Effect of Dexmedetomidine combined with sufentanil for post- thoracotomy intravenous analgesia:a randomized, controlled clinical study.

BACKGROUND: Few studies have investigated the use of dexmedetomidine in patient-controlled intravenous analgesia (PCIA) after thoracic surgery. This study to evaluate the effect of dexmedetomidine combined with sufentanil for PCIA after thoracotomy under general anaesthesia. METHODS: Ninety-seven adults patients scheduled for thoracotomy surgery. All two groups received PCIA with either sufentanil alone (control group) or combining dexmedetomidine with sufentanil (dexmedetomidine group). Hemodynamic measurements, visual analog scale (VAS) scores at rest and at coughing, Ramsay sedation score (RSS), analgesic consumption, and postoperative nausea and vomiting (PONV) as well as drug-related adverse effects were compared at 2, 6, 12, 24, 36 and 48 h postoperatively. RESULTS: In the patients of the dexmedetomidine group, compared to the control group, the pain scores at rest or at coughing during 48 h postoperatively were lower (P < 0.001), the sedation scores were lower, the consumption of sufentanil and rescue meperidine were lower, and the number of episode of moderate PONV was three times lower. No signs of toxicity or local complications were observed. There was a non-significant trend for a lower HR and BP in the dexmedetomidine group vs. CONCLUSION: The combining dexmedetomidine with sufentanil for post-thoracotomy PCIA can improve pain control together with the decrease in sufentanil requirements, and improve postoperative patient's satisfaction compared with sufentanil alone in PCIA. TRIAL REGISTRATION: This trial was retrospectively registered on 27 April 2016 at the Chinese Clinical Trial Register (number: ChiCTR-ONC-16008376 ).

Remote intrathecal morphine preconditioning confers cardioprotection via spinal cord nitric oxide/cyclic guanosine monophosphate/protein kinase G pathway.

BACKGROUND: Remote intrathecal morphine preconditioning (RMPC) induces cardioprotection, but the underlying mechanisms of this effect is unknown. The aim of this study was to investigate the role of spinal cord nitric oxide/cyclic guanosine monophosphate/protein kinase G (NO/cGMP/PKG) signal pathway in the cardioprotection of RMPC in rats. MATERIALS AND METHODS: Anesthetized, open chest, male Sprague-Dawley rats were assigned to one of eight treatment groups 3 d after intrathecal catheter placement. Before ischemia and reperfusion, RMPC received intrathecal morphine (3 µg/kg) by three cycles of 5-min infusions interspersed with 5-min infusion free periods. Intrathecally administrated a nonspecific nitric oxide synthase (NOS) inhibitor Nω-Nitro-L-arginine methyl ester (30 nmol), a specific guanylate cyclase inhibitor oxadiazolo [4,3-a] quinoxalin-1-one (11 nmol) and PKG inhibitor KT-5823 (20 pmol) 10 min before RMPC was used to evaluate the role of NO/cGMP/PKG of spinal cord. Ischemia and reperfusion injury were then induced by 30 min of left coronary artery occlusion, followed by 120 min of reperfusion. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. The content of cyclic guanosine monophosphate in the thoracic spinal cord was determined by radioimmunity protocol; the contents of nitric oxide and activity of NOS in the thoracic spinal cord were determined by nitrate reductase reduction and colorimetric methods; the expression of neuronal NOS (nNOS) and PKG in the thoracic spinal cord were determined by immunohistochemical and Western blotting method; the expression of nNOS messenger RNA was determined by reverse transcription-polymerase chain reaction method. RESULTS: RMPC group markedly reduced the infarct size compared with the control group. However, the cardioprotection of RMPC could be abolished by pretreatment with Nω-Nitro-L-arginine methyl ester, Oxadiazolo [4,3-a] quinoxalin-1-one, and KT-5823. RMPC enhanced nitric oxide , NOS, and cyclic guanosine monophosphate levels in the spinal cord. Meanwhile, RMPC increased PKG and nNOS protein or messenger RNA expression in the spinal cord. CONCLUSIONS: Spinal cord NO/cGMP/PKG signaling pathway mediates RMPC-induced cardioprotective effect.

Effect of Pericapsular Nerve Group Block with Different Concentrations and Volumes of Ropivacaine on Functional Recovery in Total Hip Arthroplasty: A Randomized, Observer-Masked, Controlled Trial.

