Sympathetic nervous system contribution to high-altitude–induced increases in pulmonary artery systolic pressure: a pilot stellate ganglion block study

Ascent to high-altitude elicits an exaggerated hypoxic pulmonary vasoconstriction response, producing acute increases in pulmonary artery systolic pressure (PASP). This response is accompanied by heightened sympathetic outflow to the systemic and pulmonary circulations. Although these parallel responses imply a potential mechanistic link, the degree to which sympathetic activation directly contributes to altitude-induced elevations in PASP remains unresolved. Hypothesis: We hypothesized that high-altitude-induced increases in sympathetic activity contribute to the rise in PASP observed in lowlanders. Objective: To determine whether stellate ganglion blockade (SGB) – a temporary interruption of efferent sympathetic traffic via local anesthetic injection – attenuates PASP in lowlanders exposed to high-altitude. Methods: Four male lowlanders (31 ± 9 yrs, 78 ± 19 kg, 175 ± 9 cm, 25 ± 5 kg/m 2 ) who had resided at high altitude (3,800 m; ~12,467 ft) for 2–7 days underwent measurements of mean blood pressure (MBP; sphygmomanometer), heart rate (HR; ECG), oxygen saturation (SaO2; pulse oximetry), and PASP (transthoracic echocardiography). PASP was calculated as the peak systolic pressure gradient across the tricuspid valve plus estimated right atrial pressure (via inferior vena cava collapsibility). Measurements were obtained before and approximately two hours after a right-sided SGB (10 mL of 2% lidocaine). In two participants, repeat measurements were obtained one week later before and after a 2-hour time-control period to account for nonspecific time effects. Results: Following SGB, MBP (103 ± 23 to 109 ± 24 mmHg; p = 0.018) and HR increased (67 ± 8 to 75 ± 7 bpm; p = 0.016), whereas SaO2 was unchanged (88 ± 3% vs. 89 ± 3%; p = 0.141). SGB elicited an ~11% reduction in PASP (33 ± 9 to 29 ± 6 mmHg; p = 0.050). No significant changes in MBP (113 ± 34 vs. 107 ± 40 mmHg; p = 0.379), HR (64 ± 9 vs. 64 ± 6 bpm; p = 0.795), SaO2 (89 ± 2% vs. 89 ± 1%; p = 0.500), or PASP (33 ± 1 vs. 32 ± 2 mmHg; p = 0.600) occurred during the time-control condition. Conclusions: These preliminary findings suggest that sympathetic activation contributes to the heightened PASP observed at high altitude, supporting a mechanistic role for sympathetic efferent activity in the pulmonary hypertensive response to altitude. Funding: Supported by the Arthur C. Guyton Award from the American Physiological Society and the American Heart Association (Grant 24CDA1273371). This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.