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At least 667 records · Page 37Linked to original sources
PubMed1985

A comparison of the relative toxicities of beta-sympathomimetic tocolytic agents.

To define the relative toxicities of ritodrine sulfate, terbutaline sulfate, hexaprenaline sulfate, and ritodrine with betamethasone mongrel dogs were treated with these agents for 19 hours. The maximum dose of ritodrine was 900 microgram/min (N = 5), terbutaline 120 micrograms/min (N = 4) and hexaprenaline 1.5 micrograms/min (N = 4). Betamethasone was given intramuscularly (12 mg) at initiation of ritodrine and repeated in 12 hours in four animals. Arrhythmias were responsible for five deaths; 2/4 terbutaline, 2/4 ritodrine and beta-methasone, 1/5 ritodrine, 0/4 hexaprenaline treated animals. Terbutaline-treated animals developed arrhythmias during more treatment cycles (50%) and at lower drug concentrations, whereas hexaprenaline-treated animals developed arrhythmias at higher drug concentrations, with an overall arrhythmia frequency of 14%. Terbutaline animals had the highest heart rate (P = 0.02) and lowest mean arterial pressure (P = 0.18); the least effect on these parameters being seen with hexaprenaline. Cardiac index was higher with terbutaline and hexaprenaline compared to ritodrine with or without beta-methasone (P = 0.02). Hypoxemia was most severe with terbutaline (pO2 = 58 mm Hg) and least severe with hexaprenaline (pO2 = 66 mm Hg); however, this does not explain the difference in the frequency of arrhythmias since the mean pO2 during the initial arrhythmias was 76 mm Hg in terbutaline treated animals compared to a baseline control of 85 mm Hg. Although all animals developed significant acidosis during Phases II-IV, hexaprenaline treated animals were the least acidotic (P = 0.036). Hypokalemia was most pronounced with terbutaline (P = 0.08 Phase II, P = 0.07 Phase III).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Pancuronium bromide: an indirect sympathomimetic agent.

In the dog, pancuronium 0.2 mg/kg increased left ventricular systolic pressure and systemic arterial pressure, but did not change central venous pressure. Repeated doses produced diminishing responses and eventually no change in arterial pressure. After tachyphylaxis was established, a pressor response to pancuronium could be induced by an i.v. infusion of noradrenaline. Desipramine, a noradrenaline blocking agent, prevented the restoration of the pressor effect of noradrenaline. Guanethidine and reserpine abollished the restoration of the pressor response to pancuronium by noradrenaline. These findings are consistent with the hypothesis that pancuronium acts on the postganglionic nerve endings and causes release of noradrenaline.

Animals↗
PubMed2005

Examples of doping control analysis by liquid chromatography-tandem mass spectrometry: ephedrines, beta-receptor blocking agents, diuretics, sympathomimetics, and cross-linked hemoglobins.

The application of modern and powerful analytical instruments consisting of liquid chromatographs (LCs), sophisticated atmospheric pressure ion sources, and sensitive mass analyzers has improved quality as well as speed of doping control analyses markedly during the last 5 years. Numerous compounds such as beta-receptor blocking agents or diuretics require derivatization prior to gas chromatographic (GC) and mass spectrometric (MS) measurement, which is the reason for extended sample preparation periods. In addition, several substances demonstrate poor GC-MS properties even after chemical modification, and peptide hormones such as cross-linked hemoglobins cannot be analyzed at all by means of GC-MS. With the availability of electrospray ionization and robust tandem MSs (e.g., triple-stage quadrupole or ion trap instruments) many new or complementary screening and confirmation assays have been developed, providing detailed qualitative and quantitative information on prohibited drugs. With selected categories of compounds (ephedrines, beta-blockers, b2-agonists, diuretics, and bovine hemoglobin-based oxygen therapeutics) that are banned according to the rules of the World Anti-Doping Agency and International Olympic Committee, the advantages of LC-MS-MS procedures over conventional GC-MS assays are demonstrated, such as enhanced separation of analytes, shorter sample pretreatment, and identification of substances that are not identified by GC-MS.

