February 1, 1993Journal of Cardiovascular Pharmacology
Effects of Halothane on p-Adrenoceptors and M-Cholinoceptors in Human Myocardium
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Discussion
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Implication
Halothane may sensitize beta-adrenoceptors in diseased myocardium in vitro; leaves open clinical relevance for anesthesia in heart disease.
Key Points
- To determine whether halothane induces postsynaptic sensitization to beta-adrenoceptor-mediated effects in diseased human myocardium and to identify the underlying cellular mechanisms.
- Assayed isolated, electrically driven atrial and ventricular muscle preparations and membrane fractions obtained from human hearts during cardiac surgery.
- Conducted radioligand binding assays using [3H]quinuclidinylbenzilate for M-cholinoceptors and 125-iodocyanopindolol for beta-adrenoceptors alongside agonist competition binding.
- Measured contractility changes in isolated myocardium following exposure to isoprenaline and carbachol in the presence or absence of halothane.
- Halothane concentration-dependently inhibited [3H]quinuclidinylbenzilate binding to M-cholinoceptors and decreased high-affinity binding of isoprenaline to beta-adrenoceptors without altering equilibrium saturation binding.
- Halothane augmented the potency and efficacy of the positive inotropic response to isoprenaline in both atrial and ventricular tissues, while carbachol-mediated negative inotropic responses remained unaltered.
- Myocardial sensitization to catecholamines occurred at the postsynaptic level via direct interaction of halothane with the G-protein-coupled adenylate cyclase complex rather than altered receptor coupling.
Cite This Study
Böhm et al. (1993) studied this question.