Baicalein attenuates neuropathic pain and improves sciatic nerve function recovery in rats with partial sciatic nerve transection.

BACKGROUND: Modulating the inflammatory response to nerve injury may provide therapeutic opportunities by aborting the neurobiological alterations that support the development of persistent pain. Baicalein, a 12-lipoxygenase inhibitor, has anti-inflammation properties. It also demonstrates anti-inflammatory functions by inhibiting lipopolysaccharide-induced barrier disruption, expression of cell adhesion molecules, and adhesion and migration of leukocytes. The aim of the present study was to assess the possibility of early treatment of neuropathic pain via the systemic injection of baicalein in rats with left partial sciatic nerve transection (PST). METHODS: Wistar rats were divided into Sham, Vehicle, and Baicalein groups. The Vehicle and Baicalein rats underwent PST, whereas the Sham rats were not transected. Baicalein was administered 20 mg/kg/day intraperitoneally for 7 days after PST and after behaviour tests. After PST, rats developed mechanical and cold allodynia, and impaired sciatic nerve function. RESULTS: Baicalein attenuated mechanical and cold allodynia and improved sciatic nerve function after PST. Baicalein significantly inhibited the expression of tumour necrosis factor α (TNF-α), interleukin 6 (IL-6), and IL-1ß on days 14 and 28, and attenuated the activation of astrocytes in the L4-5 spinal cord less than day 28 after PST. CONCLUSION: Our study revealed that early and multiple doses of systemic baicalein attenuated neuropathic pain and improved sciatic nerve function by inhibiting pro-inflammatory cytokine expression and attenuating the activation of astrocytes in the spinal cord.

Confounding factors to predict the awakening effect-site concentration of propofol in target-controlled infusion based on propofol and fentanyl anesthesia.

We conducted a large retrospective study to investigate the confounding factors that predict Ce ROC under propofol-based TIVA with TCI. We recorded sex, age, height, weight, Ce LOC, Ce ROC, total propofol and fentanyl consumption dose, and anesthetic time. Simple linear regression models were used to identify potential predictors of Ce ROC, and multiple linear regression models were used to identify the confounding predictors of Ce ROC. We found that Ce ROC correlated with age, sex, Ce LOC, and both total fentanyl and propofol consumption dose. The prediction formula was: Ce ROC = 0.87 - 0.06 × age + 0.18 × Ce LOC + 0.04 (if fentanyl consumption > 150 µg; if not, ignore this value) + 0.07 × (1 or 2, according to the total propofol consumption dose, 1 for a propofol amount 1000-2000 mg and 2 for a propofol amount > 2000 mg). We simplified the formula further as Ce ROC = 0.87 - 0.06 × age + 0.18 × Ce LOC. In conclusion, Ce ROC can be predicted under TCI with propofol- and fentanyl-based TIVA. The confounding factors that predicted propofol Ce ROC are age, sex, Ce LOC, and total consumption dose of propofol and fentanyl.

A rare case of pneumocephalus and pneumorrhachis after epidural anesthesia.

Both pneumocephalus and pneumorrhachis are rare but serious complications following epidural anesthesia. We report a rare case of simultaneous pneumocephalus and pneumorrhachis in a patient after undergoing epidural anesthesia. The patient lost consciousness and received emergent external ventricular drainage for pneumocephalus in another medical center. The patient was clear after external ventricular drain placement until 4 days later, when sudden onset of subdural hemorrhage occurred and an emergent craniectomy was performed. The patient passed away 2 days after craniectomy, due to multiorgan failure. Pneumocephalus with or without pneumorrhachis should be kept in mind when there is a sudden change of consciousness or persistent convulsions after epidural anesthesia.

Rosiglitazone attenuates cerebral vasospasm and provides neuroprotection in an experimental rat model of subarachnoid hemorrhage.

BACKGROUND: Glutamate and oxidative stress play important roles after subarachnoid hemorrhage (SAH). The ability to modulate glutamate transporter 1 (GLT-1) and the antioxidative effect of rosiglitazone have been demonstrated. We investigated the neuroprotective effect of rosiglitazone after SAH. METHODS: SAH was induced by double blood injection. The rats were randomly divided into sham, SAH + vehicle, and SAH + rosiglitazone groups and treated with dimethyl sulfoxide, dimethyl sulfoxide, and 6 mg/kg of rosiglitazone, respectively, at 2 and 12 h after SAH induction and then daily for 6 days. Cerebrospinal fluid dialysates were collected 30 min before SAH induction and then daily for 7 days for glutamate measurement. Mortality, body weight, and neurological scores were also measured daily. On day 7 after SAH, the wall thickness and the perimeter of the basilar artery (BA), neuron variability, GLT-1 levels, glial fibrillary acidic protein (GFAP) expression and activity, and malondialdehyde, superoxide dismutase, and catalase activities were also evaluated. RESULTS: Rosiglitazone improved survival (relative risk = 0.325) and neurological functions and reduced neuronal degeneration (5.7 ± 0.8 vs. 10.0 ± 0.9; P < 0.001) compared with the SAH + vehicle group. Rosiglitazone also lowered glutamate levels by 43.5-fold and upregulated GLT-1 expression by 1.5-fold and astrocyte activity by 1.8-fold compared with the SAH + vehicle group. The increase in BA wall thickness was significantly attenuated by rosiglitazone, whereas the perimeter of the BA was increased. In addition, rosiglitazone abated the 1.9-fold increase in malondialdehyde levels and the 1.6-fold increase in catalase activity after SAH. CONCLUSION: Rosiglitazone reduced SAH mortality, neurological deficits, body weight loss, GFAP loss, and cerebral vasospasm by preventing the neurotoxicity induced by glutamate and oxidative stress.

Review of aneurysmal subarachnoid hemorrhage--focus on treatment, anesthesia, cerebral vasospasm prophylaxis, and therapy.

Aneurysmal subarachnoid hemorrhage (aSAH) is a serious and debilitating condition that leads to the development of many complications, which are followed by mortality and morbidity. As anesthesiologists, we may require to manage aSAH at various settings such as in the perioperative period or in a nonoperative setting such as the neuroradiology suite for diagnostic and therapeutic interventions. Therefore, it is important to understand the pathophysiology of aSAH and anesthetic management for operations and interventions. For decades, early brain injury and cerebral vasospasm have played major roles in the outcome following aSAH. The purpose of this article is to review recent advances and future perspectives in the treatment of aSAH, early brain injury, and cerebral vasospasm.