Adrenergic beta-Antagonists↗
PubMed1992

Action of nimodipine on sympathomimetic mydriatics in humans.

In 12 healthy volunteers, the effects of a single oral dose of nimodipine (40 mg) on pupil size and on the mydriasis induced by conjunctival instillation of tyramine and phenylephrine were studied by using a TV monocular infrared pupillometer. Nimodipine alone was unable to modify the pupil area. When compared with placebo, the Ca2+ entry blocker reduced the pupil dilation caused by tyramine, whereas it did not affect the phenylephrine-induced mydriasis. Since tyramine provokes mydriasis by releasing neuronal norepinephrine, a full adrenoceptor agonist, whereas phenylephrine acts only on alpha 1-adrenoceptors insensitive of extracellular Ca2+, the hypothesis may be advanced that a heterogeneous population of alpha-adrenoceptors, located in the human iris dilator muscle and differently sensitive to Ca2+ entry blockade, is responsible for the reduction of the tyramine-induced mydriasis. Apart from this putative mechanism, the results suggest that nimodipine reduces the pupillary response to adrenergic activation in the human eye.

Administration, Oral↗
PubMed1983

Treatment of hypertension with beta-blockers with and without intrinsic sympathomimetic activity.

In a randomized double-blind trial 36 patients with essential hypertension were treated with either metoprolol or pindolol for 6 months following a 6-week placebo period. At the end of the placebo period and after 6 weeks and 6 months of active therapy peripheral hemodynamics at rest and during maximal vasodilatation were studied. Exercise heart rate was reduced to the same extent with both metoprolol and pindolol, indicating that the doses used (metoprolol average 179 mg/day; pindolol average 12 mg/day) were equipotent as regards beta-adrenoceptor blocking effect. The antihypertensive effect was identical with both compounds. However, metoprolol caused a significant reduction of heart rate at rest both at 6 weeks and 6 months. With pindolol the reduction in heart rate was not significant at 6 weeks, and it was clearly much less than with metoprolol. On the other hand, no change in calf vascular resistance was seen during metoprolol therapy, whereas a marked and statistically significant reduction was caused by pindolol. Resistance at maximal dilatation in the forearm did not change with metoprolol, but tended to fall with pindolol after 6 weeks and was significantly reduced after 6 months. This indicates that although metoprolol and pindolol have the same antihypertensive potency, the two agents appear to reduce blood pressure through different mechanisms. Thus, cardiac mechanisms seem to play the most important role with metoprolol, whereas pindolol mainly acts by a reduction in vascular resistance. It also seems that treatment with pindolol normalizes the structural arteriolar abnormality present in hypertension as indicated by the reduction in resistance at maximal vasodilation.

Adrenergic beta-Antagonists↗
PubMed1987

Cardiovascular effects of KM-13, a new, orally effective, cardiotonic sympathomimetic amine.

Dobutamine's chemical structure was modified to make it orally effective, while its pharmacological profile was preserved. Testing on anesthetized dogs showed that replacement of the para hydroxyl group with carboxyamide at the phenyl end of the molecule increased inotropic potency threefold, but it introduced pressor activity that spoiled the inotropic selective profile of dobutamine. However, shifting carboxyamide to the meta position avoided pressor activity and further enhanced inotropic potency to nine times that of dobutamine. When administered orally to conscious dogs, this compound, KM-13 (5 mg/kg), produced a sustained increase in left ventricular dP/dt with only immediate changes in heart rate; 10 mg/kg dobutamine was without cardiovascular effects. The (-) isomer of KM-13 contained twice the inotropic activity of the (+) isomer; in contrast, the (-) isomer had no effect on diastolic blood pressure, while the (+) isomer lowered blood pressure. The inotropic and chronotropic effects of dobutamine and KM-13 are both largely due to beta-adrenergic stimulation as shown by propranolol blockade. In contrast to dobutamine, KM-13 is an agent that is active by either oral or buccal administration and has greater inotropic potency.

Anesthesia↗