Purpose: The pericapsular nerve group (PENG) block provides satisfactory postoperative analgesia without hampering motor function for total hip arthroplasty (THA); however, unexpected motor block has been observed clinically. It is unknown whether this motor block is related to the dose of ropivacaine. We aimed to conduct a prospective randomized trial to test whether reducing the volume or concentration of ropivacaine was better for less motor block after PENG block. Patients and Methods: Ninety-nine patients with fracture or femoral head necrosis scheduled for THA were randomly allocated to receive 20 mL 0.5% ropivacaine (Group A), 20 mL 0.25% ropivacaine (Group B), and 10 mL 0.5% ropivacaine (Group C). The primary outcome was the incidence of postoperative quadriceps motor block at 6 hours. Secondary outcomes were the incidence of postoperative quadriceps motor block at 0, 12, 24 and 48 hours; pain scores on the numeric rating scale (NRS) at all postoperative time points (0, 6, 12, 24, and 48 hours); the time to first walk; the incidence of rescue analgesia; side effects such as dizziness, ache, nausea, and vomiting; and patient satisfaction. Results: Compared with Group A, Group C resulted in a lower incidence of quadriceps motor block at 0 hours, 6 hours and 12 hours postoperatively (P < 0.05), while Group B only resulted in a lower incidence of motor block at 12 hours postoperatively (P < 0.05). No intergroup differences were found in terms of postoperative pain scores, the incidence of rescue analgesia, adverse events or patient satisfaction (P > 0.05). Conclusion: A higher incidence of motor blockade was observed when 20 mL of 0.5% ropivacaine was administered, which was mainly caused by the excessive volume. Therefore, we recommend performing PENG block with 10 mL 0.5% ropivacaine.

Morphine reduces the threshold of remote ischemic preconditioning against myocardial ischemia and reperfusion injury in rats: the role of opioid receptors.

OBJECTIVES: Opioid receptors mediate the cardioprotection of remote ischemic preconditioning (RIPC). The authors tested the hypothesis that morphine reduces the threshold of cardioprotection produced by RIPC. METHODS: A randomized, prospective study. SETTING: A university research laboratory. PARTICIPANTS: Forty-five male Sprague-Dawley rats. INTERVENTIONS: Anesthetized, open-chest, male Sprague-Dawley rats were assigned randomly to 1 of 7 treatment groups. RIPC1 and RIPC3 were, respectively, induced by 1 or 3 cycles of 5 minutes of femoral artery ischemia interspersed with 5 minutes of reperfusion. Morphine (MOR, 0.1 mg/kg) and the opioid receptor antagonist naloxone (NAL, 6 mg/kg) were administered 30 minutes before sustaining ischemia. MOR + RIPC1 and NAL + MOR + RIPC1 groups received the combination of MOR and RIPC1 in the absence or presence of NAL before coronary artery occlusion. Ischemia and reperfusion injury then were induced by 30 minutes of left coronary artery occlusion followed by 120 minutes of reperfusion. MEASUREMENTS AND MAIN RESULTS: Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. RIPC3 and the combination of MOR and RIPC1 groups significantly reduced the infarct size compared with the control group. RIPC1, MOR, and NAL did not affect infarct size. NAL pretreatment reversed cardioprotection of the combination of MOR and RIPC1 treatments. CONCLUSIONS: MOR reduces the threshold of RIPC, and opioid receptors mediate this augmentative effect.

The dose response of sufentanil as an adjuvant to ropivacaine in cesarean section for relief from somato-visceral pain under epidural anesthesia in parturients with scarred uterus.

Visceral pain is common during epidural anesthesia with mini dose local anesthetics in parturients during cesarean section. To reduce or avoid this complication caused by traction on the abdominal viscera, this study aimed to determine the 50% effective dose (ED50) and 95% effective dose (ED95) of epidural sufentanil as an adjuvant combination with local anesthetics for relief visceral pain in parturients with scarred uterus undergoing elective cesarean section.One hundred parturients with scarred uterus undergoing elective cesarean section under epidural anesthesia were enrolled in this randomized, double-blinded, dose-ranging study. Parturients received 5, 10, 15, 20, and 25 µg epidural sufentanil as an adjuvant with 10 mL of 0.65% ropivacaine. Successful epidural anesthesia was defined as a sixth thoracic vertebra (T6) sensory level achieved within 20 minutes after epidural drugs administration and/or no visceral pain by traction on the abdominal viscera during the cesarean section. The ED50 and ED95 were calculated with a logistic regression model.ED50 and ED95 of epidural sufentanil for successful of the pain-free from visceral pain were 10.7 µg [95% confidence interval (CI): 2.4-14.4 µg) and 28.1 µg (95% CI: 19.4-44.0 µg), respectively. The onset time to sensory block, maximum Bromage scale and duration of motor block were significant different with dose of sufentanil >20 µg (P < .05, compared with the other dose groups). With the dose of epidural sufentanil >20 µg could result in an increase of incidence of maternals' adverse effects. Compared with a different dose of sufentanil, epidural administed sufentanil between 15 µg and 20 µg can maximize parturients' satisfaction.Our study showed that sufentanil could be used in combination with ropivacaine for relief from somato-visceral pain in patients with scarred uterus during elective cesarean section during epidural anesthesia, and that maximized parturients' satisfaction could be achieved when the use of sufentanil with the dose between 15 µg and 20 µg for epidural anesthesia.

