In pain control after laparoscopic cholecystectomy, subhepatic administration of bupivacaine immediately after the creation of pneumoperitoneum has been shown to be more effective than administration before the withdrawal of the trocars. We aimed to investigate the effect of intraperitoneal bupivacaine administration to the subhepatic area before the creation of the pneumoperitoneum. Eighty patients undergoing elective laparoscopic cholecystectomy under general anesthesia were included in a prospective, randomized study. Patients received 20 mL of 0.5% bupivacaine in the subhepatic area just after intubation, before pneumoperitoneum (group 1), immediately after the creation of the pneumoperitoneum (group 2), just before the removal of the trocars (group 3), or received no local anesthetic (group 4). The degree of the postoperative pain was assessed at 0, 4, 8, 12, and 24 hours after the surgery. The consumption of analgesics (diclofenac sodium) was also recorded. The pain scores and analgesic consumption did not differ among groups 1, 3, and 4. The pain scores of group 2 were lower at each time point compared to the other groups (P < 0.001). Postoperative analgesic consumption in group 2 was reduced compared to the other groups (23.4 +/- 35.9 mg vs. 80.0 +/- 66.3 mg, P = 0.005 [group 1], 69.6 +/- 62.2 mg, P = 0.026 [group 3], and 70.0 +/- 59.9 mg, P = 0.022 [group 4]). The subhepatic infiltration of 20 mL of 0.5% bupivacaine offers good postoperative analgesia when applied just after the creation of the pneumoperitoneum, not before the pneumoperitoneum or after the termination of the pneumoperitoneum.

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Sir,Despite a lack of analgesic effectiveness by itself, magnesium potentiates the effect of analgesic drugs (1). This potentiating effect is suggested to be related to NMDA-receptor blockade (2) or inhibition of catecholamine release (3). But the mechanism is not clearly defined. Some studies demonstrated that nitric oxide (NO) modulates the transmission of pain (4). In addition, magnesium seems to alter NO synthesis (5). We thought that the analgesic effect of magnesium could be related to NO synthesis. Our study included three steps. We investigated firstly the analgesic effect of MgSO 4 used alone, secondly its potentiating effect on morphine sulphate (MS) analgesia, and lastly the effect of N G -Nitro L-Arginine Methyl Ester (L-NAME) on the analgesia offered by the combination of MS with MgSO 4 .After the approval of the Institutional Animal Care and Use Committee 77 mice were allocated into nine groups receiving the following drugs: Group 1 (n ¼ 8): no drug, group 2 (n ¼ 15): MS 1 mg kg À1 , group 3 (n ¼ 4): MgSO 4 1 g kg À1 , group 4 (n ¼ 13): MS 1 mg kg À1 þ MgSO 4 1 g kg À1 , group 5 (n¼ 7): MS 1 mg kg À1 þ MgSO 4 1 g kg À1 þ L-NAME 10 mg kg À1 , group 6 (n¼ 8): MS 0.1 mg kg À1 , group 7 (n¼ 5): MgSO 4 0.5 g kg À1 , group 8 (n¼ 10): MS 0.1 mg kg À1 þ MgSO 4 0.5 g kg À1 , and group 9 (n ¼ 7): MS 0.1 mg kg À1 þ MgSO 4 0.5 g kg À1 þ L-NAME 10 mg kg À1 . Before and 15, 30, 60, 120, 240 min after intraperitoneal drug injections, animals were placed on a hot plate, and the time to hind-paw licking or jumping was recorded as the hot-plate latency (HPL). The HPLs were compared within groups using Wilcoxon Signed Rank test and between groups using the Mann-Whitney U-test. P < 0.05 was considered statistically significant.Morphine sulphate used alone at two doses increased HPL. MgSO 4 used alone at two doses did not change HPL. Morphine sulphate 1 mg kg À1 combined with MgSO 4 1 g kg À1 increased HPL more than MS 1 mg kg À1 used alone. Morphine sulphate 0.1 mg kg À1 combined with MgSO 4 0.5 g kg À1 did not alter HPL when compared to MS 0.1 mg kg À1 used alone. When L-NAME was added to MS and MgSO 4 combinations, the HPL did not change.MgSO 4 did not offer analgesia when used alone and its potentiating effect on morphine analgesia was dose-related. These findings support the results of McCarthy's study (2). Our study was the first to investigate the role of NO on the analgesiapotentiating effect of MgSO 4 . As a NO synthase inhibitor, L-NAME added to the MS and MgSO 4 combination did not alter HPL, this potentiating effect seems not to be related to NO synthesis.

Central venous access plays an increasingly important role in the delivery of modern care. Many studies on the venous access sites for central venous catheterization have been conducted. [1][2][3][4][5] The preferred access site for central venous catheter placement continues to be the right internal jugular vein (IJV).When the right IJV is not available for central venous access, the second access site remains variable. Although the left IJV and the subclavian veins (SCV) have been used for second access, several studies suggest that both SCVs and the left IJV should be avoided because of a high incidence of procedural complications (pneumothorax, arterial puncture) as well as central venous stenosis and thrombosis. [2][3][4][5][6] The left IJV is also related with a high incidence of catheter malfunction. 6 Some authors believe that the second venous access after the right IJV should be the right external jugular vein (EJV). 3,7 One reason for use of the right EJV is its relatively straightforward course and short length, which are very similar to those of right IJV. A second reason is that the EJV is easily accessed, given its superficial location on the neck.7 However, it is suggested that the incidence of malpositioned catheters via the EJV approach makes this route unreliable. 8 To decrease the incidence of catheter dislodgement, vessel wall erosion, thromboembolism and catheter malfunction, accurate positioning of the catheter tip near or at the junction of the superior vena cava (SVC) and right atrium (RA) is necessary.9 It is possible to decrease the incidence of malposition with the use of additional techniques. French) under intra-atrial ECG guidance. The presence of an increase in P-wave size was recorded. Just after the surgery, a portable chest X-ray was taken. The method was considered to be successful when a change in P-wave could be seen and the catheter was in the superior vena cava, as well as when there was no change in P-wave and the catheter was not in the superior vena cava. Results: In six patients (12%), we were not able to advance the guidewire. In the remaining 44 patients, the catheter was inserted without problem. Eight of these 44 catheters were positioned in the innominate vein, with a malposition ratio of 18%. The success rate of external jugular vein cannulation with intra-atrial ECG was 95%. No complications occured related to the EJV cannulation. Conclusion: Considering that it is easily accessed without complication, and the malposition is successfully detected by intra-atrial ECG, EJV is a suitable access for central venous cannulation when internal jugular vein (IJV) is not usable.

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