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At least 1,585 records · Page 88Linked to original sources
PubMed1993

The hemodynamic effects of antenatal indomethacin and a beta-sympathomimetic agent on the fetus and the newborn: a randomized study.

To study the effect of antenatal indomethacin or nylidrin hydrochloride treatment on the fetal and neonatal ductus arteriosus and tricuspid valve function, 84 pregnant women with threatened premature birth between 22.9 and 34.0 wk gestation and 94 of their offspring born at 24.7 to 41.6 wk of gestation were studied by Doppler echocardiography. Forty-six women were treated with indomethacin and 38 with nylidrin. Both peak systolic and peak diastolic velocities in the ductus increased after administration of indomethacin and exceeded the corresponding velocities in the fetuses of the nylidrin group (p = 0.0001). Ductal constriction occurred in 42 of 49 fetuses treated with indomethacin (86%). Tricuspid valve regurgitation (TR) was evident in 11 of 49 fetuses treated with indomethacin (22%). The mean gestational age of the fetuses with TR (30.0 wk) tended to be higher than those without TR (28.3 wk, p = 0.056). In the nylidrin group, no fetus had ductal constriction or TR. A significant increase in peak systolic velocity (r = 0.54, p = 0.0001) and in peak diastolic velocity (r = 0.46, p = 0.0001) in the ductus with advancing gestational age was demonstrated in the indomethacin group; however, in the nylidrin group, there was a less remarkable increase in peak systolic velocity (r = 0.35, p = 0.04) and no increase in peak diastolic velocity (r = 0.02, p = 0.93). In infants born at or before 35 wk gestation, incidences of both spontaneous closure and indomethacin-induced closure of ductus were similar in both study groups (p > 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Interaction of sympathomimetics and insulin with hepatic glucose production by isolated perfused rat livers: effects of continuous versus pulsatile infusion.

To elucidate the efficacy of continuous vs. intermittent exposure to epinephrine, phenylephrine, and insulin, hepatic glucose production was monitored in isolated perfused rat livers (means +/- SE, n = 6 each). To this end livers of fed rats were perfused with 5 mM glucose Krebs-Ringer buffer in a nonrecirculating system. Using this model it was shown that intermittent exposure (3 min on/off period, dose reduction -50%) to epinephrine (0.4 microM, alpha + beta-agonist) and phenylephrine (5 microM, alpha-agonist) elicited an almost identical rise in hepatic glucose production [epinephrine: 0.72 +/- 0.08 mmol/(86 min X 100 g BW); phenylephrine: 0.68 +/- 0.07 mmol/(86 min X 100 g BW) as their continuous administration (epinephrine: 0.78 +/- 0.06 mmol/(86 min X 100 g BW); phenylephrine: 0.74 +/- 0.09 mmol/(86 min X 100 g BW)]. Inhibition by insulin (100 mU/liter) given either continuously or intermittently (3 min on/off intervals; dose reduction -50%) was equipotent for epinephrine- and phenylephrine-stimulated hepatic glucose production. When the off period was doubled to 6 min, thereby reducing the total insulin dose to 33%, no significant suppression of epinephrine- and phenylephrine-stimulated hepatic glucose production was observed. From this we conclude that 1) the effect on hepatic glucose production of pulsatile (3 min on/off, dose reduction 50%) and continuous administration is equipotent for the respective action of epinephrine, phenylephrine as well as of insulin; and 2) insulin is more effective (P less than 0.02) in inhibiting hepatic glucose production stimulated by an alpha-agonist (phenylephrine; 5.0 microM) than in counteracting alpha + beta-agonist action (epinephrine; 0.4 microM). The characteristics of hepatic glucose release as stimulated by alpha- and/or beta-adrenergic agonists and its inhibition by continuously or intermittently infused insulin were simulated and described by a computer model. Thereby, no qualitative difference could be demonstrated in alpha- vs. beta-adrenergic agonists action on stimulated hepatic glucose production.

Animals↗
PubMed1979

Antifertility effect of sympathomimetic drugs on male rats when applied locally to the vas deferens.

Local application of collars containing 25% methoxamine, 50% or 75% tyramine or 50% norephedrine to both vasa deferentia of rats caused a reduction in fertility but not in their ability to mate. A gradual return to fertility was seen in those animals which received the lower dose of tyramine or norephedrine, while the other treatments caused a permanent reduction in fertility. The cause of sterility was production of azoospermic ejaculates resulting from either a block in sperm transport in the vas deferens or from a deficiency in the ejaculatory mechanism. Only methoxamine caused a mechanical obstruction of the vas deferens, but it is possible that the other drugs caused a sustained spasm. An emission defect could have been due to transmitter depletion, receptor-specific desensitization or presynaptic alpha-adrenoreceptor-mediated inhibition. Spermatozoa from the cauda epididymidis were immotile following the treatments.

Animals↗
PubMed1999

Sympathomimetic preference and ethnicity in male felons.

