Sevoflurane reduces endothelium-dependent vasorelaxation: role of Superoxide anion and endothelin

Arriero, Maria; Alameda, L. Muñoz; López‐Farré, Antonio; Burgos, M.; Carrasco, Carolina; Millás, Inmaculada; Celdrán, Ángel; Pinta, J.C. de la

doi:10.1007/bf03017923

Cited by 15 publications

(5 citation statements)

References 28 publications

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“…In the current study, Dex significantly increased serum NO concentration, concomitant with decreased shunt fraction and increased PaO2, which indicates that Dex may have induced vasodilation in the ventilated lung by enhancing NO release. In the current study isoflurane did not inhibit NO activation after OLV, while studies found that volatile anesthetics inhibit the NO-mediated relaxation in many vascular beds [ 39 , 40 ], which may partly explain why volatile anesthetics inhibit HPV.…”

Section: Discussioncontrasting

confidence: 48%

Intravenous Infusion of Dexmedetomidine Combined Isoflurane Inhalation Reduces Oxidative Stress and Potentiates Hypoxia Pulmonary Vasoconstriction during One-Lung Ventilation in Patients

Xia

Yin

et al. 2015

Mediators of Inflammation

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Inhalation anesthetic isoflurane inhibits hypoxia pulmonary vasoconstriction (HPV), while dexmedetomidine (Dex) could reduce the dose of isoflurane inhalation and potentiate HPV, but the mechanism is unclear. Inhibition of reactive oxygen species (ROS) production can favor HPV during one-lung ventilation (OLV). Similarly, nitric oxide (NO), an important endothelium-derived vasodilator in lung circulation, can decrease the regional pulmonary vascular resistance of ventilated lung and reduce intrapulmonary shunting. We hypothesized that Dex may augment HPV and improve oxygenation during OLV through inhibiting oxidative stress and increasing NO release. Patients undergoing OLV during elective thoracic surgery were randomly allocated to either isoflurane + saline (NISO, n = 24) or isoflurane + dexmedetomidine (DISO, n = 25) group. Anesthesia was maintained with intravenous remifentanil and inhalational isoflurane (1.0–2.0%), with concomitant infusion of dexmedetomidine 0.7 μgkg−1h−1 in DISO and saline 0.25 mL kg−1h−1 in NISO group. Hemodynamic variables or depth of anesthesia did not significantly differ between groups. Administration of Dex significantly reduced Qs/Qt and increased PaO2 after OLV, accompanied with reduced lipid peroxidation product malondialdehyde and higher levels of SOD activity as well as serum NO (all P < 0.05 DISO versus NISO). In conclusion, reducing oxidative stress and increasing NO release during OLV may represent a mechanism whereby Dex potentiates HPV.

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Section: Discussioncontrasting

confidence: 48%

Intravenous Infusion of Dexmedetomidine Combined Isoflurane Inhalation Reduces Oxidative Stress and Potentiates Hypoxia Pulmonary Vasoconstriction during One-Lung Ventilation in Patients

Xia

Yin

et al. 2015

Mediators of Inflammation

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“…In most previous studies, halothane, 156,178 -183 enflurane, 160,178 isoflurane, 133,160,178,184 desflurane, 177 sevoflurane, 135,160,163,180,185,186 thiopental, 187 ketamine, 188 propofol, 189 -191 and etomidate 188,[192][193][194] inhibited endothelium-dependent, presumed nitric oxidemediated vasodilator responses (table 2). However, most of those anesthetics did not inhibit the endotheliumindependent vasodilator response to nitrovasodilators (table 2) and the associated increases in cGMP level in VSMCs.…”

Section: Anesthetic Effects On Vasodilator Responsementioning

confidence: 87%

General Anesthetics and Vascular Smooth Muscle

Akata

2007

Anesthesiology

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General anesthetics threaten cardiovascular stability by causing changes in cardiac function, vascular reactivity, and cardiovascular reflexes and significantly alter distribution of cardiac output to various organs. Their overall impact is often systemic hypotension, which is attributable to myocardial depression, peripheral vasodilation, and attenuated sympathetic nervous system activity. However, one could be more causative than the others, depending on anesthetic agents and cardiovascular factors inherent in patients (e.g., coexisting heart disease). It is generally believed that most general anesthetics attenuate sympathetic nervous system outflow from the central nervous system, thereby decreasing vascular resistance in peripheral circulations. Indeed, in previous in vivo studies, during administration of various general anesthetics, vascular resistance was decreased in most peripheral circulations; however, it was unaffected or increased in some peripheral circulations. General anesthetics may act directly on vascular smooth muscle and/or endothelial cells in various vascular beds, influencing total peripheral and/or regional vascular resistance, and hence organ blood flow. This article reviews previously reported direct (i.e., nonneural) vascular actions of general anesthetics and discusses their underlying mechanisms, their in vivo relevance, and the future of research for general anesthetic vascular pharmacology.

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“…Sevoflurane inhibits the pathway leading from acetylcholine signalling to the transduction of NO from the endothelium to smooth muscle cells. 19 Our results indicate that sevoflurane may attenuate the activity of endothelial NO synthase. The expressions of HO-1, 2 were not elevated after sevoflurane anaesthesia in this study, indicating that CO was not involved in the vasodilatory mechanisms of sevoflurane.…”

Section: Discussionmentioning

confidence: 56%

Expression of pulmonary vasoactive factors after sevoflurane anaesthesia in rats: a quantitative real-time polymerase chain reaction study

Takemori

Kobayashi

Sakamoto

2008

British Journal of Anaesthesia

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Sevoflurane reduces endothelium-dependent vasorelaxation: role of Superoxide anion and endothelin

Cited by 15 publications

References 28 publications

Intravenous Infusion of Dexmedetomidine Combined Isoflurane Inhalation Reduces Oxidative Stress and Potentiates Hypoxia Pulmonary Vasoconstriction during One-Lung Ventilation in Patients

Intravenous Infusion of Dexmedetomidine Combined Isoflurane Inhalation Reduces Oxidative Stress and Potentiates Hypoxia Pulmonary Vasoconstriction during One-Lung Ventilation in Patients

General Anesthetics and Vascular Smooth Muscle

Expression of pulmonary vasoactive factors after sevoflurane anaesthesia in rats: a quantitative real-time polymerase chain reaction study

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