[Protective effect of shenfu injection pretreatment on brain of patients receiving aortic valve replacement undergoing cardiopulmonary bypass].

OBJECTIVE: To observe the protective effect of Shenfu Injection (SFI) pretreatment on brain of patients receiving aortic valve replacement (AVR) undergoing cardiopulmonary bypass (CPB). METHODS: Thirty AVR patients undergoing CPB were randomly assigned to 2 groups, the control group and the experimental group, 15 cases in each group. SFI at 1.5 mL/kg (dissolved in 250 mL 5% glucose solution) was intravenously dripped to those in the experimental group 5 days before operation, once daily for 5 successive days. SFI at 1.5 mL/kg (dissolved in 250 mL 5% glucose solution) was intravenously dripped to those 30 min before anesthesia induction. Equal dose of normal saline was intravenously dripped to those in the control group, and the other procedures were the same as those for patients in the experimental group. The venous blood sample (2 mL) was drawn from the right internal carotid vein immediately after induction of anesthesia (T1),10 min after CPB (T2), 30 min after GPB (T3), 2 h after CPB (T4), 24 h after CPB (T5), and 48 h after CPB (T6), thus detecting the plasma levels of S100beta and neuron specific enolase (NSE). And patients' cognitive function was assessed with mini-mental state examination (MMSE) scale on the day before operation, the 2nd and the 7th day after operation. RESULTS: There was no statistical difference in the levels of S1001 and NSE between the two groups at T1 (P > 0.05). There was statistical difference in the levels of S100beta and NSE between the two groups at T2, T3, T4, T5, T6, when compared with those at T1 (P <0.05). Besides, the levels of S100beta and NSE at T2, T3, T4, T5, T6 were lower in the experimental group than in the control group, showing statistical difference (P <0.05). The MMSE scores decreased on the 2nd day after operation in the two groups, showing statistical difference when compared with those on the day before operation (P <0.05). It was lowered more obviously in the control group. There was no statistical difference in the MMSE score between the 7th day post-operation and the day before operation (P >0.05). CONCLUSION: SFI pretreatment had protective effect on brain in AVR patients undergoing CPB.

Dual isoflurane-induced preconditioning improves neuroprotection in rat brain in vitro and the role of extracellular signal--regulated protein kinase.

OBJECTIVE: To test the ability of isoflurane-induced preconditioning against oxygen and glucose deprivation (OGD) injury in vitro. METHODS: Rat hippocampal slices were exposed to 1 volume percentage (vol%), 2vol% or 3vol% isoflurane respectively for 20 minutes under normoxic conditions (95% O2/5% CO2) once or twice (12 slices in each group) before OGD, with 15-minute washout after each exposure. During OGD experiments, hippocampus slices were bathed with artificial cerebrospinal fluid (ACSF) lacking glucose and perfused with 95% N2 and 5% CO2 for 14 minutes, followed by a 30-minute reperfusion in normal ACSF. The CA1 population spike (PS) was measured and used to quantify the degree of neuronal function recovery after OGD. To assess the role of mitogen-activated protein kinases (MAPKs) in isoflurane preconditioning, U0126, an inhibitor of extracellular signal-regulated protein kinase (ERK1/2), and SB203580, an inhibitor of p38 MAPK, were used before two periods of 3vol% isoflurane exposure. RESULTS: The degree of neuronal function recovery of hippocampal slices exposed to 1vol%, 2vol%, or 3vol% isoflurane once was 41.88%±9.23%, 55.05% ± 11.02%, or 63.18% ± 10.82% respectively. Moreover, neuronal function recovery of hippocampal slices exposed to 1vol%, 2vol%, or 3vol% isoflurane twice was 53.75% ± 12.04%, 63.50% ± 11.06%, or 76.25% ± 12.25%, respectively. Isoflurane preconditioning increased the neuronal function recovery in a dose-dependent manner. U0126 blocked the preconditioning induced by dual exposure to 3vol% isoflurane (6.13% ± 1.56%, P < 0.01) and ERK1/2 activities. CONCLUSIONS: Isoflurane is capable of inducing preconditioning in hippocampal slices in vitro in a dose-dependent manner, and dual exposure to isoflurane with a lower concentration is more effective in triggering preconditioning than a single exposure. Isoflurane-induced neuroprotection might be involved with ERK1/2 activities.

Duplicate preconditioning with sevoflurane in vitro improves neuroprotection in rat brain via activating the extracellular signal-regulated protein kinase.

OBJECTIVE: Sevoflurane preconditioning has been demonstrated to reduce cerebral ischemia-reperfusion (IR) injury, but the underlying mechanisms have not been fully elucidated. Besides, different protocols would usually lead to different results. The objective of this study was to determine whether dual exposure to sevoflurane improves the effect of anesthetic preconditioning against oxygen and glucose deprivation (OGD) injury in vitro. METHODS: Rat hippocampal slices under normoxic conditions (95% O2/5% CO2) were pre-exposed to sevoflurane 1, 2 and 3 minimum alveolar concentration (MAC) for 30 min, once or twice, with 15-min washout after each exposure. The slices were then subjected to 13-min OGD treatment (95% N2/5% CO2, glucose-free), followed by 30-min reoxygenation. The population spikes (PSs) were recorded in the CA1 region of rat hippocampus. The percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment was calculated, since it could indicate the recovery degree of neuronal function. In addition, to assess the role of mitogen-activated protein kinases (MAPKs) in preconditioning, U0126, an inhibitor of extracellular signal-regulated protein kinase (MEK-ERK1/2, ERK1/2 MAPK), and SB203580, an inhibitor of p38 MAPK, were separately added 10 min before sevoflurane exposure. RESULTS: Preconditioning once with sevoflurane 1, 2, and 3 MAC increased the percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment, from (15.13+/-3.79)% (control) to (31.88+/-5.36)%, (44.00+/-5.01)%, and (49.50+/-6.25)%, respectively, and twice preconditioning with sevoflurane 1, 2, and 3 MAC increased the percentage to (38.53+/-4.36)%, (50.74+/-7.05)% and (55.86+/-6.23)%, respectively. The effect of duplicate preconditioning with sevoflurane 3 MAC was blocked by U0126 [(16.23+/-4.62)%]. CONCLUSION: Sevoflurane preconditioning can induce neuroprotection against OGD injury in vitro, and preconditioning twice enhances this effect. Besides, the activation of extracellular signal-regulated protein kinase (MEK-ERK1/2, ERK1/2 MAPK) may be involved in this process.