Progress on perioperative monitoring of cerebral blood flow autoregulation / 浙江大学学报·医学版

Cerebral blood flow autoregulation is physiologically protective mechanism to maintain the stability of cerebral blood flow. Once autoregulation is impaired, the cerebral blood flow fluctuates with blood pressure, leading to the risk of brain ischemia or cerebral hyperemia. Multiple research results indicate that cerebral blood flow can be monitored indirectly and continuously with transcranial Doppler, near infrared spectroscopy or ICP. The correlation coefficient calculated by the surrogate for cerebral blood flow and blood pressure is used to judge cerebral blood flow autoregulation. When the correlation coefficient is close to 1, cerebral blood flow will be passively fluctuated by blood pressure, indicating autoregulation is impaired. When the coefficient is less than 0, cerebral blood flow will not be changed with blood pressure, indicating autoregulaiton is intact. The status of autoregualtion is closely associated with mortality or poor neurological outcomes in patients with cardiac surgery underwent cardiopulmonary bypass, liver transplantation patients or patients with deep trendelenburg position for long time or beach chair position. Continuous monitoring of cerebral blood flow autoregulation can identify the lower or the upper limit of autoregulation, and provide information to individualize the perioperative management of blood pressure.

Epidural fentanyl decreases the minimum local analgesic concentration of epidural lidocaine / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Epidural lidocaine can be used when regional anesthesia needs to be established quickly, but the effect of co-administering epidural fentanyl on the minimum local analgesic concentration (MLAC) of lidocaine is not known. We compared the MLAC of epidural lidocaine in combination with different doses of fentanyl for epidural anesthesia in adults.</p><p><b>METHODS</b>One hundred and twenty patients requiring epidural analgesia were randomly allocated to receive 20 ml of one of four solutions: lidocaine, or lidocaine plus fentanyl 1 µg/ml, 2 µg/ml, or 3 µg/ml. The first patient in each group was administered 1% lidocaine weight by volume; subsequent patients received a concentration determined by the response of the previous patient to a higher or lower concentration according to up and down sequential allocation in 0.1% increments. Efficacy was assessed using a visual analog pain scale, and accepted if this was = 10 mm on a 100 mm scale within 30 minutes. The extent of motor block and of nausea and vomiting were recorded at 30 minutes after administration of the epidural solution and two hours after surgery, respectively.</p><p><b>RESULTS</b>The MLAC of lidocaine in those receiving lidocaine alone was 0.785% (95%CI 0.738 - 0.864). A significant dose-dependent reduction was observed with the addition of fentanyl: the MLAC of lidocaine with fentanyl at 2 µg/ml was 0.596% (95%CI 0.537 - 0.660) and 0.387% with fentanyl at 3 µg/ml (95%CI 0.329 - 0.446, P < 0.001).</p><p><b>CONCLUSION</b>Epidural fentanyl significantly reduces the dose of lidocaine required for effective epidural analgesia in adults without causing adverse side effects.</p>

Ammonia induces upregulation of aquaporin-4 in neocortical astrocytes of rats through the p38 mitogen-activated protein kinase pathway / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Astrocyte swelling is an important consequence of hepatic encephalopathy, and aquaporin-4 has been reported to play a vital role in this swelling. Ammonia causes astrocyte swelling and is also known to modulate aquaporin-4 expression in the astrocyte foot processes. The purpose of this study was to explore the mechanism of ammonia-induced aquaporin-4 expression, which has been suggested to involve the p38 mitogen-activated protein kinase pathway.</p><p><b>METHODS</b>We exposed cultured astrocytes to ammonium chloride, an in vitro model of hepatic encephalopathy. The purity of cultured astrocytes was evaluated by fluorescent glial fibrillary acidic protein labeling; cell morphology was assessed by light microscopy; the expression of aquaporin-4, phospho-p38, and p38 were detected by Western blotting analysis. Statistical analysis was performed by one-way factorial analysis of variance, and the relationship between variables was calculated by linear regression using SPSS version 13.0 program for Windows (SPSS, Chicago, IL, USA).</p><p><b>RESULTS</b>The purity of cultured astrocytes was (96.6 +/- 1.4)%. Astrocytes swelled significantly when exposed to 5 mmol/L ammonium chloride for 24 hours as compared to non-exposed astrocytes. Co-treatment with 10 micromol/L SB203580 (an inhibitor of p38) attenuated the degree of ammonium chloride induced astrocyte swelling. Western blotting analysis revealed that the expression levels of phospho-p38 and aquaporin-4 in ammonium chloride treated cells were significantly increased relative to the control group (P < 0.001); SB203580 co-treatment inhibited the increased expression of phospho-p38 and aquaporin-4 relative to the ammonium chloride treated group (P = 0.002 and P = 0.015 respectively). The phosphorylation of p38 and upregulation of aquaporin-4 were highly correlated (r = 0.909). There were no significant differences in total p38 expression among the groups (P = 0.341).</p><p><b>CONCLUSIONS</b>Ammonium chloride induced upregulation of aquaporin-4 in astrocytes is regulated by the p38 mitogen-activated protein kinase pathway. Inhibiting p38 activation prevented ammonium chloride induced aquaporin-4 protein upregulation.</p>

Tramadol inhibits c-fos expression in spinal cord dorsal horn and serum IL-6 levels induced by plantar incision in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate effect of tramadol on c-fos expression in spinal cord dorsal horn and serum IL-6 levels induced by plantar incision in rats.</p><p><b>METHODS</b>The Brennan pain model was induced by incision on the planter surface of left hind paw in rats. Forty-eight rats were randomly divided into six groups: Sham group (Group C), control group (Group I,pretreatment with saline 5 ml), three tramadol pretreatment groups (Group T1, T10 and T20,pretreated with 1 mg/kg, 10 mg/kg and 20 mg/kg tramadol, respectively) and one tramadol treatment group (Group PT10, treated with tramadol 10 mg/kg immediately after operation). Pain behavior was assessed by withdrawal threshold to von Frey filament stimulation intensity, response latency of the hind paw to radiant thermal and a cumulative pain score 2 h after incision. Fos-positive neurons in spinal cord were identified by the immunohistochemical technique. Serum IL-6 levels were measured by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>WithdrawIal threshold to von Frey filament stimulation intensity and response latency of the hind paw to radiant thermal in Group I were significantly lower than those in Group C (P<0.01). Cumulative pain score in Group I was significantly higher than that in Group C (P<0.01). In Groups of T10 and T20, withdrawal threshold to von Frey filament stimulation intensity and response latency of the hind paw to radiant thermal were significantly higher than those in Group I (P<0.01), cumulative pain score was significantly lower than that in Group I in a dose-dependent manner (P<0.01), and were also those in Group PT10. The greatest density of Fos-positive neurons was located in lamine I-II in Group I. Serum IL-6 levels were significantly elevated in Group I. Pretreatment with tramadol showed a dose-depended inhibitory effect on c-fos expression and serum IL-6 production,but not in Group T1. Administration of tramadol postoperatively also suppressed the c-fos expression and serum IL-6 production as showed in PT10 but were weaker than those in Group T10.</p><p><b>CONCLUSION</b>Pretreatment with tramadol can produce dose-dependent inhibitory effect on c-fos expression in spinal cord dorsal horn and then suppress the inflammatory response to the trauma.</p>