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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 χ 2 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 purpose of this study was to identify the relationship between sensitivity of arterial baroreflex and plasma concentrations of lidocaine. Using twelve mongrel dogs anesthetized with alpha-chloralose, the left kidney was exposed retroperitoneally, and renal sympathetic nerve activity was recorded continuously. Lidocaine was infused in four different doses: 2 mg.kg BW-1 bolus + 100 micrograms.BW-1 x min; 3 mg.kg BW-1 bolus + 200 micrograms.kg BW-1 x min; 6 mg.kg BW-1 bolus + 400 micrograms.kg BW-1 x min; and 12 mg.kg BW-1 + 800 micrograms.kg BW-1 x min. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after beginning lidocaine infusion. Plasma lidocaine concentrations determined by high performance liquid chromatography revealed that the steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at plasma concentrations of lidocaine below 5 micrograms.ml-1. However, cardiac and sympathetic baroreflex sensitivity were significantly attenuated (P < 0.01) when plasma lidocaine concentrations were well above human convulsion levels (10 micrograms.ml-1). The results indicate that hemodynamic derangement observed in the lidocaine-induced central nervous system toxicity is, at least in part, due to the attenuated arterial baroreflex.

The mechanism of arterial hypotension induced by non-depolarizing neuromuscular blocking agents may be multifactorial and differ between drugs. The purpose of this study was to evaluate the effect of high-dose atracurium and equivalent doses of other non-depolarizing neuromuscular blocking agents on haemodynamic state and sympathetic nervous activity. In studies on 24 mongrel dogs anaesthetized with alpha-chloralose, the left kidney was exposed retroperitoneally and renal sympathetic nerve activity was recorded continuously after bilateral sino-aortic denervation and cervical vagi section. The dogs were allocated to four groups; atracurium 1.5 mg kg-1, tubocurarine 0.3 mg kg-1, pancuronium 0.3 mg kg-1 or vecuronium 0.3 mg kg-1 was administered to six dogs in each group. Histamine 1 micrograms kg-1 was given to two dogs in each group, 1 h before administration of neuromuscular blocking agents. We observed that atracurium and tubocurarine significantly decreased arterial pressure, heart rate and renal sympathetic nerve activity (P < 0.05), but pancuronium and vecuronium did not Histamine-induced arterial hypotension but did not affect heart rate or renal sympathetic nerve activity. As both arterial and cardiopulmonary baroreflex pathways were inactivated in these animals, we conclude that atracurium decreased arterial pressure by suppressing efferent sympathetic nerve activity in a manner similar to that of tubocurarine.