No abstract

TREM-2 plays an important role in the host defense response to sepsis by enhancing bacterial clearance.

Scalp nerve block with ropivacaine has been shown to provide perioperative analgesia. However, the best concentration of ropivacaine is still unknown for optimal analgesic effects. We performed a prospective study to evaluate the effects of scalp nerve block with varied concentration of ropivacaine on postoperative pain and intraoperative hemodynamic variables in patients undergoing craniotomy under general anesthesia. Eighty-five patients were randomly assigned to receive scalp block with either 0.2% ropivacaine, 0.33% ropivacaine, 0.5% ropivacaine, or normal saline. Intraoperative hemodynamics and post-operative pain scores at 2, 4, 6, 24 hours postoperatively were recorded. We found that scalp blockage with 0.2% and 0.33% ropivacaine provided adequate postoperative pain relief up to 2 h, while administration of 0.5% ropivacaine had a longer duration of action (up to 4 hour after craniotomy). Scalp nerve block with varied concentration of ropivacaine blunted the increase of mean arterial pressure in response to noxious stimuli during incision, drilling, and sawing skull bone. 0.2% and 0.5% ropivacaine decreased heart rate response to incision and drilling. We concluded that scalp block using 0.5% ropivacaine obtain preferable postoperative analgesia compared to lower concentrations. And scalp block with ropivacaine also reduced hemodynamic fluctuations in craniotomy operations. About 10% to 20% patients undergoing craniotomy suffered severe pain and more than 30% experienced moderate pain as per Guilfoyle et al. 1. These experiences with pain may disturb patient sleep patterns and prolong hospital stays 2. Abrupt increases in heart rate (HR) and blood pressure (BP) resulting from dramatic stimuli like incisions, drilling, and screwing cause potential morbidities and mortalities due to elevation of intracranial pressure (ICP) in patients 3,4. Generally, opioids are used for relieving hemodynamic fluctuations and reducing postoperative pain, however, it may delay recovery time, contribute to extreme sedation, and interfere with postoperative neurological examinations. In addition, adverse effects of opioids such as nausea and vomiting, and respiratory depression may result in a rise of ICP or mask the signs of increased ICP. Since there is such an emphasis on controlling the adverse effects of opioid administration, postoperative pain after craniotomy is frequently uncontrolled 1. Easing hemodynamic perturbation and relieving postoperative pain are important concerns of neuroanesthesiologists and are also necessary components of the Enhanced Recovery After Surgery (ERAS). With advances in modern anesthesia come the development of short-acting analgesics, mainly remifentanil, transition analgesics, and conjunction analgesics that can be used instead of opioids to treat postoperative pain 5. Scalp never block (SNB), the blockage of nerves that innervate the involved region of the scalp about surgery 6 , was developed due to its potential benefits for effective regional anesthesia administration 7 , which promotes d...

Volatile anesthetics induce hyperactivity during induction while producing anesthesia at higher concentrations. They also bidirectionally modulate many neuronal functions. However, the neuronal mechanism is unclear. The effects of isoflurane on sodium channel currents were analyzed in acute mouse brain slices, including sodium leak (NALCN) currents and voltage-gated sodium channels (Na v) currents. Isoflurane at sub-anesthetic concentrations increased the spontaneous firing rate of CA3 pyramidal neurons, whereas anesthetic concentrations of isoflurane decreased the firing rate. Isoflurane at sub-anesthetic concentrations enhanced NALCN conductance but minimally inhibited Na v currents. Isoflurane at anesthetic concentrations depressed Na v currents and action potential amplitudes. Isoflurane at sub-anesthetic concentrations depolarized resting membrane potential (RMP) of neurons, whereas hyperpolarized the RMP at anesthetic concentrations. Isoflurane at low concentrations induced hyperactivity in vivo, which was diminished in NALCN knockdown mice. In conclusion, enhancement of NALCN by isoflurane contributes to its bidirectional modulation of neuronal excitability and the hyperactivity during induction.

No abstract