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At least 379 records · Page 21Linked to original sources
PubMed1994

Torsades de pointes ventricular tachycardia associated with overdose of astemizole.

An overdose of astemizole predisposes the myocardium to ventricular dysrhythmias, including torsades de pointes. Herein we describe a case of astemizole-induced torsades de pointes ventricular tachycardia and also review previous case reports in the literature. All the patients were young, and dysrhythmias developed only in those with corrected QT intervals greater than 500 ms. Although several mechanisms have been postulated, no clear explanation has been provided for why astemizole promotes myocardial dysrhythmias. Treatment of astemizole-induced torsades de pointes includes discontinuing use of astemizole, intravenous administration of magnesium sulfate and isoproterenol, temporary cardiac pacing, and, when necessary, direct current cardioversion. A cardiac cause of syncope or convulsions must not be overlooked, especially in patients taking H1 antagonists because they often have these symptoms before hospitalization or detection of torsades de pointes (or both).

Adult↗
PubMed2002

Effects of quinupristin/dalfopristin on vasomotor tone in the intact peripheral microcirculation.

The purpose of this study was to determine whether quinupristin/dalfopristin modulates vasomotor tone in the intact peripheral microcirculation. Using intravital microscopy, we found that superfusion of quinupristin/dalfopristin (120 mg/L) on the intact hamster cheek pouch microcirculation had no significant effects on arteriolar diameter. In addition, superfusion of quinupristin/dalfopristin (120 mg/L) had no significant effects on vasodilation evoked by bradykinin and acetylcholine, two endothelium-dependent agonists, or by vasoactive intestinal peptide, an endothelium-independent agonist, on to the cheek pouch. Collectively, these data indicate that quinupristin/dalfopristin has no significant effects on vasomotor tone in the intact peripheral microcirculation.

Animals↗
PubMed1975

Analysis of coronary vascular beta receptors in situ.

Observations were conducted in the isolated potassium-arrested dog heart to determine the direct vasodilator effects of adrenergic agonists and antagonists on the coronaryvascular beta receptors, independent of cardiac inotropic and chronotropic influences. Practocol (a selective beta-1-receptor antagonist) blocked coronary vasodilation activated by isoproternol (a combined beta-1-and beta-2-receptor agonist) only at the very high dose of 10-minus 3 M, whereas propranolol (a combined beta-1- and beta-2-receptor antagonist) blocked coronary vasodilation at 10-minus 7 to 10-minus 5 M. Salbutamol (a selective beta-2-receptor agonist) was one-eighth as potent as isoproterenol in producing coronary vasodilation. The potency ratio (1/8) is similiar to valuesreported for other beta receptors classified as type 2. It is concluded that the coronary vasodilator beta receptors are type 2, similiar to those found in peripheral bloodvessels.

Albuterol↗
PubMed1980

Arachidonate raises vascular resistance but not permeability in lungs of awake sheep.

Prostaglandins have been implicated as mediators of pulmonary hypertension in a variety of reactions, but the agents responsible for pathological increases in lung vascular permeability have not been determined. To test the hypothesis that products of arachidonic acid metabolism produce pulmonary vasoconstriction and alter lung vascular permeability, we infused purified sodium arachidonate (25-100 micrograms . kg-1 . min-1) into chronically instrumented unanesthetized sheep prepared for collection of lung lymph. Arachidonate produced dose-related increases in pulmonary artery pressure and lung lymph flow with corresponding decreases in the lymph-to-plasma protein concentration ratio. Lung lymph responses were like those caused by mechanically elevating left atrial pressure. Infusion of indomethacin or sodium eicosatetraynoate inhibited hemodynamic and lung lymph responses to arachidonate. We conclude a) that arachidonate must be converted to prostaglandin cyclic endoperoxides to produce pulmonary hypertension and increased flow of protein-poor lung lymph and b) that under normal conditions, no detectable increase in lung vascular permeability results from either arachidonate itself or the combined products of arachidonate metabolism via cyclooxygenase and/or lipoxygenase.

Animals↗
PubMed1998

A comparison of psychological and pharmacological treatment of pediatric migraine.

A comparison was carried out of the efficacy of psychological and drug treatments for children with migraine. Forty-three children aged between 8 and 16 years (mean age: 11.3 years) who suffered from migraine received either progressive relaxation or cephalic vasomotor feedback, both with stress management training, or metoprolol, a beta-blocker. Psychological treatment was administered in ten sessions lasting six weeks and the drug treatment lasted ten weeks. Relaxation and stress management training reduced the headache index (frequency x intensity of headache episodes), more effectively than metoprolol with cephalic vasomotor feedback and stress management training in between. An overall improvement over time was found with regard to frequency and intensity of headache episodes and analgesics intake. When comparing pre- to post-treatment data, children treated with relaxation training improved significantly in headache frequency and intensity, whereas those treated with cephalic vasomotor feedback improved significantly in headache frequency and duration as well as mood. The clinical improvement was stable at an 8-months follow-up.

