Lidocaine attenuates hyperoxic lung injury in rabbits

Takao, Yumiko; Mikawa, Katsuya; Nishina, Kahoru; Maekawa, Nobuhiro; Obara, Hidefumi

doi:10.1111/j.1399-6576.1996.tb04439.x

Cited by 85 publications

(45 citation statements)

References 28 publications

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“…In rabbits, Mikawa et al (1994) used 2mg/kg in a single dose of intravenous lidocaine 10min before infusion of LPS and thereafter infused it at a rate of 2mg/kg/h until 6h after the start of LPS administration and in another study (Nishina et al, 1995) the rabbits received 10min after the end of infusion of endotoxin, a bolus injection followed by continuous infusion of lidocaine (2mg/kg+2mg/kg/h). Others researchers (Takao et al, 1996), used the same dosage of lidocaine, but after exposing animals to 100% oxygen. Dogs (Fletcher and Ramwell, 1978) received a continuous infusion of lidocaine (1mg/kg/h) from 45min before to 2h after an LD 60 dose of endotoxin.…”

Section: Discussionmentioning

confidence: 99%

Effects of lidocaine on lipopolysaccharide-induced synovitis in horses

Campebell¹,

Peiró

Valadão

et al. 2004

Arq. Bras. Med. Vet. Zootec.

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Lidocaine (100mg 2%) injected into the carpal joint was used to evaluate the inflammatory response induced by injection (1.5ng) of intra-articular E. coli lipopolysaccharide (LPS) endotoxin. Seventeen male Mangalarga horses aged two to three years were divided into three groups and in all animals was injected 0.9% saline (SAL) in the left carpus (LC), and in the right carpus (RC) one of the following combinations were injected: group A (n=6) LPS plus SAL; group B (n=6) LPS plus lidocaine; group C (n=5) lidocaine plus SAL. Synovial fluid and blood samples were collected immediately before the injection of LPS (T0), and at 1.5 (T1), 3 (T2), 6 (T3), 12 (T4) and 36 hours (T5) after the injection. Clinical and physical variables and cellular and biochemical characteristics of the synovial fluid were evaluated at the same time. The local and systemic inflammatory response was evaluated by measurement of mean serum and synovial fluid TNF-α concentration. A rise in TNF-α concentration in LPS injected joints at 3h in group A and from 1.5h to 3h in group B was observed. It is concluded that LPS triggered an inflammatory process and that lidocaine did not inhibit or attenuate the LPS-induced synovitis nor the synthesis and release of TNF-α.Keywords: horse, synovitis, lipopolysacharide, TNF-α, lidocaine RESUMO Injetou-se lidocaína (100mg 2%) na articulação do carpo para avaliar a resposta inflamatória induzida pela injeção (1,5ng) intra-articular de lipopolissacarídeo (LPS) de E. coli. Utilizaram-se 17 cavalos Mangalarga não castrados, entre dois e três anos, divididos em três grupos. No carpo esquerdo (CE) administrou-se solução fisiológica a 0,9% (SAL) e no carpo direito (CD) uma das seguintes combinações: grupo A (n=6) LPS mais SAL, grupo B (n=6) LPS mais lidocaína e grupo C (n=5) lidocaína mais SAL. Amostras do líquido sinovial e de sangue foram colhidas imediatamente antes da injeção de LPS (T0) e às 1,30 (T1), 3 (T2), 6 (T3), 12 (T4) e 36 horas (T5) após a injeção. Variáveis clínicas e físicas, e características bioquímicas e celulares do líquido sinovial foram avaliadas nos mesmos tempos. A resposta inflamatória local e sistêmica foi mensurada pela concentração do TNF-α no

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Section: Discussionmentioning

confidence: 99%

Effects of lidocaine on lipopolysaccharide-induced synovitis in horses

Campebell¹,

Peiró

Valadão

et al. 2004

Arq. Bras. Med. Vet. Zootec.

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“…The lung damage that develops during hyperoxia consists of lung tissue and alveolar edema (2,3,8,14,15,34), surfactant dysfunction (10,11,13,14,21), lung inflammation (2-5, 10, 11), and subsequent deterioration of the lung function (2,8,10,11,13,14,25,26,31,34,35). Studies on oxygen toxicity have primarily focused on parenchymal damage (2-5, 10, 11, 25), whereas the potential adverse effects of prolonged oxygen exposure on the airways have not been characterized.…”

mentioning

confidence: 99%

Hyperoxia-induced changes in mouse lung mechanics: forced oscillations vs. barometric plethysmography

