Transcutaneous Electrical Acupoints Stimulation Improves Spontaneous Voiding Recovery After Laparoscopic Cholecystectomy: A Randomized Clinical Trial.

BACKGROUND: Facilitating the recurrence of spontaneous voiding is considered to be a way to prevent urinary retention after surgery, which is of great importance in cholecystectomy. This study aimed to assess the effect of transcutaneous electrical acupoint stimulation (TEAS) on spontaneous voiding recovery after laparoscopic cholecystectom. METHODS: Participants who underwent elective laparoscopic cholecystectomy were randomly assigned to either the TEAS group or the sham group. Active TEAS or sham TEAS at specific acupuncture points was conducted intraoperatively and postoperatively. The primary outcome was the recovery speed of spontaneous voiding ability after surgery and secondary outcomes included postoperative urinary retention (POUR), voiding dysfunction, pain, anxiety and depression, and early recovery after surgery. RESULTS: A total of 1,948 participants were recruited and randomized to TEAS (n = 975) or sham (n = 973) between August 2018 and June 2020. TEAS shortens the time delay of the first spontaneous voiding after laparoscopic cholecystectomy (5.6 h [IQR, 3.7-8.1 h] in the TEAS group vs 7.0 h [IQR, 4.7-9.7 h] in the sham group) (p < 0.001). The TEAS group experienced less POUR (p = 0.020), less voiding difficulty (p < 0.001), less anxiety and depression (p < 0.001), reduced pain (p = 0.007), and earlier ambulation (p = 0.01) than the sham group. CONCLUSIONS: Our results showed that TEAS is an effective approach to accelerate the recovery of spontaneous voiding and reduce POUR which facilitates recovery for patients after laparoscopic cholecystectomy.

Electroacupuncture protects against bladder dysfunction induced by acute urinary retention via TRPV1/ATP signaling pathway: An animal and human research study.

Electroacupuncture (EA) can protect against acute urinary retention (AUR); however, the underlying mechanism remains unclear. Non-vesicular ATP release mediated by transient receptor potential (TRP) channels were identified as a key contributor to signaling in urothelial cells. In this study, the AUR model was established by urethral outlet obstruction in female Sprague-Dawley rats. EA was performed at SP6 and BL32 for 0.5 h prior to induction of AUR. EA reduced TRPV1 expression and urinary ATP concentrations in rat bladder, decreased the peak intravesical pressure during AUR, and attenuated abnormal voiding patterns and bladder pathological injury induced by AUR. Besides, 179 patients who experienced postoperative urinary retention were recruited and found that EA reduced urinary ATP concentrations and accelerated the recovery of spontaneous voiding. These observations indicate that EA exerts protection against AUR-induced bladder dysfunction by reducing urinary ATP concentrations through the regulation of TRPV1.

Electroacupuncture Improves Cognition in Rats With Sepsis-Associated Encephalopathy.

BACKGROUND: Sepsis-associated encephalopathy (SAE) is a common complication of sepsis. Although sepsis is effectively managed with the administration of antibiotics and source control, which may include surgical intervention, SAE usually leads to prolonged cognitive dysfunction affecting the quality of life of the patients. In this study, we investigated the possible effect of electroacupuncture (EA) on cognition in a model of SAE induced by cecal ligation and puncture (CLP). MATERIALS AND METHODS: The rats were randomly divided into four groups: the control group, the CLP group, the CLP with EA treatment group (CLP + EA), and the CLP with sham EA treatment group (CLP + sham EA). EA at DU20, LI11, and ST36 or sham EA was performed 30 min daily for 10 consecutive days starting from 2 days before CLP. Then cognitive function was examined by the Morris water maze test. On day 14 after CLP surgery, the synaptic injury, neuron loss, and oxidative stress were studied. RESULTS: Rats with EA treatment showed improved survival rate, spatial learning, and memory abilities. The dendritic spine density, the synaptic proteins, and the hippocampal neuron number were also increased after EA treatment. Furthermore, EA suppressed oxidative stress through regulating the level of malondialdehyde and superoxide dismutase and enhanced the expression of antioxidant nuclear factor erythroid-2-related factor-2 and hemeoxygenase-1. But sham EA did not have the same effect. CONCLUSIONS: EA may protect against SAE-induced cognitive dysfunction by inhibiting synaptic injury, neuronal loss, and oxidative stress, and the nuclear factor erythroid-2-related factor-2/hemeoxygenase-1 signaling pathway may be involved in this effect.

PI3K/Akt pathway-mediated HO-1 induction regulates mitochondrial quality control and attenuates endotoxin-induced acute lung injury.

Sepsis-related acute lung injury (ALI) remains a major cause of mortality in critically ill patients and lacks specific therapy. Mitochondrial dysfunction is involved in the progression of septic lung injury. Mitochondrial dynamics, mitophagy, and biogenesis converge to constitute the assiduous quality control of mitochondria (MQC). Heme oxygenase-1 (HO-1) protects against sepsis-induced ALI through the modulation of mitochondrial dynamics. However, the causal relationship between HO-1 and the general processes of MQC, and their associated cellular pathways in sepsis-related ALI remain ill-defined. Herein, lipopolysaccharide (LPS)-induced ALI in Sprague-Dawley rats together with LPS-induced oxidative injury in RAW264.7 macrophages were used to investigate whether the PI3K/Akt pathway-mediated induction of HO-1 preserves MQC and alleviates septic lung injury. After pretreatment with hemin, a potent inducer of HO-1, LPS-induced cell apoptosis, enhanced mitochondrial fragmentation, and mitochondrial membrane potential damage were significantly reduced in macrophages. In rats, these effects were accompanied by a higher survival rate, less damage to lung tissue, a 28.5% elevation in lung mitochondria MnSOD activity, and a 39.2% increase in respiratory control ratios. Concomitantly, HO-1 induction preserved the dynamic process of mitochondrial fusion/fission (Mfn2, OPA1, Drp1), promoted mitochondrial biogenesis (NRF1, PGC1α, Tfam), and facilitated the key mediators of mitochondrial mitophagy (Parkin, PINK1) at mRNA and protein levels. Notably, LY294002, a PI3K inhibitor, or knockdown of PI3K by small interfering RNA significantly suppressed Akt phosphorylation, attenuated HO-1 induction, and further reversed these beneficial effects evoked by hemin pretreatment in RAW264.7 cells or rats received LPS, indicating a direct involvement of PI3K/Akt pathway. Taken together, our results indicated that HO-1 activation, through PI3K/Akt pathway, plays a critical role in protecting lung from oxidative injury in the setting of sepsis by regulating MQC. HO-1 may therefore be a therapeutic target for the prevention sepsis-related lung injury.