Intravenous Lidocaine and Bupivacaine Dose-dependently Attenuate Bronchial Hyperreactivity in Awake Volunteers

Groeben, Harald; Schwalen, Andreas; Irsfeld, S.; Stieglitz, Sven; Lipfert, P.; Hopf, Hans‐Bernd

doi:10.1097/00000542-199603000-00007

Cited by 40 publications

(20 citation statements)

References 28 publications

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“…Plasma and interstitial concentrations of local anesthetics ranges from 5–20 µ M after intravenous [38, 39]and epidural [40, 41]injections to 1–10 m M range [42]after local nerve plexus infiltrations (e.g. interscalene or axillary block).…”

Section: Discussionmentioning

confidence: 99%

Local Anesthetics Induce Human Renal Cell Apoptosis

Lee¹,

Xu²,

Siegel³

et al. 2003

Am J Nephrol

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Renal cell apoptosis contributes significantly to the pathogenesis of acute renal failure. Local anesthetics induce apoptosis in neuronal and lymphocytic cell lines. We examined the effects of chronic (48 h) local anesthetic treatment (lidocaine, bupivacaine and tetracaine) on human proximal tubular (HK-2) cells. Apoptosis induction was assessed by detecting poly(ADP)-ribose polymerase fragmentation, caspase activation, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining, DNA laddering and by cellular morphology. Cell death was quantified by measuring neutral red dye uptake and lactate dehydrogenase released into the cell culture medium. All 3 local anesthetics caused concentration-dependent cell death, induced HK-2 cell apoptosis and potentiated TNF-α induced apoptosis. Local anesthetics induced HK-2 cell apoptosis by activation of caspases 3, 6, 7, 8 and 9. ZVAD-fmk, a pan-caspase inhibitor, blocked the local anesthetic induced HK-2 cell apoptosis. Local anesthetics also inhibited the activities of anti-apoptotic kinases protein kinase B (Akt) and extracellular signal regulated mitrogen-activated protein kinase. Local anesthetic’s pro-apoptotic effects are independent of sodium channel inhibition as tetrodotoxin, a selective voltage-gated sodium channel blocker, failed to mimic local anesthetic-mediated induction or potentiation of HK-2 cell apoptosis. We conclude that local anesthetics induce human renal cell apoptotic signaling by caspase activation and via inhibition of pro-survival signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Local Anesthetics Induce Human Renal Cell Apoptosis

Lee¹,

Xu²,

Siegel³

et al. 2003

Am J Nephrol

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“…This way, autonomic reflexes such as the coughing reflex or reflex bronchoconstriction can be suppressed with lidocaine plasma concentrations of 1.0-2.0 µg·ml −1 , i.e., far below the toxic threshold of 5.0 µg·ml −1 [76][77][78]. In asthmatic volunteers, intravenous lidocaine doses of 1.0-2.0 mg·kg −1 body weight significantly attenuated histamine-induced bronchoconstriction [65,67].…”

Section: The Effects Of Local Anesthetics On Lung Function and Bronchmentioning

confidence: 99%

“…This effect is comparable to a moderate dose of a β2-adrenergic agonist such as salbutamol, and leads, in combination with salbutamol, to an additive effect [79]. Therefore, in cases of expected airway irritation, prophylactic treatment with lidocaine and a β2-adrenergic agonist can be recommended [72,77]. As well as its use as a prophylactic agent, intravenous administration of lidocaine has been used successfully to treat bronchospasm [69,80].…”

Section: The Effects Of Local Anesthetics On Lung Function and Bronchmentioning

confidence: 99%

Epidural anesthesia and pulmonary function

Groeben¹

2006

J Anesth

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107

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The epidural administration of local anesthetics can provide anesthesia without the need for respiratory support or mechanical ventilation. Nevertheless, because of the additional effects of epidural anesthesia on motor function and sympathetic innervation, epidural anesthesia does affect lung function. These effects, i.e., a reduction in vital capacity (VC) and forced expiratory volume in 1 s (FEV(1.0)), are negligible under lumbar and low thoracic epidural anesthesia. Going higher up the vertebral column, these effects can increase up to 20% or 30% of baseline. However, compared with postoperative lung function following abdominal or thoracic surgery without epidural anesthesia, these effects are so small that the beneficial effects still lead to an improvement in postoperative lung function. These results can be explained by an improvement in pain therapy and diaphragmatic function, and by early extubation. In chronic obstructive pulmonary disease (COPD) patients, the use of thoracic epidural anesthesia has raised concerns about respiratory insufficiency due to motor blockade, and the risk of bronchial constriction due to sympathetic blockade. However, even in patients with severe asthma, thoracic epidural anesthesia leads to a decrease of about 10% in VC and FEV(1.0) and no increase in bronchial reactivity. Overall, epidural administration of local anesthetics not only provides excellent anesthesia and analgesia but also improves postoperative outcome and reduces postoperative pulmonary complications compared with anesthesia and analgesia without epidural anesthesia.

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“…4e6 Intravenous administration of lidocaine or bupivacaine has been reported to attenuate bronchial hyperreactivity in awake humans. 7 It has been demonstrated that bupivacaine or lidocaine applied topically to the smooth muscle of isolated rat tail arteries can inhibit vascular contraction in response to adrenergic activation. 8 The effect of bupivacaine topically applied to the trachea has not been well explored.…”

Section: Introductionmentioning

confidence: 99%