Peták

Habre

Donati

et al. 2001

Journal of Applied Physiology

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.-Hyperoxia-induced lung damage was investigated via airway and respiratory tissue mechanics measurements with low-frequency forced oscillations (LFOT) and analysis of spontaneous breathing indexes by barometric whole body plethysmography (WBP). WBP was performed in the unrestrained awake mice kept in room air (n ϭ 12) or in 100% oxygen for 24 (n ϭ 9), 48 (n ϭ 8), or 60 (n ϭ 9) h, and the indexes, including enhanced pause (Penh) and peak inspiratory and expiratory flows, were determined. The mice were then anesthetized, paralyzed, and mechanically ventilated. Airway resistance, respiratory system resistance at breathing frequency, and tissue damping and elastance were identified from the LFOT impedance data by model fitting. The monotonous decrease in airway resistance during hyperoxia correlated best with the increasing peak expiratory flow. Respiratory system resistance and tissue damping and elastance were unchanged up to 48 h of exposure but were markedly elevated at 60 h, with associated decreases in peak inspiratory flow. Penh was increased at 24 h and sharply elevated at 60 h. These results indicate no adverse effect of hyperoxia on the airway mechanics in mice, whereas marked parenchymal damage develops by 60 h. The inconsistent relationships between LFOT parameters and WBP indexes suggest that the changes in the latter reflect alterations in the breathing pattern rather than in the mechanical properties. It is concluded that, in the presence of diffuse lung disease, Penh is inadequate for characterization of the mechanical status of the respiratory system.

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“…The ability of Lidocaine to attenuate inflammation in ALI has been recently demonstrated in rabbits with hyperoxic [45], HCl [33], as well as endotoxin-induced ALI [31], and in a rabbit model simulating pancreatitis [19]. The attenuation in lung injury in these studies was associated with a reduction in cytokines and activated complement levels, as well as decreased wet-dry lung ratio, decreased albumin in bronchial alveolar lavage fluid, and a reduction in the sequestration of neutrophils in the lungs [19,31,33,45].…”

Section: Discussionmentioning

confidence: 99%

“…Based on the expected surfactant lavage retention of ∼30%, it was estimated that a dose of 2 mg/kg of Lidocaine would be administered, similar to the initial intravenous Lidocaine dose used in previous ALI experiments [19,31,33,45].…”

Section: Lidocaine Preparationmentioning

confidence: 99%

“…We chose to combine Lidocaine with surfactant lavage. Lidocaine has shown anti-inflammatory properties when given intravenously in various rabbit models of ALI [19,31,33,45]. We theorized that the immunomodulating effects of Lidocaine would act synergistically with surfactant lavage in improving pulmonary function parameters in neonatal piglets after HCl induced ALI.…”

Section: Introductionmentioning

confidence: 99%

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Surfactant Lavage with Lidocaine Improves Pulmonary Function in Piglets after HCl-Induced Acute Lung Injury

Huang

Uyehara

Balaraman

et al. 2004

Lung

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Acute respiratory distress syndrome (ARDS) is associated with significant morbidity and mortality. The pathophysiology of ARDS includes abnormalities of surfactant function as well as pulmonary inflammation. Immunomodulating drugs, like Lidocaine, have shown some success in decreasing inflammation in ARDS. We attempted to combine surfactant lavage's ability to reverse the surfactant dysfunction, while acting as a vehicle to deliver Lidocaine. Gravity-driven surfactant (Infasurf) lavage (35 ml/kg) was administered alone or mixed with Lidocaine after severe HCl acid injury (0.3N; 3cc/kg) in neonatal piglets. Treatment groups included: control (C) (n = 5), surfactant lavage (SL) (35 ml/kg-diluted Infasurf) (n = 7) and SL mixed with Lidocaine (SL+L) (n = 7). About 26-27% of the lavage was retained (phospholipid 73-74 mg/kg; Lidocaine 1.8 mg/kg). Oxygenation progressively increased in the SL and SL+L groups over the 4-hour period (at 240 min: C = 99 ± 14; SL = 154 ± 39; SL+L = 230 ± 40 mmHg) (p < 0.05). PaCO 2 increased in all groups from 43± 0.3to 55 ± 0.7 mmHg. Only SL+L showed a reduction in PaCO 2 (at 240 min: C = 54 ± 4; SL = 53 ± 7; SL +L = 49 ± 2 mmHg) (p < 0.05). Finally, SL and SL + L had superior characteristics during the quasistatic pressure volume (PV) procedure as compared to Control (p < 0.05). In our HCl ALI model, SL improved oxygenation and quasi-static lung compliance over C. The pulmonary function effects of SL were further enhanced by the addition of Lidocaine to the surfactant suspension. Combining therapeutic agents with surfactant lavage may be an effective strategy in ALI.

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Lidocaine attenuates hyperoxic lung injury in rabbits

Cited by 85 publications

References 28 publications

Effects of lidocaine on lipopolysaccharide-induced synovitis in horses

Effects of lidocaine on lipopolysaccharide-induced synovitis in horses

Hyperoxia-induced changes in mouse lung mechanics: forced oscillations vs. barometric plethysmography

Surfactant Lavage with Lidocaine Improves Pulmonary Function in Piglets after HCl-Induced Acute Lung Injury

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