Paravertebral dexmedetomidine as an adjuvant to ropivacaine protects against independent lung injury during one-lung ventilation: a preliminary randomized clinical trial

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Abstract

Background

To investigate the effect of paravertebral dexmedetomidine as an adjuvant to ropivacaine on independent lung injury during one-lung ventilation.

Methods

In total, 120 patients who underwent elective radical resection of pulmonary carcinoma were randomly assigned to one of six groups ( n = 20): normal saline (C group), ropivacaine (R group), intravenous dexmedetomidine (Div group), 0.5 μg/kg paravertebral dexmedetomidine as an adjuvant to ropivacaine (RD0.5 group), 1.0 μg/kg paravertebral dexmedetomidine as an adjuvant to ropivacaine (RD1.0 group), or 2.0 μg/kg paravertebral dexmedetomidine as an adjuvant to ropivacaine (RD2.0 group).

Patients in the R, Div, RD0.5, RD1.0 and RD2.0 groups underwent a thoracic paravertebral block, and normal saline was administered as a control to C group. Small marginal lung samples next to the tumor were harvested immediately after the tumor tissues were excised.

Lung injury was evaluated as follows: an injury score was determined via light microscopy, and cell apoptosis was determined via a TUNEL assay. TNF-α, IL-6, miRNA-210, HIF-1α, Tom20 and ISCU2 were also detected.

Results

Both intravenous and paravertebral dexmedetomidine attenuated independent lung injury. Downregulation of HIF-1α and miRNA-210 and upregulation of Tom20 and ISCU2 may be the underlying mechanism. No difference was observed between the Div and RD0.5 groups, and no further improvement of lung injury was found in the RD1.0 and RD2.0 groups with increased paravertebral dexmedetomidine doses.

Conclusions

Paravertebral dexmedetomidine as an adjuvant to ropivacaine, which is comparable to intravenous dexmedetomidine, could protect against independent lung injury during one-lung ventilation.

Trial registration

ISRCTN, 13000406; retrospectively registered on 22.05.2018.

Related collections

Most cited references 23

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Lung Injury After One-Lung Ventilation: A Review of the Pathophysiologic Mechanisms Affecting the Ventilated and the Collapsed Lung.

Jens Lohser, Peter Slinger (2015)

Lung injury is the leading cause of death after thoracic surgery. Initially recognized after pneumonectomy, it has since been described after any period of 1-lung ventilation (OLV), even in the absence of lung resection. Overhydration and high tidal volumes were thought to be responsible at various points; however, it is now recognized that the pathophysiology is more complex and multifactorial. All causative mechanisms known to trigger ventilator-induced lung injury have been described in the OLV setting. The ventilated lung is exposed to high strain secondary to large, nonphysiologic tidal volumes and loss of the normal functional residual capacity. In addition, the ventilated lung experiences oxidative stress, as well as capillary shear stress because of hyperperfusion. Surgical manipulation and/or resection of the collapsed lung may induce lung injury. Re-expansion of the collapsed lung at the conclusion of OLV invariably induces duration-dependent, ischemia-reperfusion injury. Inflammatory cytokines are released in response to localized injury and may promote local and contralateral lung injury. Protective ventilation and volatile anesthesia lessen the degree of injury; however, increases in biochemical and histologic markers of lung injury appear unavoidable. The endothelial glycocalyx may represent a common pathway for lung injury creation during OLV, because it is damaged by most of the recognized lung injurious mechanisms. Experimental therapies to stabilize the endothelial glycocalyx may afford the ability to reduce lung injury in the future. In the interim, protective ventilation with tidal volumes of 4 to 5 mL/kg predicted body weight, positive end-expiratory pressure of 5 to 10 cm H2O, and routine lung recruitment should be used during OLV in an attempt to minimize harmful lung stress and strain. Additional strategies to reduce lung injury include routine volatile anesthesia and efforts to minimize OLV duration and hyperoxia.

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MicroRNA-210 Regulates Mitochondrial Free Radical Response to Hypoxia and Krebs Cycle in Cancer Cells by Targeting Iron Sulfur Cluster Protein ISCU

Elena Favaro, Anassuya Ramachandran, Robert L. McCormick … (2010)

Background Hypoxia in cancers results in the upregulation of hypoxia inducible factor 1 (HIF-1) and a microRNA, hsa-miR-210 (miR-210) which is associated with a poor prognosis. Methods and Findings In human cancer cell lines and tumours, we found that miR-210 targets the mitochondrial iron sulfur scaffold protein ISCU, required for assembly of iron-sulfur clusters, cofactors for key enzymes involved in the Krebs cycle, electron transport, and iron metabolism. Down regulation of ISCU was the major cause of induction of reactive oxygen species (ROS) in hypoxia. ISCU suppression reduced mitochondrial complex 1 activity and aconitase activity, caused a shift to glycolysis in normoxia and enhanced cell survival. Cancers with low ISCU had a worse prognosis. Conclusions Induction of these major hallmarks of cancer show that a single microRNA, miR-210, mediates a new mechanism of adaptation to hypoxia, by regulating mitochondrial function via iron-sulfur cluster metabolism and free radical generation.

