Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SYMPATHOMIMETICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources
PubMed1978

Studies on the sympathomimetic effects of guanoxan on smooth muscles of rat.

In anococcygeus muscle and vas deferens preparations of rat, guanidinomethyl-2-benzo-(1,4)-dioxane (guanoxan) potentiated responses to norepinephrine (NF) in concentrations which exerted a neurone blocking effect. The potentiation was significantly reduced in reserpinized preparations and was abolished in the presence of nialamide. The possible mechanisms of potentiation have been discussed. Higher concentrations of guanoxan produced concentration-related contractions. The contractions were significantly less in reserpinized preparations. Phentolamine both prevented and reversed the contractions while methysergide was ineffective in this respect. Thus the effect of guanoxan appears to be mediated through the activation of alpha-receptors by the released NE.

Animals↗
PubMed1978

Differential beta-adrenergic sensitivity of atrial tissue assessed by chronotropic and inotropic responses to several sympathomimetic amines.

The relative inotropic and chronotropic activity of epinephrine, norepinephrine, isoproterenol, dopamine, dobutamine and ethylephrine was studied on isolated rat atria at 31 C. Dose-response curves were expressed as a percentage of the maximum response. Both atria were used for testing chronotropic effects. Inotropic dose-response curves were performed on left atria driven at 1 Hz, 1.6 Hz, 2.8 Hz and 6.6 Hz. Epinephrine and norepinephrine had a greater chronotropic action than their inotropic one throughout the range of stimulation employed. Their pD2-values changed from 8.12 +/- 0.06 and 8.05 +/- 0.05 to 7.19 +/- 0.03 and 7.14 +/- 0.05, respectively. Isoproterenol, dopamine and ethylephrine produced the same degree of chronotropic and inotropic stimulation. Dobutamine exerted the same effect on heart rate and developed tension at 1 Hz. pD2-values for dobutamine were significantly lower (p less than 0.01, p less than 0.001, p less than 0.001) when the frequency of stimulation was increased to 1.6, 2.8 and 6.6 Hz. These findings may be due to the influence of the negative staircase phenomenon, the temperature and the distribution of beta 1 and beta 2 receptors.

Animals↗
PubMed1975

Treatment of circulatory shock. Use of sympathomimetic and related vasoactive agents.

Reduction of effective blood flow represents the primary disturbance accounting for circulatory shock. Four categories of circulatory shock are identified: cardiogenic, hypovolemic, distributive, and obstructive. The pharmacology and clinical implications for treatment of shock with vasoactive drugs are reviewed in this context. Except for epinephrine, when it is used for treatment of anaphylactic shock, there is no specific indication for the routine use of alpha- or beta-adrenergic receptor agonists. These agents may increase blood pressure or cardiac output, but nutritive flow is not necessarily improved. Comparable limitations are observed with alpha-adrenergic receptor blocking agents. However, selective effects on the myocardium and on the resistance, exchange, and capacitance vessels may be advantageous as an interim and complementary measure. Since vasoactive drugs frequently intensify the fundamental defect accounting for perfusion failure, their selective rather than routine employment is mandatory.

Adrenergic alpha-Agonists↗
PubMed1989

Celiprolol does not protect against ventricular tachycardia or sudden death in the conscious canine: a comparison with pindolol in assessing the role of intrinsic sympathomimetic activity.

The antiarrhythmic and antifibrillatory effects of the beta-1 adrenoceptor antagonist celiprolol were evaluated in a chronic canine model of myocardial infarction and sudden death. Programmed electrical stimulation (PES) was performed in conscious animals 3 to 5 days after a 2-hr occlusion/reperfusion of the left anterior descending coronary artery. Dogs in which PES resulted in a reproducible nonsustaining or sustained ventricular tachycardia (VT) were randomized to receive i.v. celiprolol (3 mg/kg, n = 10) or vehicle (n = 10). PES and measurement of electrophysiologic (parameters were repeated after 30 min and the animals were entered into the sudden death protocol by introducing a 150-microA anodal current to the lumen of the left circumflex coronary artery via a surgically implanted silver wire electrode. Celiprolol failed to prevent the induction of VT, and the outcome of the sudden death protocol did not differ from vehicle with respect to either sudden (within 1 hr of ischemia) or delayed (greater than 1 hr) mortality. VT cycle length and ventricular refractoriness were prolonged (P less than .05) by celiprolol, but other electrophysiologic parameters were unaffected. Heart rate was not altered after drug, but celiprolol antagonized the ischemia-induced increase in rate seen in the vehicle group. Similar electrophysiologic results and mortality data were apparent in a third group of dogs which received pindolol (0.09 mg/kg, n = 8). The failure of both drugs to protect against ischemic ventricular fibrillation in a model in which beta adrenoceptor antagonism has previously proved beneficial may be due in part to related cardiostimulant properties shared by celiprolol and pindolol.

