• T A Thurston and B P Mathew.
• Department of Anesthesiology, University of Texas Medical Branch at Galveston 77555, USA.
• Can J Anaesth. 1995 Oct 1; 42 (10): 944-7.

AbstractThe purpose of this study was to determine the importance of inhibition of beta-adrenergic function in thiopentone-induced myocardial depression. Using an isolated, electrically stimulated rat left atria model, contractile dose-response curves to thiopentone (200 microM, 400 microM, 600 microM, 800 microM) were shifted to the right in preparations treated with 10(-3)M dibutyryl cyclic adenosine monophosphate (cAMP) compared with atria stimulated with 10(-6) M dibutyryl cyclic isoprenaline, demonstrating that inhibition of beta-adrenergic mechanisms by thiopentone is physiologically important. Depression by thiopentone was similar in atria treated with 10(-5) M forskolin compared with preparations stimulated with 10(-6) M isoprenaline, indicating that thiopentone does not block beta-adrenergic receptors. It is concluded that thiopentone depresses myocardial function by several mechanisms, one of which involves inhibition of the adenyl cyclase cascade. The adenyl cyclase enzyme is a likely site where thiopentone inhibits the system; however, other components of the cascade may also be involved.

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