Key result
Infusion of atenolol, metoprolol, and timolol, or bolus of propranolol, significantly inhibited norepinephrine-induced cardiac responses in isolated rat hearts, unlike bolus of the other agents.
Why the study?
Do beta-blockers (atenolol, metoprolol, timolol, propranolol) inhibit norepinephrine-induced cardiac responses in isolated rat hearts?
Do beta-blockers (atenolol, metoprolol, timolol, propranolol) inhibit norepinephrine-induced cardiac responses in isolated rat hearts?
The route of administration (bolus vs. infusion) and lipophilicity of beta-blockers significantly affect their ability to inhibit norepinephrine-induced cardiac responses in isolated rat hearts.
Rat heart data warrant no clinical changes; leaves open whether route or lipophilicity effects translate to patients.
The effects of atenolol and another three beta-adrenoceptor blocking agents on norepinephrine (NE)-induced cardiac responses were examined in isolated and perfused rat hearts following a Langendorff method. Bolus injection of atenolol did not show significant inhibitory effects on NE-induced increases in myocardial contractile force (MCF) and heart rate. Bolus injections of metoprolol and timolol were also ineffective for inhibiting NE-responses. However, both bolus injection and infusion of propranolol or infusion of atenolol, metoprolol and timolol all significantly inhibited NE-responses. On sustained increase in MCF induced by infusion of NE, the inhibitory effect of atenolol was transient, while that of propranolol was continuous. From these results, it is concluded that atenolol displays a different time course of action on NE-induced cardiac responses by bolus injection or infusion because of its pharmacological properties, which may be due to its low lipophilicity.
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Nakasone et al. (1988) studied Norepinephrine-induced cardiac responses. Atenolol, metoprolol, timolol, and propranolol was evaluated on Norepinephrine-induced increases in myocardial contractile force (MCF) and heart rate. Infusion of atenolol, metoprolol, and timolol, or bolus of propranolol, significantly inhibited norepinephrine-induced cardiac responses in isolated rat hearts, unlike bolus of the other agents.
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