Phrenic Nerve Block at the Azygos Vein Level Versus Sham Block for Ipsilateral Shoulder Pain After Video-Assisted Thoracoscopic Surgery: A Randomized Controlled Trial.

BACKGROUND: Ipsilateral shoulder pain (ISP) is a common problem after pulmonary surgery. We hypothesized that phrenic nerve block (PNB) at the azygos vein level, near the location of the surgical operation, would be effective for reducing ISP. Our primary aim was to assess the effect of PNB on postoperative ISP, following video-assisted thoracic surgery (VATS). METHODS: This prospective, randomized, patient-blinded, single-institution trial was registered at the University Hospital Medical Information Network (UMIN000030464). Enrolled patients had been scheduled for VATS under general anesthesia with epidural analgesia. Patients were randomly allocated to receive infiltration of the ipsilateral phrenic nerve at the azygos vein level with either 10 mL of 0.375% ropivacaine (PNB group) or 0.9% saline (control group) before chest closure. Postoperative ISP was assessed using a numerical rating scale (NRS, 0-10) at rest at 2, 4, 8, 16, and 24 hours. The incidence of ISP was defined as the proportion of patients who reported an NRS score of ≥1 at least once within 24 hours after surgery. In the primary analysis, the proportion of patients with ISP was compared between PNB and control groups using the χ2 test. NRS values of ISP and postoperative incision pain within 24 hours were investigated, as was the frequency of postoperative analgesic use. Incision pain was assessed using an NRS at the time of ISP assessment. Finally, the incidence of postoperative nausea and vomiting and shoulder movement disorders were also evaluated. RESULTS: Eighty-five patients were included, and their data were analyzed. These patients were randomly assigned to either PNB group (n = 42) or control group (n = 43). There were no clinically relevant differences in demographic and surgical profiles between the groups. There was no significant difference in the incidence of ISP (the control group 20/43 [46.5%] versus the PNB group 14/42 [33.3%]; P = .215). The severity of ISP was lower in the PNB group than in the control group (linear mixed-effects model, the main effect of treatment [groups]: P < .001). There were no significant differences between groups in terms of postoperative incision pain. The frequency of postoperative analgesic use was significantly higher in the control group (Wilcoxon rank sum test, P < .001). Postoperative nausea and vomiting did not significantly differ between the 2 groups. There were no changes in the range of shoulder joint movement. CONCLUSIONS: Azygos vein level PNB did not significantly affect the incidence of ISP after VATS.

The effect of aging on dopamine release and metabolism during sevoflurane anesthesia in rat striatum: an in vivo microdialysis study.

We have previously reported that halothane anesthesia increases extracellular concentrations of dopamine (DA) metabolites in rat striatum using in vivo microdialysis techniques. Aging induces many changes in the brain, including neurotransmission. However, the relationship between aging and changes in neurotransmitter release during inhalational anesthesia has not been fully investigated. The aim of the present investigation was to evaluate the effect of sevoflurane on methamphetamine (MAPT)-induced DA release and metabolism in young and middle-aged rats. Male Sprague-Dawley rats were implanted with a microdialysis probe into the right striatum. The probe was perfused with a modified Ringer's solution and 40µl of dialysate was directly injected to an HPLC every 20min. Rats were administered saline, the same volume of 2mgkg(-1) MAPT intraperitoneally, or 5µM MAPT locally perfused. After treatments, the rats were anesthetized with 1% or 3% sevoflurane for 1h. Sevoflurane anesthesia significantly increased the extracellular concentration of DA only in middle-aged rats (52-weeks-old). In young rats (8-weeks-old), sevoflurane significantly enhanced MAPT-induced DA when administered both intraperitoneally and perfused locally, whereas no significant additive interaction was found in middle-aged rats. These results suggest that aging changes DA release and metabolism in rat brains primarily by decreasing the DA transporter.

Pentobarbital decreased nitric oxide release in the rat striatum but ketamine increased the release independent of cholinergic regulation.

Pentobarbital (PB) and ketamine (Ket) influence the concentration of neurotransmitters in the brain. PB has been reported to decrease the extracellular nitric oxide (NO) concentration through a decrease in acetylcholine (ACh) release, while Ket has been shown to increase the NO concentration via an increase in ACh release. Here, we investigated effects of PB and Ket on NO release and the relationship between NO and ACh in the rat striatum by in vivo microdialysis experiments. Male Sprague-Dawley rats were used. A microdialysis probe was inserted into the right striatum and perfused with modified Ringer's solution. Samples were collected every 15 min and injected into an HPLC system. The rats were freely moving, and PB and Ket were administered intraperitoneally. Neostigmine (1 and 10 µM) and mecamylamine (100 µM) were added to the perfusate. Calcium and magnesium concentrations were modified for each anesthetic to influence ACh release. PB decreased NO products (NOx) while Ket increased them. While perfusion with neostigmine showed no effect on baseline NOx concentrations, it diminished the PB-induced NOx reduction at low concentrations and abolished it at high concentrations. Magnesium-free perfusion had no effect on baseline NOx concentrations, whereas perfusion at a low magnesium concentration antagonized the PB-induced NOx reduction. Mecamylamine and calcium-free perfusion had no effect on baseline NOx concentrations and Ket-induced NOx increases. PB may decrease NO release through reduction in ACh release, whereas Ket may increase NO release independent of ACh regulation.

Dexmedetomidine and hydroxyzine synergistically potentiate the hypnotic activity of propofol in mice.

PURPOSE: Investigation into the characteristics of anesthetic interactions may provide clues to anesthesia mechanisms. Dexmedetomidine, an α(2)-adrenergic receptor agonist, has become a popular sedative in intensive care, and hydroxyzine, a histamine receptor antagonist, is well known as a tranquilizing premedication for anesthesia. However, no experimental or pharmacological evaluation has been reported concerning their combination with propofol. Thus, we studied their combined effect with a hypnotic dose of propofol in ddY mice. METHODS: Male adult mice were intravenously administered either dexmedetomidine (30 µg/kg) or hydroxyzine (5 mg/kg) with propofol (3.75-10 mg/kg) to induce hypnosis, defined as a loss of the righting reflex (LRR). Other mice were intravenously administered propofol, dexmedetomidine (300 µg/kg), or hydroxyzine (50 mg/kg) alone, and subsequent behavioral changes were observed. The 50% effective dose (ED(50)) for LRR was calculated, and the duration of LRR was determined. RESULTS: The hypnotic dose of propofol was 9.95 ± 1.04 mg/kg (ED(50) ± SEM) without combination. Dexmedetomidine and hydroxyzine reduced the ED(50) of propofol to 5.32 ± 0.57 and 5.63 ± 0.57 mg/kg, respectively. Coadministration of dexmedetomidine significantly extended LRR duration compared with propofol alone, whereas hydroxyzine significantly shortened LRR duration. A maximal dose of dexmedetomidine or hydroxyzine alone did not induce hypnosis. CONCLUSIONS: Dexmedetomidine and hydroxyzine demonstrated no hypnotic action alone; however, their coadministration potentiated the hypnotic activity of propofol. Although reduction in the dose of propofol was similar, only dexmedetomidine prolonged the duration of hypnosis.