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[Effects of 2[p-(dimethylamino)styryl] pyridine methiodide on mouse and rabbit]
Abstract:
The effects of 2[p-(dimethylamino)styryl] pyridine methiodide on mouse and rabbit ECG and on the contraction of isolated rabbit atrial muscles were studied. DSPM produced long-lasting bradycardia and A-V block in a dose-dependent manner, but did not effect intraventricular conduction. DSPM antagonized the positive chronotropic and dromotropic effects of isoprenaline (Iso) in vivo, and antagonized the inotropic effects of Iso and CaCl2 non-competitively in vitro. The pD'2 were 4.49 and 4.52, respectively. It is suggested that DSPM may be a Ca2+ antagonist.
Insights
2[p-(dimethylamino)styryl] pyridine methiodide (DSPM) causes dose-dependent bradycardia and A-V block in mice and rabbits. DSPM acts as a calcium antagonist, inhibiting isoprenaline and calcium chloride effects.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Context:
- Investigating the cardiovascular effects of novel chemical compounds.
- Assessing the impact of 2[p-(dimethylamino)styryl] pyridine methiodide (DSPM) on cardiac function.
Purpose:
- To determine the electrophysiological and mechanical effects of DSPM on mammalian hearts.
- To elucidate the mechanism of action of DSPM, particularly its interaction with calcium channels.
Summary:
- DSPM induced dose-dependent bradycardia and atrioventricular (A-V) block in vivo without affecting intraventricular conduction.
- In vitro, DSPM non-competitively antagonized the inotropic effects of isoprenaline and calcium chloride, with pD'2 values of 4.49 and 4.52.
- These findings suggest that DSPM functions as a calcium antagonist.
Impact:
- Provides evidence for DSPM as a potential calcium channel blocker.
- Contributes to understanding drug-induced cardiac electrophysiological and mechanical changes.
- Informs future research on DSPM for potential therapeutic applications in cardiovascular conditions.