Midazolam inhibits cardiac nociception evoked by coronary artery occlusion in rats

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Background and objectives

This study was designed to investigate the potential existence of the response of neurons in the parafascicular nucleus of the thalamus to acute myocardial ischaemia induced by selective coronary artery occlusion and the effects of midazolam on the response in rats.


The left anterior descending branch of the coronary artery was instrumented with a snare occluder in anaesthetized Sprague-Dawley rats. A single-barrel glass microelectrode was used for recording the unit discharges of the neuron in the parafascicular nucleus. The neuron responding only to noxious somatic stimulation was further examined for the response to coronary artery occlusion. Once the effect of coronary artery occlusion on the discharges was detected, the pharmacological effects of midazolam and flumazenil were examined.


It was observed that the discharge rate of the neuron was markedly increased following coronary artery occlusion. Midazolam attenuated the increase in the discharges of the neuron induced by coronary artery occlusion (P < 0.05). The effect of midazolam was reversed by flumazenil.


The parafascicular nucleus is involved in the modulation of cardiac nociception and midazolam possesses antinociceptive property in modulating cardiac pain.

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