The effects of preoperative single-dose thoracic paravertebral block on acute and chronic pain after thoracotomy: A randomized, controlled, double-blind trial.

BACKGROUND: Patients undergoing thoracotomy frequently experience acute pain and chronic post-thoracotomy pain (CPTP). There are few articles relating to the investigations on the effects of preoperative single-dose thoracic paravertebral block (PSTPVB) on acute pain and CPTP. We tested the hypothesis that adding PSTPVB to intravenous (IV) patient-controlled analgesia (PCA) would reduce acute pain scores and decrease the incidence and intensity of CPTP. METHODS: Fifty-six patients undergoing elective thoracotomy were randomized to receive PSTPVB in addition to IV PCA (group T) or IV PCA alone (group C). A single 20-mL injection of 0.50% ropivacaine plus 10 mg dexamethasone in saline was administered preoperatively under ultrasound guidance; sufentanil was used for IV PCA. The acute pain intensity at rest and at coughing based on verbal rating scale, postoperative sufentanil consumption, and complications were evaluated at 6, 24, 48, and 72 hours after surgery. The incidence and intensity of CPTP were evaluated at 3 months after surgery. RESULTS: Group T had significantly less acute pain compared with group C at all measurement times both at rest and at coughing (P < .05). The PCA cumulative sufentanil consumption, complications, and the incidence of CPTP between the 2 groups was not statistically significant (P > .05). The intensity of CPTP was significantly higher in group C than in group T (P < .05). CONCLUSION: This study indicated that adding PSTPVB to IV PCA improved acute postoperative pain and chronic pain in patients undergoing thoracotomy, but did not reduce the incidence of CPTP.

Ginsenoside Rb1 Attenuates Isoflurane/surgery-induced Cognitive Dysfunction via Inhibiting Neuroinflammation and Oxidative Stress.

OBJECTIVE: Anesthetic isoflurane plus surgery has been reported to induce cognitive impairment. The underlying mechanism and targeted intervention remain largely to be determined. Ginsenoside Rb1 was reported to be neuroprotective. We therefore set out to determine whether ginsenoside Rb1 can attenuate isoflurane/surgery-induced cognitive dysfunction via inhibiting neuroinflammation and oxidative stress. METHODS: Five-months-old C57BL/6J female mice were treated with 1.4% isoflurane plus abdominal surgery for two hours. Sixty mg/kg ginsenoside Rb1 were given intraperitoneally from 7 days before surgery. Cognition of the mice were assessed by Barnes Maze. Levels of postsynaptic density-95 and synaptophysin in mice hippocampus were measured by Western blot. Levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in mice hippocampus were measured by ELISA. RESULTS: Here we show for the first time that the ginsenoside Rb1 treatment attenuated the isoflurane/surgery-induced cognitive impairment. Moreover, ginsenoside Rb1 attenuated the isoflurane/surgery-induced synapse dysfunction. Finally, ginsenoside Rb1 mitigated the isoflurane/surgery-induced elevation levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in the mice hippocampus. CONCLUSION: These results suggest that ginsenoside Rb1 may attenuate the isoflurane/surgery-induced cognitive impairment by inhibiting neuroinflammation and oxidative stress pending future studies.

Optimum end-tidal concentration of sevoflurane to facilitate supraglottic airway device insertion with propofol at induction allowing spontaneous respiration in obese patients: A prospective observational study.

Obese patients are more likely to encounter with difficult airway management, and supraglottic airway device has been adopted to facilitate tracheal intubation. The optimum anesthetic concentration for obese patients to insert a supraglottic airway device with spontaneous respiration has not been investigated. This study was designed to determine the end-tidal concentration of sevoflurane that would provide acceptable condition for supraglottic airway device insertion with propofol at induction in obese patients without using neuromuscular blockade.Thirty elective obese patients [body mass index (BMI) 30-50 kg/m] scheduled for bariatric surgery were enrolled in this study. Sevoflurane was inhaled at a concentration of 5% after infusion of 1 mg/kg propofol (within 1 minute) according to lean body weight. The target concentration of sevoflurane was initiated at 2.5% with 0.5% as a step size using a modified Dixon up-and-down method. Five minutes after target concentration achieved, the insertion of supraglottic airway device was attempted.The minimum alveolar concentration of sevoflurane for successful insertion of supraglottic airway device calculated using up-and-down method were 2.25 (0.53) % for obese patients. The values of the effective concentration of sevoflurane for successful supraglottic airway device insertion in 50% (EC50) and 95% (EC95) of the obese patients obtained by probit regression analysis were 2.09% (95% confidence interval 1.48-2.68) and 3.31% (95% confidence interval 2.70-8.12), respectively.We conclude that sevoflurane at a minimum alveolar concentration of 2.25% can provide optimal conditions for insertion of supraglottic airway device with spontaneous respiration in obese patients with 1 mg/kg propofol at induction.