Adrenergic beta-Antagonists↗
PubMed1989

The role of sympathetic innervation and sympathomimetics in gastric secretion in vivo.

It can, I believe, be argued in summary that pentagastrin-stimulated acid and pepsin secretion from innervated or denervated fundic mucosa is inhibited by doses of epinephrine and isoproterenol that produce an unequivocal cardiac stimulation, but this cannot be said of either histamine-, bethanechol-, or methacholine-, or food-stimulated secretion. There is substantial old evidence that epinephrine and isoproterenol, in doses that depress the pentagastrin effect, actually augment that of histamine and cholinomimetics. Large doses, of course, inhibit unequivocally. Sympathectomy, chemical or surgical, seems to increase the responsiveness of the fundus to acid stimuli, but again there is little uniformity; both less acid following feeding, after sympathectomy, and more following propranolol have been reported. It would be rash to draw any conclusions from the action of either sympathetic stimulation or ablation. The evidence that beta-adrenergic blocking agents can prevent insulin-stimulated increases in gastrin is fairly good, but the evidence that these agents have any effect on food-stimulated gastrin levels (whether the food is a meal or sham) is not good. Almost every aspect of this subject remains confused and confusing. At the end of a paper such as this, most readers would expect conclusions, but any conclusions other than those given above would be invention or else bias. This subject, at present unfashionable for research, represents a black hole in our knowledge.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Neurologic complications caused by use of cocaine, amphetamines and sympathomimetics].

Drug abuse has become a social and medical problem. Amphetamine and cocaine have a potent sympathicomimetic action, so they have important effects on the Central Nervous and Cardiovascular Systems. Their neurological complications are principally: psychic alterations, seizures and stroke (hemorrhagic and ischemic). The latter are the most important in the clinical practice. Their capacity to produce transit arterial hypertension and cerebral vascular constriction could be the physiopathological substrate of such alterations. Angiographic studies have shown lesions suggesting vasculopathy. In the last ten years cocaine abuse has become an authentic epidemic. We have reviewed its neurological complications, particularly the vascular ones--42 hemorrhagic and 24 ischemic--and the following conclusions were drawn: it should be considered as a risk factor in the younger age group; a short period of time between the last drug dose and the clinical picture is frequently seen; clinical features may appear with the first drug administration; no characteristic lesion in relation to the way of administration or consumption time was elicited.

Amphetamines↗
PubMed1985

[Intrinsic sympathomimetic action and its special features as demonstrated by the beta-1-receptor blocker celiprolol].

The Intrinsic Sympathetic Activity (ISA) of the beta-1-adrenoceptor blocker celiprolol was tested in a series of pharmacological and clinical investigations. Celiprolol shows much more pronounced positive chronotropic effects in spontaneously beating atria of cats than in those of guinea-pigs and rats. Positive inotropic effects of celiprolol are much pronounced in the left kitten atrium, but scarcely demonstrable in the kitten papillary muscle. Celiprolol has no influence on the adenylyl cyclase activity of the dog heart. In reserpinized rats and reserpinized, adrenalectomized, vagotomized cats celiprolol increases the heart rate to the same extent as the beta-blocker pindolol. In ganglion-blocked dogs celiprolol distinctly increases heart rate and left ventricular contraction force. Celiprolol relaxes isolated human arterial and venous strips and induces a transient increase of the femoral arterial blood flow in anaesthetized dogs. Celiprolol relaxes isolated bovine tracheal muscle preparations and reduces the airway resistance in anaesthetized cats infused with serotonin. The intrinsic chronotropic effects of celiprolol in cat atria in vitro and in reserpinized rats in vivo and the relaxing effects of celiprolol in isolated bovine tracheal muscles are antagonized by propranolol, and therefore these actions may be explained by the ISA of celiprolol. However the vascular relaxing effects of celiprolol in vitro and in vivo and the bronchodilating effects in the serotonin-infused cat are not blocked by propranolol. In order to obtain a more precise characterization of these surprising effects, further pharmacological investigations were done. In the isolated femoral artery of the dog the concentration-response curve of calcium chloride is not influenced by celiprolol while it is antagonized by verapamil. A serotonin antagonistic effect cannot be demonstrated for celiprolol either in receptor binding studies or on the blood pressure of anaesthetized dogs. Celiprolol inhibits the methacholine bronchospasm in rats and the prostaglandin F2 alpha-induced bronchoconstriction in cats. The histamine-induced bronchoconstriction in dogs is scarcely affected by celiprolol while it is enhanced by propranolol. In radioligand studies celiprolol shows a tenfold higher affinity for alpha-2 in comparison to alpha-1 receptors. Celiprolol enhances the inhibitory effect of clonidine in the electrically stimulated vas deferens of the rat in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