A double-blind comparison of lidocaine and mepivacaine during epidural anaesthesia

The effects of epidural anaesthesia with plain 2% lidocaine or mepivacaine were compared in 200 patients undergoing extracorporeal shock wave lithotripsy in a double-blind manner. The onset, spread, duration and quality of analgesia were similar in both groups. The numbers of patients who needed vasoconstrictor or atropine were almost equal in both the lidocaine and the mepivacaine groups. Mild but significant hypotension continued for a longer period in the mepivacaine group than in the lidocaine group. A transient decrease in arterial oxygen saturation was seen in two patients receiving lidocaine and in three patients receiving mepivacaine. Mild systemic toxicity was observed in eight patients in both groups, although serious complications such as convulsions did not occur. It is concluded that both drugs can be used equally safely for epidural anaesthesia, although the maximum recommended doses differ.     

Lidocaine-induced hemodynamic effects are enhanced by the inhibition of endothelium-derived relaxing factor in dogs

Background: Lidocaine has been shown to have direct vasoconstrictive effects at low concentrations. Since lidocaine inhibits endothelium-dependent vasodilation in vitro , the vasoconstrictor effect of lidocaine may be due to inhibition of endothelium-derived relaxing factor(EDRF/NO). Therefore, the current study was designed to determine the effects of N^G-nitro-L-arginine (L-NNA), a potent inhibitor of nitric oxide synthase, on systemic and pulmonary hemodynamics during lidocaine infusion.
Methods: Systemic and pulmonary hemodynamic effects of lidocaine infusion, 1 mg kg^-1 min^-1, for 10 min were measured in dogs anesthetized with 1% halothane in oxygen. Dogs were studied twice with an interval of 1 week in a cross-over study, and were assigned to one of two groups that received saline or L-NNA intravenously in group 1 (n=8), or L-NNA or L-NNA+L-arginine which reverses the nitric oxide synthesis inhibitor effect of L-NNA, intravenously in group 2 (n=8) prior to lidocaine infusion. The free serum concentration of and protein-binding ratio for lidocaine were measured.
Results: With saline pretreatment in group 1, lidocaine infusion significantly decreased cardiac index (CI) and significantly in-
Conclusion: In contrast to in vitro study, vasoconstrictor effect of lidocaine is enhanced when a capacity for compensatory vasodilation including EDRF/NO pathway is exhausted in halo-thane-anesthetized dogs.     

Bupivacaine does not suppress cardiac sympathetic nerve activity during halothane anesthesia in the cat

Background: The finding that IV lidocaine suppresses cardiac sympathetic nerve activity during 1 MAC halothane, but not during 2 MAC or 3 MAC halothane, suggests that the neurally mediated circulatory effects of IV local anesthetics may vary with background autonomic activity. This study aimed to compare the effects of IV lidocaine and bupivacaine on cardiac sympathetic nerve activity (CSNA) during normal and high levels of CSNA.
Methods: Cats were anesthetized with halothane and allocated to three groups. In groups I-L and I-B, sympathetic hyperactivity was induced by electrical stimulation of the posterior hypothala-mus. CSNA, heart rate and mean arterial pressure were then measured before and after administration of lidocaine 2 mgkg BW^-l IV (Group I-L, n=7) or bupivacaine 0.5 mgkg BW^-1 IV (Group I-B, n=7) during 1% halothane anesthesia. In Group II (n=7), following administration of bupivacaine 0.5 mgkg BW^-1 IV, CSNA, sinus cycle length (SCL), and subintervals of atrio-ventricular conduction time (A-H, H-V, and H-S) at pacing were measured during O.8%, 1.6% and 2.4% halothane anesthesia without sympathetic hyperactivity.
Results: Lidocaine suppressed CSNA hyperactivity and tachycardia significantly in Group I-L, but bupivacaine did not do so in Group I-B. In Group 11, bupivacaine did not affect CSNA at any concentrations of halothane, but lengthened SCL, A-H, H-V and H-S intervals significantly at each concentration of halothane.
Conclusions: We conclude that IV bupivacaine, unlike IV lidocaine, does not suppress CSNA during either normal or high CSNA under halothane anesthesia although IV bupivacaine has stronger depressive effects on cardiac conduction than does IV lidocaine during deep halothane anesthesia.     

