Two Novel Approaches to Improve Otolaryngology Resident Wellness: The ACGME Back to Bedside Initiative.

Rates of burnout, mental illness, and suicide are disproportionately elevated among physicians, and surgical specialists, including otolaryngologists, are at even higher risk for professional burnout. These trends have been identified at both the trainee and attending level. To combat resident burnout, the Accreditation Council for Graduate Medical Education (ACGME) Council of Review Committee Residents (CRCR) designed the Back to Bedside Initiative, the goals of which are to foster meaning in the learning environment and to help trainees to engage more deeply with patients. Two funded Back to Bedside proposals involve otolaryngology training programs. Herein, we discuss these 2 approaches in an effort to foster additional novel resident wellness initiatives and awareness thereof across our subspecialty.

Selective mu and kappa Opioid Agonists Inhibit Voltage-Gated Ca2+ Entry in Isolated Neonatal Rat Carotid Body Type I Cells.

It is known that opioids inhibit the hypoxic ventilatory response in part via an action at the carotid body, but little is known about the cellular mechanisms that underpin this. This study's objectives were to examine which opioid receptors are located on the oxygen-sensing carotid body type I cells from the rat and determine the mechanism by which opioids might inhibit cellular excitability.Immunocytochemistry revealed the presence of µ and κ opioid receptors on type I cells. The µ-selective agonist DAMGO (10 µM) and the κ-selective agonist U50-488 (10 µM) inhibited high K(+) induced rises in intracellular Ca(2+) compared with controls. After 3 h incubation (37 °C) with pertussis toxin (150 ng ml(-1)), DAMGO (10 µM) and U50-488 (10 µM) had no significant effect on the Ca(2+) response to high K(+).These results indicate that opioids acting at µ and κ receptors inhibit voltage-gated Ca(2+) influx in rat carotid body type I cells via G(i)-coupled mechanisms. This mechanism may contribute to opioid's inhibitory actions in the carotid body.

Acutely Administered Leptin Increases [Ca2+] i and BK Ca Currents But Does Not Alter Chemosensory Behavior in Rat Carotid Body Type I Cells.

Obesity related pathologies are the health care crisis of our generation. The fat cell derived adipokine leptin has been shown to be a central stimulant of respiration. Very high levels of leptin, however, are associated with the depressed ventilatory phenotype observed in obesity hypoventilation syndrome. Leptin receptors have been identified on carotid body type I cells but how their activation might influence the physiology of these cells is not known.The acute application of leptin evoked calcium signaling responses in isolated type I cells. Cells increased their Fura 2 ratio by 0.074 ± 0.010 ratio units (n = 39, P < 0.001). Leptin also increased the peak membrane currents in 6 of 9 cells increasing the peak macroscopic currents at +10 mV by 61 ± 14 % (p < 0.02). Leptin administered in the presence of the selective BK(Ca) channel inhibitor Paxilline (0.5 µM) failed to increase membrane currents (n = 5). Interestingly, leptin did not significantly alter the resting membrane potential of isolated type I cells (n = 9) and anoxic/acidic depolarizations were unaffected by leptin (n = 7, n = 6).These data suggest that leptin receptors are functional in type I cells but that their acute activation does not alter chemosensory properties. Future studies will use chronic models of leptin dysregulation.