A disproportionate number of Euro-American inmates given either an amphetamine- or cocaine-abuse diagnosis upon admission to prison were given a diagnosis of amphetamine abuse. A disproportionate number of African-American inmates were given a cocaine-abuse diagnosis. Of the 800 consecutively admitted inmates who were given one diagnosis or the other, 68% of the cocaine abusers, but only 4% of the amphetamine abusers, were African American.

Adult↗
PubMed1978

Inhibition of gastric acid secretion in dogs by a new sympathomimetic drug.

The effect of salmefamol, a new beta 2-agonist, on pentagastrin-induced gastric acid secretion was studied in conscious gastric fistula dogs. Salmefamol inhibited the acid secretion, an effect which was dose dependent. The volume as well as the acidity was inhibited. Salmefamol caused an increase in the pulse rate. Propranolol prevented the inhibition of acid output as well as the increase in pulse rate. Practolol, a beta 1-adrenoceptor blocker, had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with 6 doses of pentagastrin and 1 dose of salmefamol showed a decrease in calculated maximal response (CMR) and an unchanged D50. It is concluded that salmefamol strongly inhibits pentagastrin-induced acid output in the dog, and the inhibition follows a non-competitive kinetic. The mechanism of gastric secretion probably involves a beta 2-receptor.

Animals↗
PubMed1980

Effect of beta 2-sympathomimetic on pentagastrin- and histamine-stimulated gastric acid secretion in vagotomized gastric fistula dogs.

The effect of a beta 2-adrenoceptor agonist on pentagastrin- and histamine-stimulated gastric acid secretion was studied in conscious vagotomized gastric fistula dogs. A dose-dependent inhibition was found after pentagastrin stimulation, whereas minor differences were found after histamine stimulation. No major differences between truncal, selective, and parietal cell vagotomy were found after pentagastrin stimulation, whereas one truncal vagotomy dog showed a high inhibition after histamine stimulation. Dose-response experiments with five doses of pentagastrin or histamine (single-dose studies) and two doses of beta 2-agonist suggested a change after vagotomy in the mechanisms of inhibition of gastric acid secretion: for pentagastrin, from a non-competitive type to an uncompetitive type, and for histamine, from a competitive type to a non-significant inhibition. Furthermore, the dose-response curves for the vagotomized dogs were very similar to the curve from intact innervated dogs inhibited by a beta 2-agonist, from an earlier study. These findings may indicate that a decrease in cholinergic tone and an increase in sympathetic tone have identical effects on pentagastrin- and histamine-stimulated gastric acid secretion, and a counterbalance between the two nervous systems on gastric acid secretion is suggested.

Adrenergic beta-Agonists↗
PubMed1981

Effect of a beta2-sympathomimetic on urecholine-stimulated gastric acid secretion in dogs.

The effect of a selective beta2-adrenoceptor agonist on urecholine-stimulated gastric acid secretion was studied in conscious gastric fistula dogs. A dose-dependent inhibition was found, most pronounced for the highest doses of urecholine. The inhibition was primarily on volume, whereas the acidity showed a decreasing tendency only. The pulse rate was increased by the beta2-agonist and by urecholine in high doses. Propranolol prevented both the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with five doses of urecholine and two doses of the beta2-agonist showed a decrease in maximal response, and transformation of the curve suggested an unchanged D50. It is concluded that the beta2-agonist inhibits urecholine-stimulated acid secretion in the dog to the same degree as pentagastrin-induced acid secretion, and much stronger than found for histamine-induced acid secretion in earlier experiments. The inhibition seems to follow a noncompetitive kinetic, and beta2-receptors are probable involved.

Adrenergic beta-Agonists↗
PubMed1981

Effect of a beta 2-sympathomimetic on gastrin release, acid secretion, and blood glucose during basal conditions and in response to insulin, 2-deoxy-D-glucose, and feeding in the dog.

The effect of a selective beta 2-adrenoceptor agonist on basal volume and on insulin-, 2-deoxy-D-glucose (2-DG)-, and food-induced gastrin release was studied in conscious gastric fistula dogs. Acid output and blood glucose changes were also studied, except in the food experiments. Basal acid secretion and serum gastrin were unchanged after beta 2-sympathetic infusion, whereas a slight increase in blood and glucose was found. The beta 2-agonist almost prevented acid output and gastrin release after insulin hypoglycaemia. However, the hypoglycaemia was also inhibited. Gastric acid secretion stimulated by 2-DG was inhibited, as was probably the gastrin release. 2-DG increased the blood glucose level, and no significant differences were found after beta 2 infusion. After feeding, gastrin release was initially decreased for one of five doses of the beta 2-agonist, and higher doses of the beta 2-agonist prevented the subsequent fall in serum gastrin after the initial peak value. This pattern was also found for the histamine H2-blocker cimetidine in a dose that blocks acid output. The beta 2-agonist and 2-DG increased pulse rate. It is concluded that beta 2-sympathetic stimulation inhibits acid output and gastrin release after insulin and 2-DG stimulation, but one should be cautions in drawing conclusions from the insulin experiments. The effect on gastrin release is small compared with the effect on the acid secretion, and it is unlikely that the inhibition of acid secretion acts through a change in gastrin release.

Animal Feed↗