Dexmedetomidine (DEX) is known to provide neuroprotection against cerebral ischemia and reperfusion injury (CIRI), but the exact mechanisms remain unclear. This study was conducted to investigate whether DEX pretreatment conferred neuroprotection against CIRI by inhibiting neuroinflammation through the JAK2/STAT3 signaling pathway. Middle cerebral artery occlusion (MCAO) was performed to establish a cerebral ischemia/reperfusion (I/R) model. Specific-pathogen-free male Sprague-Dawley rats were randomly divided into Sham, I/R, DEX, DEX+IL-6, and AG490 (a selective inhibitor of JAK2) groups. The Longa score, TTC staining, and HE staining were used to evaluate brain damage. ELISA was used to exam levels of TNF-α. Western blotting was used to assess the levels of JAK2, phosphorylated-JAK2 (p-JAK2), STAT3, and phosphorylated-STAT3 (p-STAT3). Our results suggested that both pretreatment with DEX and AG490 decreased the Longa score and cerebral infarct areas following cerebral I/R. After treatment with IL-6, the effects of DEX on abrogating these pathological changes were reduced. HE staining revealed that I/R-induced neuronal pathological changes were attenuated by DEX application, consistent with the AG490 group. However, these effects of DEX were abolished by IL-6. Furthermore, TNF-α levels were significantly increased in the I/R group, accompanied by an increase in the levels of the p-JAK2 and p-STAT3. DEX and AG490 pretreatment down-regulated the expressions of TNF-α, p-JAK2, and p-STAT3. In contrast, the down-regulation of TNF-α, p-JAK2, and p-STAT3 induced by DEX was reversed by IL-6. Collectively, our results indicated that DEX pretreatment conferred neuroprotection against CIRI by inhibiting neuroinflammation via negatively regulating the JAK2/STAT3 signaling pathway.

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Trigeminocardiac reflex (TCR) can result in bradycardia and even cardiac arrest, and is reversible with elimination of the stimulus. Here, we report the case of a 68-year-old man who experienced cardiac arrest during percutaneous balloon compression for the treatment of trigeminal neuralgia. In this patient, sinus rhythm did not recover after stimulation removal, causing us to successfully perform cardiopulmonary resuscitation (CPR). The patient regained a sinus rhythm and was pretreated with atropine 0.5 mg, allowing the operation to be started again. The operation was completed successfully and the patient experienced no complications. Subsequent heart rate variability (HRV) analysis showed that parasympathetic activity predominated before anesthesia induction and after tracheal intubation. It further elevated during foramen ovale puncture, leading to prolonged asystole. Fortunately, sympathetic activity predominated after atropine was administered, which manifested as an increase in sympathetic activity and a decrease in parasympathetic activity. This could be beneficial for patients with TCR. This case indicates that TCR-related cardiac arrest might not be reversed with stimulus cessation, and atropine played a key role in preventing TCR. Moreover, HRV analysis might be essential for preoperative screening for high-risk patients. We also reviewed the literature for cases of TCR with prolonged asystole.