Why the study?
The clinical significance of the parasympathomimetic effects of opioids prompted investigation into whether the nucleus of the solitary tract mediates opioid-induced heart rate changes without nociceptive input across wakefulness and slow-wave sleep.
Do opioid agonists microinjected into the nucleus of the solitary tract alter heart rate variations independently of nociception and EEG states in cats?
Do opioid agonists microinjected into the nucleus of the solitary tract alter heart rate variations independently of nociception and EEG states in cats?
Opioids directly stimulate the parasympathetic component of heart rate by activating mu and delta receptors in the nucleus of the solitary tract, independent of pain or EEG-behavioral states.
Should not yet change HRV-guided opioid titration; leaves open whether this NST mechanism explains monitor signals in humans.
The present study aims to elucidate the involvement of the Nucleus of the Solitary Tract (NST) in opioid-induced heart rate (HR) changes in the absence of nociceptive input across different behavioral states, including wakefulness (W) and slow-wave sleep (SWS), given the clinical significance of the parasympathomimetic effects of opioids. Three adult cats with a stereotactic-guided implanted cannula aimed at the NST and with electrodes for electroencephalogram (EEG), electromyogram (EMG), electrooculogram (EOG) to identify W-SWS states and EKG recordings to obtain RR-intervals were used. After microinjections of saline, morphine sulphate, morphiceptin (mu-agonist), D-pen-2-D-pen-5-enkephalin (delta-agonist), or U-50488H (kappa-agonist) and after morphine preceded by naloxone, 60-min polygraph recordings were obtained “in vivo”. RR-intervals 60 min after NST administration were significantly increased (p < 0.001) after morphine (542 ± 108 ms), mu-agonist (525 ± 102 ms) and delta-agonist (472 ± 70 ms) as compared with saline (429 ± 68 ms), and the three substances also caused an EEG synchronization with a statistically significant increase of time spent in SWS (p < 0.05). These RR-interval changes were also statistically significant during both W (p < 0.015) and SWS states (p < 0.001). All the morphine induced EKG and EEG changes were blocked by prior administration of naloxone. NST injection of kappa-agonist was not followed by any significant effect. Therefore, opioids, by activating the mu and delta opioid receptors located in the NST, directly stimulate the parasympathetic component of HRindependently on EEG-behavioral states and even in the absence of pain.
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Reinoso‐Barbero et al. (2024) studied this question.
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