Adolescent↗
PubMed1963

DEPRESSION OF THE VASOMOTOR CENTRE BY MECAMYLAMINE, INDEPENDENT OF ITS GANGLION-BLOCKING ACTIVITY.

Mecamylamine depressed the vasomotor centre independently of its ganglion-blocking action. The central action was elicited by small amounts of the drug when it was confined to the central nervous system of dogs and cats anaesthetized with pentobarbital sodium and of spinal cats. The spinal site of action was shown by the inhibition of vasomotor responses due to spinal compression in cats, when mecamylamine was introduced intrathecally in a dose too small to block autonomic ganglia. The supraspinal site of action was shown by intravertebral arterial injection of mecamylamine into cats, which caused hypotension and selectively blocked the electrically evoked pressor responses from the medulla without affecting the "nicotinic" ganglionic responses to acetylcholine. Injection of mecamylamine into the cerebral ventricles of dogs produced hypotension, and the reflex vasomotor responses to stimulation of afferent fibres in the vagus nerves and to occlusion of the common carotid arteries were inhibited without any change in the response of the nictitating membrane to preganglionic nervous stimulation.

Acetylcholine↗
PubMed1999

Ten days' use of oxymetazoline nasal spray with or without benzalkonium chloride in patients with vasomotor rhinitis.

CONTEXT: In most countries, the use of topical nasal decongestants is limited to a maximum of 10 days because of the risk of developing rebound mucosal swelling and rhinitis medicamentosa. OBJECTIVE: To determine whether topical nasal decongestants can be safely used for 10 days in patients with chronic inflammation of the nasal mucosa. DESIGN: Double-blind, randomized, controlled, parallel study. PATIENTS: Thirty-five patients with vasomotor rhinitis selected from our outpatient department. INTERVENTION: Eighteen patients received oxymetazoline hydrochloride (0.5 mg/mL) nasal spray containing the preservative benzalkonium chloride (0.1 mg/mL), and the other 17 were treated with oxymetazoline nasal spray without benzalkonium chloride. Before and after the treatment, recordings of the nasal mucosa and minimal cross-sectional area were made with rhinostereometry and acoustic rhinometry, followed by histamine hydrochloride challenge tests. Symptoms of nasal stuffiness were estimated on visual analog scales (0-100) in the morning and the evening, just before the nasal spray was used. RESULTS: No rebound swelling was found after the 10-day treatment in the 2 groups with either of the methods or as estimated by symptom scores. In the group receiving oxymetazoline containing benzalkonium chloride, but not in the other group, the histamine sensitivity was significantly reduced after treatment (P<.001). CONCLUSIONS: It is safe to use topical nasal oxymetazoline with or without benzalkonium chloride for 10 days in patients with vasomotor rhinitis. However, this study indicates that benzalkonium chloride in nasal decongestant sprays affects the nasal mucosa also after short-term use.

Benzalkonium Compounds↗
PubMed1998

Interaction of the dopamine D2 receptor agonist quinpirole with sympathetic vasomotor tone and the central action of rilmenidine in conscious rabbits.

Previous studies in conscious rats have shown that systemic administration of the dopamine D2 receptor agonist quinpirole causes a centrally-mediated increase in blood pressure which is associated with increased plasma levels of noradrenaline and adrenaline. In addition, treatment with quinpirole caused a marked inhibition of the antihypertensive effect of centrally-acting sympatho-inhibitory drugs such as clonidine, rilmenidine and alpha-methyldopa, suggesting an interaction at the level of sympathetic vasomotor tone. The main aim of the present study was investigate in conscious rabbits the effect of quinpirole on renal sympathetic nerve activity. In addition, we studied the effect of pretreatment with quinpirole on responses to additional quinpirole injections or rilmenidine treatment. Quinpirole treatment caused a prolonged dose-dependent increase in blood pressure and heart rate. Additional injection of quinpirole, 30 min after the first treatment, caused a significantly smaller pressor response (7+/-2 vs. 17+/-2 mm Hg). Injection of rilmenidine caused a larger decrease in blood pressure in rabbits which had been pretreated with quinpirole than in controls (-28+/-3 vs. -14+/-3 mm Hg). Total renal sympathetic nerve activity was markedly increased by quinpirole treatment (3.5-fold), an effect which could be attributed to both increased amplitude and increased frequency of the renal nerve signal. After a second injection of quinpirole, 30 min after the first treatment, only total renal sympathetic nerve activity and amplitude were increased and the effects were reduced. These results show marked actions of quinpirole on renal sympathetic nerve activity in conscious rabbits. However, the previously described apparent desensitisation to the antihypertensive effect of rilmenidine could not be observed in rabbits, suggesting marked species differences in the mechanism and site of action of rilmenidine.

Adrenergic alpha-Agonists↗