Opposing Effects of Isoflurane and Sevoflurane on Neurogenic Pulmonary Edema Development in an Animal Model

Kandatsu, Nobuhisa; Nan, Yongshan; Feng, Guo-Gang; Nishiwaki, Kimitoshi; Hirokawa, Mitsuru; Ishikawa, Kiyonori; Komatsu, Toshimitsu; Yokochi, Takashi; Shimada, Yasuhiro; Ishikawa, Naohisa

doi:10.1097/00000542-200506000-00018

Cited by 35 publications

(23 citation statements)

References 22 publications

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“…Effect of preventive atropine injection in rats anesthetized with 1.5% isoflurane (groups [7][8][9]. The administration of atropine 2 min before balloon inflation caused a significant BP decrease prior to spinal cord injury without affecting the HR.…”

Section: Spinal Cord Injury Under Different Degrees Of Isoflurane Anementioning

confidence: 99%

“…blood pressure; heart rate; atropine NEUROGENIC PULMONARY EDEMA (NPE) is an acute life-threatening complication following spinal cord or brain injury (4). It is characterized by marked pulmonary vascular congestion, extravasation of protein-rich edema fluid, and intra-alveolar hemorrhage (7)(8)(9)(10). Many pathophysiological mechanisms have been implicated in the development of NPE, but the exact cascade leading to its development is still unclear (9,10).…”

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confidence: 99%

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The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions

Šedý

Zicha

Kuneš

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Neurogenic pulmonary edema (NPE) is an acute life-threatening complication following an injury of the spinal cord or brain, which is associated with sympathetic hyperactivity. The role of nitric oxide (NO) in NPE development in rats subjected to balloon compression of the spinal cord has not yet been examined. We, therefore, pretreated Wistar rats with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) either acutely (just before the injury) or chronically (for 4 wk prior to the injury). Acute (but not chronic) L-NAME administration enhanced NPE severity in rats anesthetized with 1.5% isoflurane, leading to the death of 83% of the animals within 10 min after injury. Pretreatment with either the ganglionic blocker pentolinium (to reduce blood pressure rise) or the muscarinic receptor blocker atropine (to lessen heart rate decrease) prevented or attenuated NPE development in these rats. We did not observe any therapeutic effects of atropine administered 2 min after spinal cord compression. Our data indicate that NPE development is dependent upon a marked decrease of heart rate under the conditions of high blood pressure elicited by the activation of the sympathetic nervous system. These hemodynamic alterations are especially pronounced in rats subjected to acute NO synthase inhibition. In conclusion, nitric oxide has a partial protective effect on NPE development because it attenuates sympathetic vasoconstriction and consequent baroreflex-induced bradycardia following spinal cord injury.

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Section: Spinal Cord Injury Under Different Degrees Of Isoflurane Anementioning

confidence: 99%

mentioning

confidence: 99%

The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions

Šedý

Zicha

Kuneš

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The downstream effects of sympathetic overactivity vary depending on the cardiopulmonary effects [2]. Pathologically, there is marked pulmonary vascular congestion with perivascular edema, extravasation and intra-alveolar accumulation of protein rich edema fluid and intra-alveolar hemorrhage [8]. The clinical pathology overlaps with acute lung injury and acute respiratory distress syndrome [6].…”

Section: Discussionmentioning

confidence: 99%

Neurogenic Pulmonary Edema Following Status Epilepticus: An Unusual Case

et al. 2015

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Neurogenic pulmonary edema (NPE) is rare in pediatric patients. It occurs most commonly following brain malignancies, traumatic brain injuries, infections and seizures. It has rarely been reported in pediatric patients following status epilepticus. The pathophysiology is not completely understood and is proposed to be due to overactivity of sympathetic nervous system leading to pulmonary interstitial and alveolar edema. Here we present a case of a 4-year-old healthy boy with status epilepticus secondary to febrile seizures who developed NPE. Treatment is supportive ventilator management with low tidal volume and high positive end-expiratory pressure. Timely diagnosis and management is the key for good recovery. It should be considered in the differential diagnosis of patients with rapidly developing pulmonary edema in the setting of normal cardiac function.

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“…In the lungs exposed to isoflurane, immunohistochemical staining of bronchial epithelial cells for vascular endothelial growth factor demonstrated an increased expression. Sevoflurane exposition lacked such harmful effects [30 ]. The clinical implications of these findings remain to be established.…”

Section: Ventilation Strategy and Cerebro-pulmonary Interactionsmentioning

confidence: 94%

Management of physiological variables in neuroanaesthesia: maintaining homeostasis during intracranial surgery

Randell

Niskanen²

2006

Current Opinion in Anaesthesiology

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Opposing Effects of Isoflurane and Sevoflurane on Neurogenic Pulmonary Edema Development in an Animal Model

Abstract: Exposure to 1.5% isoflurane enhances the development of neurogenic pulmonary edema development in this animal model, most likely via release of vascular endothelial growth factor from bronchial epithelial cells, an effect not observed with sevoflurane.

Cited by 35 publications

References 22 publications

The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions

The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions

Neurogenic Pulmonary Edema Following Status Epilepticus: An Unusual Case

Management of physiological variables in neuroanaesthesia: maintaining homeostasis during intracranial surgery

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