The Role of Superior Cervical Ganglion in the Chronic Sensitization of Carotid Bodies Post-Acute Lung Injury

Abstract

Background/hypothesis of the study: Acute lung injury (ALI) increases respiratory rate (RR), induces hypoxemia. This stimulates carotid body (CB) chemoreflex to maintain oxygen homeostasis. Our previous study indicates a sensitized chemoreflex during the recovery of ALI. Chronic chemoreflex hyperactivity negatively affects the overall quality of life. The neural mechanisms underlying the sensitized CB chemoreflex during the recovery from ALI remain a gap in knowledge. Electrical stimulation of the superior cervical ganglion (SCG) sensitizes the CB chemoreflex in rats. We hypothesized that the SCG causes the CB chemoreflex sensitization post-ALI. Methods and Results: We performed a bilateral SCG ganglionectomy (SCGx) or sham-SCGx (Sx) in our male SD rats 2 weeks before inducing ALI (W-2). After 2 weeks of recovery, ALI was induced using a single intra-tracheal instillation of bleomycin (day 1) and measured the resting respiratory variables- RR, TV (Tidal Volume), and MV (Minute Ventilation). The chemoreflex response to 10% hypoxia and 5% normoxic hypercapnia were measured on W(-3) (pre-SCGx), W0 (post-SCGx/pre-ALI) and W4 (post-ALI) using whole-body plethysmography (WBP). Ganglionectomy did not alter the resting lung parameters and the chemoreflex response to either gas challenge in normal, healthy rats. An increase in resting RR at W1 post-ALI was not significantly different between Sx and SCGx rats. At W4 post-ALI, there were no significant differences in resting lung parameters between Sx and SCGx rats. Consistent with our previous study, the CB chemoreflex response to hypoxia and normoxic hypercapnia in Sx rats at W4 post-ALI was sensitized (p<0.01). However, the chemoreflex sensitivity significantly lowered in SCGx rats in response to hypoxia (p=0.01) and normoxic-hypercapnia (p=0.002). Conclusion(s): The CB chemoreflex sensitization during the recovery from the ALI may be mediated by the SCG. Further understanding of the underlying mechanism will provide important information to develop therapeutic approaches to pulmonary disease to improve clinical outcomes. This study was supported by: NIH Grant- RO1 HL-152160 and RO1 HL-126796; Lieberman Grant 2021- Dept. of Anesthesiology, UNMC; American Heart Association- Pre-doctoral fellowship, AHA. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.