Ginsenoside Rg1 Attenuates Isoflurane-induced Caspase-3 Activation via Inhibiting Mitochondrial Dysfunction.

OBJECTIVE: The inhalation anesthetic isoflurane has been shown to induce mitochondrial dysfunction and caspase activation, which may lead to learning and memory impairment. Ginsenoside Rg1 is reported to be neuroprotective. We therefore set out to determine whether ginsenoside Rg1 can attenuate isoflurane-induced caspase activation via inhibiting mitochondrial dysfunction. METHODS: We investigated the effects of ginsenoside Rg1 at concentrations of 12.5, 25, and 50 µmol/L and pretreatment times of 12 h and 24 h on isoflurane-induced caspase-3 activation in H4 naïve and stably transfected H4 human neuroglioma cells that express full-length human amyloid precursor protein (APP) (H4-APP cells). For mitochondrial dysfunction, we assessed mitochondrial permeability transition pore (mPTP) and adenosine-5'-triphosphate (ATP) levels. We employed Western blot analysis, chemiluminescence, and flowcytometry. RESULTS: Here we show that pretreatment with 50 µmol/L ginsenoside Rg1 for 12 h attenuated isoflurane-induced caspase-3 activation and mitochondrial dysfunction in H4-APP cells, while pretreatment with 25 and 50 µmol/L ginsenoside Rg1 for 24 h attenuated isoflurane-induced caspase-3 activation and mitochondrial dysfunction in both H4 naïve and H4-APP cells. CONCLUSION: These data suggest that ginsenoside Rg1 may ameliorate isoflurane-induced caspase-3 activation by inhibiting mitochondrial dysfunction. Pending further studies, these findings might recommend the use of ginsenoside Rg1 in preventing and treating isoflurane-induced neurotoxicity.

Relationship between depth of anesthesia and effect-site concentration of propofol during induction with the target-controlled infusion technique in elderly patients.

BACKGROUND: There are few studies to assess whether the effect-site concentration of propofol can predict anesthetic depth during the target-controlled infusion (TCI) induction in elderly patients. This study aimed to evaluate the relationship between effect-site concentration of propofol and depth of anesthesia during the TCI induction in elderly patients. METHODS: Ninety patients (60 - 80 years) with an American Society of Anesthesiologists (ASA) physical status of 1 - 3, undergoing scheduled abdominal and thoracic surgery under general anesthesia were randomly allocated into one of three groups, Group S1, S2 and S3 (30 patients in each group). The patients in Group S1 received propofol with a target plasma concentration of 4.0 microg/ml; patients in Group S2 received propofol with an initial target plasma concentrations of 2.0 microg/ml that was raised to 4.0 microg/ml 3 minutes later; patients in Group S3 received an infused scheme of 3 steps; starting from a target plasma concentration of 2.0 microg/ml that was increased stepwised by 1 microg/ml until a target plasma concentration of 4.0 microg/ml was achieved, the interval between the two steps was 3 minutes. When an Observer's Assessment of Alertness/Sedation (OAA/S) score of 1 was achieved, remifentanil (effect-site concentration (Ce) of 4.0 ng/ml) and rocuronium 0.9 mg/kg were administered. Tracheal intubation was started 2 minutes after rocuronium injection. Changes of propofol Ce, blood pressure (BP), heart rate (HR), and bispectral index (BIS) were recorded. RESULTS: When an OAA/S score of 1 was achieved, Ce of propofol were (1.7 +/- 0.4) microg/ml, (1.9 +/- 0.3) microg/ml, (1.9 +/- 0.4) microg/ml and the BIS values were 64 +/- 5, 65 +/- 8, and 62 +/- 8 in Groups S1, S2 and S3. Before intubation, Ce of propofol was (2.8 +/- 0.2) microg/ml, (2.8 +/- 0.3) microg/ml, (2.7 +/- 0.3) microg/ml, and the BIS values were 48 +/- 7, 51 +/- 7, and 47 +/- 5 in Groups S1, S2 and S3. By linear regression analysis, a significant correlation between Ce of propofol and BIS values was found (r = -0.580, P < 0.01). Systolic blood pressure (SBP) before intubation was significantly lower in Group S1 than in Groups S2 and S3. SBP and HR after intubation in the three groups were significantly increased when compared with pre-intubation values, but they did not exceed baseline values. CONCLUSIONS: During the TCI induction, Ce of propofol with (1.9 +/- 0.3) microg/ml may make the elderly patients unconscious. When remifentanil with a Ce of 4.0 ng/ml is added a Ce of propofol with (2.8 +/- 0.3) microg/ml is suitable for intubation. The Ce of propofol has a close correlation with the BIS values. Also, a two-step TCI technique seems to be a more suitable method of anesthesia induction in elderly patients compared with the no-stepwise TCI technique and three-step TCI technique.