Isoflurane inhibits endothelium-mediated nitric oxide relaxing pathways in the isolated perfused rabbit lung

Oshima, Yoshiaki; Ishibe, Yuichi; Okazaki, Naoto; Satô, Tôru

doi:10.1007/bf03019235

Cited by 9 publications

(3 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, endothelium-denuded aortas from Iso group presented increases in KCl and Phe-induced contractions, suggesting endotheliumderived NO protects vascular smooth muscle cells against isoflurane effects on receptor-operated calcium channels [30,31]. Moreover, we found that isoflurane and sevoflurane did not affect ACh-induced vasodilation, which is not in accordance with previous reports [27,32].…”

Section: Discussioncontrasting

confidence: 88%

Sevoflurane and isoflurane anesthesia induce redox imbalance, but only sevoflurane impairs vascular contraction

Rocha

Borges

Rodrigues

et al. 2023

Fundamemntal Clinical Pharma

View full text Add to dashboard Cite

Volatile anesthetics may cause vascular dysfunction; however, underlying effects are unclear. The aim of the present study was to investigate whether sevoflurane and isoflurane affect vascular function, nitric oxide (NO) bioavailability, and biomarkers of oxidative stress and inflammation. Wistar rats were divided into three experimental groups: Not anesthetized (control group) or submitted to anesthesia with isoflurane (Iso group) or sevoflurane (Sevo group). Hemodynamic parameters were monitored during anesthesia, and blood gas values and biochemical determinants were analyzed. Isometric contractions were recorded in aortic rings. Vasoconstriction induced by potassium chloride (KCl) and phenylephrine (Phe) were measured. No differences in hemodynamic parameters and blood gasses variables were observed. Impaired KCl and Phe‐induced contractions were observed in endothelium‐intact aorta of Sevo compared to Iso and Control groups. Redox imbalance was found in Sevo and Iso groups. Reduced NO bioavailability and increased activity of matrix metalloproteinase 2 (MMP‐2) were observed in Sevo, but not in the Iso group. While reduced IL‐10 and IL‐1β were observed in Sevo, increases in IL‐1β in the Iso group were found. Sevoflurane, but not isoflurane, anesthesia impairs vasocontraction, and reduced NO and cytokines and increased MMP‐2 activity may be involved in vascular dysfunction after sevoflurane anesthesia.

show abstract

Section: Discussioncontrasting

confidence: 88%

Sevoflurane and isoflurane anesthesia induce redox imbalance, but only sevoflurane impairs vascular contraction

Rocha

Borges

Rodrigues

et al. 2023

Fundamemntal Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…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

101

View full text Add to dashboard Cite

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.

show abstract

“…Immediately after killing, sterilize the ventral body surface with 70% EtOH and use the rough scissor to cut the skin along the ventral midline from the chin to the pelvis. Note: Since it is known that inhalative anesthetics such as isoflurane have an impact on the vascular tone 18,19 , do not use volatile anesthetics. 2.…”

Section: Isolation Of Murine Lungs and Preparation Of Precision Cut Lmentioning

confidence: 99%

Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices

Paddenberg

Mermer

Goldenberg

et al. 2014

JoVE

View full text Add to dashboard Cite

Acute alveolar hypoxia causes pulmonary vasoconstriction (HPV) -also known as von Euler-Liljestrand mechanism -which serves to match lung perfusion to ventilation. Up to now, the underlying mechanisms are not fully understood. The major vascular segment contributing to HPV is the intra-acinar artery. This vessel section is responsible for the blood supply of an individual acinus, which is defined as the portion of lung distal to a terminal bronchiole. Intra-acinar arteries are mostly located in that part of the lung that cannot be selectively reached by a number of commonly used techniques such as measurement of the pulmonary artery pressure in isolated perfused lungs or force recordings from dissected proximal pulmonary artery segments 1,2 . The analysis of subpleural vessels by real-time confocal laser scanning luminescence microscopy is limited to vessels with up to 50 µm in diameter 3 .We provide a technique to study HPV of murine intra-pulmonary arteries in the range of 20-100 µm inner diameters. It is based on the videomorphometric analysis of cross-sectioned arteries in precision cut lung slices (PCLS). This method allows the quantitative measurement of vasoreactivity of small intra-acinar arteries with inner diameter between 20-40 µm which are located at gussets of alveolar septa next to alveolar ducts and of larger pre-acinar arteries with inner diameters between 40-100 µm which run adjacent to bronchi and bronchioles. In contrast to real-time imaging of subpleural vessels in anesthetized and ventilated mice, videomorphometric analysis of PCLS occurs under conditions free of shear stress. In our experimental model both arterial segments exhibit a monophasic HPV when exposed to medium gassed with 1% O 2 and the response fades after 30-40 min at hypoxia.

show abstract

Isoflurane inhibits endothelium-mediated nitric oxide relaxing pathways in the isolated perfused rabbit lung

Cited by 9 publications

References 22 publications

Sevoflurane and isoflurane anesthesia induce redox imbalance, but only sevoflurane impairs vascular contraction

Sevoflurane and isoflurane anesthesia induce redox imbalance, but only sevoflurane impairs vascular contraction

General Anesthetics and Vascular Smooth Muscle

Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices

Contact Info

Product

Resources

About