed. Six cases are described in which hexoprenaline (Ipradol), a beta2-selective sympathomimetic drug, has been administered as a 10 microgram intravenous bolus in the treatment of acute fetal distress in labor.

Apgar Score↗
PubMed1980

Treatment of premature labor with beta sympathomimetics: results with isoxsuprine.

This prospective study presents a protocol for the treatment of premature labor with beta sympathomimetics and the results when isoxsuprine was used. Seventy-two patients from 25 to 36 weeks' gestation were treated. All patients were placed at bed rest, hydrated, and given parenteral sedation prior to the intravenous use of isoxsuprine. Treatment was continued via the intramuscular and oral routes until the thirty-seventh week of gestation. Three patients (4.2%) were delivered of infants during the initial infusion, and 15 (20.2%) were delivered of infants within 2 weeks after the onset of therapy. Forty-nine (68%) were delivered of infants after 37 weeks' gestation, and their infants weighed more than 2,500 grams. Maternal side effects were common, but none necessitated termination of therapy. There were six neonatal deaths, the causes of which were respiratory distress syndrome in two infants, necrotizing enterocolitis in one, group B streptococcal sepsis in one, congenital anomalies with sepsis in one, and multiple congenital anomalies in one.

Adrenergic beta-Agonists↗