Effects of intravenous lidocaine on cardiac sympathetic nerve activity and A–V conduction in halothane–anesthetized cats

To study neural contributions to the alterations in intracardiac conduction induced by IV lidocaine, we measured cardiac sympathetic nerve activity (CSNA) simultaneously with sinus cycle length (SCL) and AV conduction time using His–bundle electrocardiography following IV lidocaine in cats. Sixteen cats were anesthetized with halothane in oxygen and mid–sternotomized. The His–bundle electrogram and CSNA were recorded from an electrode placed in the interatrial septum and from the left ventrolateral or ventromedial nerve, respectively. Atrium–His (A–H), His–Purkinje (H–V), and total intraventricular (H–S) conduction times were measured during atrial pacing conducted at a cycle length of 300 ms. In eight cats, 1 MAC, 2 MAC, and 3 MAC halothane were given during IV lidocaine (Groups H–l, H–2 and H–3). In the other eight cats, anesthesia was switched from halothane to IV alpha–chloralose (30–50 mg–kgBW^-1; Group C). A significant decrease in CSNA with IV lidocaine, 2 mg–kgBW^-1' was recognized in Groups C and H–l, but not in Groups H–2 and H–3. Prolongations of SCL during the spontaneous cycle, A–H and H–V in the paced mode following IV lidocaine were significant in Groups C, H–l and H–2, but not significant in Group H–3. We conclude that IV lidocaine induces a significant decrease in CSNA during alpha–chloralose or 1 MAC halothane anesthesia which partly contributes to the control of intracardiac conduction.     

Gastric emptying and small bowel transit times in volunteers after intravenous morphine and nalbuphine

Gastric emptying half-times and small intestinal transit times were measured in a double-blind crossover study of 17 volunteers who received an intravenous injection of nalbuphine (5 or 10 mg), morphine (5 mg) or placebo. Both times were monitored using a gamma camera after a radioactive test meal and gastric emptying half-time was calculated. Small intestinal transit time was measured by the appearance of radioactivity in the caecum and also of hydrogen in end tidal air. Gastric emptying was prolonged over placebo by nalbuphine 10 mg, which had more effect than nalbuphine 5 mg or morphine 5 mg; morphine 5 mg had less effect than nalbuphine 5 mg. Small intestinal transit time was prolonged over placebo by nalbuphine 10 mg more than by nalbuphine 5 mg or morphine 5 mg, which had approximately equal effects. In these respects, the potency ratio of nalbuphine appears roughly equivalent to morphine. Small intestinal transit times measured by end tidal hydrogen concentration and gamma camera showed close agreement.     

Effects of intravenous administration of local anesthetics on the renal sympathetic nerve activity during nitrous oxide and nitrous oxide-halothane anesthesia in the cat

The effects of subseizure doses of lidocaine and bupivacaine administered intravenously (i.v.) on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were studied in cats anesthetized with nitrous oxide (N2O)-O2 and N2O-O2-halothane (1%). In cats anesthetized with N2O-O2, MAP decreased briefly (P less than 0.01) and then returned to the initial level within a minute after the i.v. injection of lidocaine (5 mg/kg, 10 mg/kg). RSNA increased at first and then decreased slightly. In cats with denervated baroreceptors, the change in RSNA after lidocaine 5 mg/kg i.v. was similar to that in cats with intact baroreceptors. In contrast, MAP, HR and RSNA decreased significantly (P less than 0.01) after i.v. injection of lidocaine during N2O-O2-halothane anesthesia. The effects of bupivacaine on RSNA were similar to those of lidocaine. It is concluded that cardiovascular depression following intravenous local anesthetics during N2O-O2-halothane anesthesia may be caused by both a decreased sympathetic activity and a direct depressant effect on the myocardium.     

Recovery of bowel motility after high dose fentanyl or morphine anaesthesia for cardiac surgery

Recovery of bowel function was investigated after cardiac surgery. The time to first passage of flatus was measured using a carbon dioxide analyser as an indication of the return of coordinated bowel motility in 22 adult patients who received high-dose fentanyl (56.3, SD 20.9 micrograms/kg) or morphine (1.3, SD 0.7 mg/kg) anaesthesia. The time from the patient's arrival in the intensive care unit to passage of the first flatus in patients who received fentanyl anaesthesia was significantly longer than in those who received morphine (p less than 0.05). There was a significant relationship between the time to first flatus and the total dose of fentanyl, but no such relationship could be demonstrated for morphine. It is concluded that high-dose fentanyl anaesthesia delays recovery of bowel motility in a dose-dependent manner.