Analgesic and Sedative Effect of Acupuncture Combined with Medicine on Patients Undergoing Cardiac Surgery.

Authors

Bixia Huang, Hailong Ding, Wei Liang, Lingen Xu

Published in

Journal of visualized experiments : JoVE. Issue 236. Oct 27, 2026. Epub Oct 27, 2026.

Abstract

Acupuncture (AP) has been reported to modulate inflammation and oxidative stress, but whether it can reduce dexmedetomidine (Dex) requirements or protect against Dex-induced diaphragm toxicity during mechanical ventilation (MV) remains unknown. This study investigated whether AP could alleviate Dex-aggravated diaphragmatic dysfunction and explored its underlying mechanisms, focusing on autophagy. Female Sprague-Dawley rats were subjected to MV and treated with Dex, AP (Baihui and Yintang), and the autophagy inducer rapamycin (RAPA). Arterial blood gas parameters, vital signs, blood cell counts, and sedative dosage were recorded. Diaphragm function was evaluated by measuring contractile force, muscle fiber cross-sectional area, apoptosis, and oxidative stress markers, including superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and angiotensin II (ANG II). Autophagy levels were assessed using the LC3-II/LC3-I ratio, p62 expression, and autophagosome accumulation. AP reduced the total Dex dosage by 54.7% (0.102 ± 0.005 mg vs. 0.225 ± 0.009 mg in the MV + Dex group, p < 0.001) while maintaining stable physiological parameters. MV decreased diaphragm contractility and myofiber cross-sectional area and increased MAFbx expression, apoptosis, and oxidative stress markers. Dex further worsened these parameters, whereas AP improved diaphragm function and attenuated atrophy, apoptosis, and oxidative stress. MV and MV + Dex groups exhibited excessive autophagy, as shown by autophagic vacuole accumulation, an increased LC3-II/LC3-I ratio, and decreased p62 expression. AP inhibited these autophagic changes, while RAPA partially reversed its protective effects. AP at Baihui and Yintang reduced Dex requirements and alleviated MV- and Dex-induced diaphragm dysfunction in rats by inhibiting excessive autophagy.

PMID:
42949155
Bibliographic data and abstract were imported from PubMed on 28 Oct 2026.

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