RESUMO
Objective: To investigate whether transcutaneous electrical acupoint stimulation (TEAS) at PC6 could reduce hypotension after spinal anesthesia (SA) in parturients and to compare the effect of TEAS at different frequencies. Methods: From February 20, 2023, to August 29, 2023, 90 parturients scheduled for c-section under SA were randomly assigned to receive no treatment (Control), TEAS at high frequency (TEAS-HF), or TEAS at low frequency (TEAS-LF). Treatments started immediately after SA and lasted for 30 min. The primary endpoint was incidence of hypotension by 30 min after SA. Secondary endpoints included lowest systolic blood pressure (SBP) during 30 min after SA, dose of ephedrine, dose of atropine, Apgar score at 1 min, and adverse events, including nausea, vomiting, dizziness, dyspnea, and chest congestion. Results: In the TEAS-HF group, the incidence of hypotension by 30 min after SA was lower (13.3%) than in the Control (53.3%, p = 0.001; OR 1.9, 95% confidence interval [CI]: 1.2-2.8) and TEAS-LF group (40.0%, p = 0.02, OR 1.4, 95% CI: 1.0-2.0). The lowest SBP during 30 min after SA was higher in the TEAS-HF group (100.0 ± 9.4 mm Hg) than in the Control group (91.5 ± 16.5 mm Hg) and TEAS-LF group (93.9 ± 16.6 mm Hg). Patients who received TEAS showed a lower score of nausea and vomiting (both p = 0.02). Patients in the group TEAS-HF showed a lower incidence of dizziness, dyspnea, and of chest congestion than those in the other two groups. There was no difference with respect to atropine consumption and neonatal Apgar score. Conclusions: TEAS-HF at PC6 reduced hypotension after SA in parturients, while TEAS-LF did not. Trial registration: ClinicalTrials.gov (NCT05724095).
RESUMO
The mechanism of electroacupuncture (EA) pretreatment-induced neuroprotection remains unclear. In this study, we found that neuronal Triggering receptor expressed on myeloid cells 2 (TREM2) expression was increased and peaked at 48 h and 72 h after ischemia/reperfusion. After specific knockdown of TREM2 in excitatory neurons, neurological function was damaged, and the infarct volume was enlarged. Furthermore, the expression of LC3II/LC3I and Beclin1 was decreased, while the expression of p62 was increased. EA pretreatment enhanced TREM2, LC3II/LC3I and Beclin1 expression while reducing p62 in the ischemic penumbra area. The EA-induced neuroprotective effects and improvements in autophagic flux were abolished by specific knockdown of TREM2 in excitatory neurons. Taken together, our findings provide novel mechanistic insight into EA-induced ischemic tolerance and suggest a promising therapeutic strategy of targeting neuronal TREM2 to treat brain ischemia.
