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Chronotropic responses in rats implanted with an acrylic orthopaedic cement
M C Camilion de Hurtado1, O A Gende
1Center of Cardiovascular Research, Faculty of Medical Sciences, La Plata, Argentina.
Pharmacology & Toxicology
|May 1, 1989
Summary
Methyl methacrylate exposure in rats impaired heart rate responses to certain stimuli. This suggests a disruption in the signaling pathway for heart rate control, specifically after receptor activation but before cyclic AMP action.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Toxicology
Background:
- Methyl methacrylate is a monomer used in various applications, including dental prosthetics and bone cement.
- Exposure to methyl methacrylate may have toxicological effects on physiological systems.
- Understanding its impact on cardiovascular function is crucial for assessing health risks.
Purpose of the Study:
- To investigate the effects of methyl methacrylate polymer exposure on cardiac chronotropic and inotropic responses in rats.
- To determine the specific mechanisms underlying any observed alterations in cardiac function.
- To assess the impact on the adenylate cyclase signaling pathway.
Main Methods:
- Isolated rat atria and papillary muscles were used.
- Animals were exposed to a methyl methacrylate polymer pellet for one week.
- Responses to isoproterenol, glucagon, dibutyryl cAMP, and calcium chloride were measured.
- Beta-receptor density and affinity were assessed.
Main Results:
- Right atria from exposed rats showed reduced responsiveness to isoproterenol and glucagon (chronotropic effects).
- Responsiveness to dibutyryl cAMP and calcium chloride remained unchanged.
- Inotropic responses in left atria and papillary muscles were not altered.
- No changes in beta-receptor density or affinity were detected.
Conclusions:
- Methyl methacrylate exposure disrupts the signal transduction pathway for chronotropic stimuli mediated by the adenylate cyclase system.
- The alteration occurs downstream of beta-receptor binding and upstream of cyclic AMP (cAMP) action.
- This suggests a specific interference with intracellular signaling components involved in regulating heart rate.