Disease relevance of Alinidin

• These observations indicate that alinidine reduces heart-rate without blocking beta-adrenoceptors and may be useful in patients with angina and in patients with tachyarrhythmias [1].
• Atenolol and alinidine significantly decreased the basic heart rate without causing more sinus arrest or higher-degree atrioventricular block [2].
• The prevalence of atrial fibrillation in alinidine patients was lower than in the atenolol patients (P = .007) but not lower than in placebo patients (P = .11) [2].
• Bradycardia was induced in rats by administering the bradycardic drug alinidine (3 mg/kg body weight) twice daily [3].
• Left ventricular weight, body weight, and their ratio were not significantly altered by alinidine treatment [3].

Psychiatry related information on Alinidin

• Acute effects of alinidine on heart rate and blood pressure in healthy subjects and patients with hyperkinetic heart syndrome [4].

High impact information on Alinidin

• Alinidine reduces heart-rate without blockade of beta-adrenoceptors [1].
• Alinidine 80 mg reduced arterial pressure in the standing and supine positions [1].
• In contrast, bFGF mRNA was not altered by alinidine treatment [3].
• In a double-blind study, we examined the effects of early intravenous and continued oral administration of a beta-blocker (atenolol), a specific bradycardiac agent (alinidine) or placebo on left ventricular function, late coronary artery patency, infarct size, exercise capacity and incidence of arrhythmias [5].
• No significant differences in clinical events were observed, with the exception of a greater incidence of nonfatal pulmonary edema in the atenolol group (6% vs. 1% in the alinidine group and 0% in the placebo group, p = 0.021) [5].

Chemical compound and disease context of Alinidin

• Since treatment of pathological cardiovascular conditions with drugs with positive inotropic and vasodilatory properties is often accompanied by tachycardia, we also studied the effects alinidine in combination with the phosphodiesterase inhibitor sulmazole [6].
• Alinidine and nadolol produced an overall mean bradycardia in comparison with saline treated animals, the effect of alinidine exceeding that of nadolol [7].
• Equal reductions in heart rate (44 beats X min-1) were obtained in cats by treatment with either the beta blocking agent timolol or alinidine, an agent claimed to cause bradycardia without interfering with beta adrenoceptor function [8].
• However alinidine and phentolamine did produce a dose-related bradycardia in the spontaneously beating right atria.(ABSTRACT TRUNCATED AT 250 WORDS)[9]
• CONCLUSIONS: During experimental septic shock, alinidine administration can reverse dobutamine-induced tachycardia and simultaneously improve ventricular function [10].

Biological context of Alinidin

• When, in the anaesthetized animals, heart rate was kept constant by atrial pacing, no changes were observed with alinidine in maxLVdP/dt and cardiac output at doses up to 0.4 mg kg-1 [6].
• The clinical pharmacology of alinidine and its side-effects [11].
• The purpose of the study was to investigate the prophylactic antiarrhythmic properties of alinidine on supraventricular tachyarrhythmias (svt), which occur with incidence after open heart surgery [12].
• The substitution of chlorine ions by other anions did not prevent the decrease in the rate of diastolic depolarisation due to alinidine but did prevent the effect on the action potential duration [13].
• Alinidine did not increase resting potential or accelerate repolarisation, suggesting that potassium conductance was not increased [14].

Anatomical context of Alinidin

• Chronotropic action of alinidine on the isolated sinus node of the rabbit heart [15].
• In pigs with normal hearts alinidine homogeneously reduced myocardial perfusion, but no imbalance in the myocardial oxygen supply-demand relationship was noticed due to a simultaneous reduction of the metabolic needs of the myocardium [6].
• The effective refractory period of the right atrium, the atrioventricular node and the right ventricle, as well as the functional refractory period of the atrioventricular node, were unaffected by alinidine in both groups of patients [16].
• Metabolic inhibition of intact B-cells by 250muM NaCN, most likely by a decrease of the ATP/ADP ratio, significantly diminished the K(ATP) channel-blocking effect of a low concentration of alinidine (10muM), whereas efaroxan proved to be susceptible even at a highly effective concentration (100muM) [17].
• Given that the rank order of potency of the antagonists was similar in all tissues (i.e. glibenclamide greater than phentolamine = alinidine), this result may suggest vascular K+ channels opened by cromakalim are quantitatively but not qualitatively different in vascular compared with non-vascular smooth muscle [9].

Associations of Alinidin with other chemical compounds

• The circadian rhythm was attenuated but not abolished by alinidine and nadolol [7].
• Compared with the control cats, in whom 87.4 (SEM 2.2)% of hypoperfused myocardium developed into necrosis, timolol reduced infarct size to 65.8 (SEM 2.6)% (p less than 0.001) and alinidine to 76.2 (SEM 3.1)% (p less than 0.01) of the hypoperfused area [8].
• Electrophysiological effects of alinidine (ST 567) on sinoatrial node fibres in the rabbit heart [13].
• Blockade of the pacemaker current of if by caesium prevented neither the alinidine effect on the diastolic depolarisation completely nor its effect on the action potential duration, but blockade of if probably was one of the determinants of the action of alinidine [13].
• 4. Experiments on pig coronary artery, where acetylcholine causes vasoconstrictor responses, showed that phentolamine and alinidine have some anti-muscarinic activity which could account for their ability to affect vasorelaxant/hyperpolarization responses to acetylcholine in the rat small mesenteric artery [18].

Gene context of Alinidin

• Pressures in the pulmonary artery and in capillary wedge position were significantly reduced after Alinidine by about 12 to 18% (mean PAP) and by about 19 to 28% (PCW) [19].

Analytical, diagnostic and therapeutic context of Alinidin

• Changes in systemic haemodynamics, regional myocardial function and perfusion induced by alinidine in pigs with and without narrowed coronary arteries [6].
• The effects of alinidine on systemic and pulmonary haemodynamics and the ECG were studied in 8 patients early after open heart surgery as a double-blind cross-over comparison between alinidine and placebo [20].
• Thirty minutes later, alinidine was administered as a bolus dosage of 1 mg/kg in five dogs; the other five dogs served as a control group [10].
• Saline or alinidine (5 mg/kg i.v.) was administered 15 min prior to ligation [21].
• Determination of alinidine in human plasma by high-performance liquid chromatography [22].

References