The Analgesic Effect of Ropivacaine Combined With Dexmedetomidine for Incision Infiltration After Laparoscopic Cholecystectomy.

BACKGROUND: Local anesthetics infiltration is one consensus efficient strategy for pain relief after laparoscopic cholecystectomy (LC). The aim of this study was to investigate analgesia efficacy of incisional infiltration with ropivacaine plus dexmedetomidine. METHODS: Patients scheduled for LC were assigned to 4 groups by different medications for trocar wound infiltration. The incidence of adverse events and the analgesic effect of ropivacaine combined with dexmedetomidine for incision infiltration were recorded. RESULTS: Incisional infiltration of ropivacaine combining with dexmedetomidine could significantly reduce postoperative pain and the amount of pethidine requirement. Furthermore, it could also reduce time to walk without assistance, improve the efficacy of analgesia and sleep quality during the first night after LC, but did not increase the incidence of surgical adverse events. CONCLUSIONS: The use of ropivacaine and dexmedetomidine may be considered as an alternative treatment for postoperative pain in patients undergoing LC.

The optimal dose of dexmedetomidine added to an sufentanil-based analgesic regimen for postoperative pain control in spine surgery: A probit analysis study.

Postoperative spinal patients remain a challenge for provision of postoperative analgesia. Patient-controlled intravenous analgesia (PCIA) is a major method in reducing the severe pain after the surgery in our institution, but some adverse effects prevent the use of adequate dosage opioids.This study was determined using the probit analysis to investigate the optimal dose of dexmedetomidine (DEX) infusion for postoperative analgesia combined with sufentanil (SUF) in spine surgery.The dose of DEX needed to produce satisfactory analgesia conditions following combination of 3.0 µg/kg SUF in PCIA pump, which was diluted to 250 mL with a 4 mL/h as background infusion. Patients were recruited with age 35 to 65 years. The satisfactory criteria of postoperative analgesia were determined with a average satisfaction level of pain control, sedation, self-satisfaction, and adverse effects, among others. The dose of DEX was determined using the modified Dixon's up-and-down method (0.5 µg/kg as a step size). The first patient was test at 3.0 µg/kg DEX. The patient was assessed at 6, 12, 36 hours, and termination of PCIA following the continuous infusion of DEX-SUF mixture in PCIA after surgery.Twenty-five patients were enrolled by predetermined criteria. The optimal dose of DEX required for satisfactory analgesic was 4.33 (SD, 0.38) µg/kg combined with 3.0 µg/kg SUF via a PCIA volume of 250 mL by background infusion of 4 mL/h. Using probit analysis, the ED50 of DEX was 4.12 µg/kg (95% confidence limits 3.74-4.52 µg/kg) for satisfactory postoperative analgesic in spine surgery, the ED95 of DEX was 4.85 µg/kg (95% confidence limits 4.48-7.13 µg/kg). There was no report of somnolence or respiratory depression, relevant bradycardia or hypotension, or over sedation in this study.The optimal dose of DEX was 4.33 (0.38) µg/kg combined with 3.0 µg/kg SUF diluted to 250 mL with a background infusion of 4 mL/h for satisfactory analgesic after spine surgery. From probit analysis, ED50 and ED95 of DEX were 4.12 µg/kg (95% confidence limits 3.74-4.52 µg/kg) and 4.85 µg.kg (95% confidence limits 4.48-7.13 µg/kg), respectively.

Preoperative dexmedetomidine prevents tourniquet-induced hypertension in orthopedic operation during general anesthesia.

This study was a double-blinded randomized control trial designed to investigate the hemodynamic effects of dexmedetomidine on prolonged tourniquet inflation. Thirty-seven patients scheduled for elective orthopedic surgery of the lower limb under general anesthesia were recruited. They were randomly assigned to receive intravenous dexmedetomidine (DEX, 0.5 µg/kg; n = 18) or normal saline (CON; n = 19) before tourniquet inflation. Arterial blood pressure and heart rate were recorded every 10 minutes until 60 minutes after the start of tourniquet inflation and again immediately after deflation. In the DEX group, arterial pressure was not significantly changed, but in the CON group arterial pressure was significantly increased at 40, 50, and 60 minutes after the start of tourniquet inflation. Development of more than 30% increase in arterial pressure during tourniquet inflation was more frequent in the CON group than in the DEX group. Preoperative intravenous dexmedetomidine could therefore prevent tourniquet-induced hypertension in patients undergoing general anesthesia.