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Operative mortality and respiratory complications after lung resection for cancer: impact of chronic obstructive pulmonary disease and time trends.

Marc Licker, Igor Widikker, John Robert … (2006)

Smoking is a common risk factor for chronic obstructive pulmonary disease (COPD), cardiovascular disease, and lung cancer. In this observational study, we examined the impact of COPD severity and time-related changes in early outcome after lung cancer resection. Over a 15-year period, we analyzed an institutional registry including all consecutive patients undergoing surgery for lung cancer. Using the receiver-operating characteristic (ROC) curve, we analyzed the relationship between forced expiratory volume in 1 second (FEV1) and postoperative mortality and respiratory morbidity. Multiple regression analysis has also been applied to identify other risk factors. A preoperative FEV1 less than 60% was a strong predictor for respiratory complications (odds ratio [OR] = 2.7, confidence interval [CI]: 1.3 to 6.6) and 30-day mortality (OR = 1.9, CI: 1.2 to 3.9), whereas thoracic epidural analgesia was associated with lower mortality (OR = 0.4; CI: 0.2 to 0.8) and respiratory complications (OR = 0.6; CI: 0.3 to 0.9). Mortality was also related to age greater than 70 years, the presence of at least three cardiovascular risk factors, and pneumonectomy. From the period 1990 to 1994, to 2000 to 2004, we observed significant reductions in perioperative mortality (3.7% versus 2.4%) and in the incidence of respiratory complications (18.7% versus 15.2%), that was associated with a higher rate of lesser resection (from 11% to 17%, p < 0.05) and increasing use of thoracic epidural analgesia (from 65% to 88%, p < 0.05). Preoperative FEV1 less than 60% is a main predictor of perioperative mortality and respiratory morbidity. Over the last 5-year period, diagnosis of earlier pathologic cancer stages resulting in lesser pulmonary resection as well as provision of continuous thoracic epidural analgesia have contributed to improved surgical outcome.

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Author and article information

Contributors

Wei Zhang: myhope2005@163.com

Shanfeng Zhang: zsf@zzu.edu.cn

Bing Li: 540026341@qq.com

Mingyang Sun: mingyangsun1986@163.com

Jiaqiang Zhang:

ORCID: http://orcid.org/0000-0002-4329-784X

457106786@qq.com

Journal

Journal ID (nlm-ta): BMC Anesthesiol

Journal ID (iso-abbrev): BMC Anesthesiol

Title: BMC Anesthesiology

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2253

Publication date (Electronic): 15 June 2018

Publication date PMC-release: 15 June 2018

Publication date Collection: 2018

Volume: 18

Electronic Location Identifier: 67

Affiliations

[1 ]GRID grid.414011.1, Department of Anesthesiology, , Henan Provincial People’s Hospital, ; No. 7, Weiwu Road, Zhengzhou City, Henan Province China

[2 ]ISNI 0000 0001 2189 3846, GRID grid.207374.5, Department of Biochemistry and Molecular Biology, , The Academy of Medical Science, Zhengzhou University, ; No. 100, Science Avenue, Zhengzhou City, Henan Province China

Author information

Jiaqiang Zhang http://orcid.org/0000-0002-4329-784X

Article

Publisher ID: 532

DOI: 10.1186/s12871-018-0532-6

PMC ID: 6003137

PubMed ID: 29907082

SO-VID: d76e26b0-c1f0-48eb-845b-c82dfecbd69b

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 12 April 2018

Date accepted : 28 May 2018

Funding

Funded by: The Natural Science Foundation of China

Award ID: 81771149

Funded by: Science and Technology Project of Henan Province

Award ID: 182102310167

Funded by: Medical Science Research Project of Henan Province

Award ID: 201602227

Custom metadata

ScienceOpen disciplines: Anesthesiology & Pain management

Keywords: paravertebral,dexmedetomidine,lung injury,one-lung ventilation

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ScienceOpen disciplines: Anesthesiology & Pain management

Keywords: paravertebral, dexmedetomidine, lung injury, one-lung ventilation

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Paravertebral dexmedetomidine as an adjuvant to ropivacaine protects against independent lung injury during one-lung ventilation: a preliminary randomized clinical trial

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Abstract

Background

Methods

Results

Conclusions

Trial registration

Related collections

Inflamed lung in vitro co-culture models

Most cited references 23

Lung Injury After One-Lung Ventilation: A Review of the Pathophysiologic Mechanisms Affecting the Ventilated and the Collapsed Lung.

MicroRNA-210 Regulates Mitochondrial Free Radical Response to Hypoxia and Krebs Cycle in Cancer Cells by Targeting Iron Sulfur Cluster Protein ISCU

Operative mortality and respiratory complications after lung resection for cancer: impact of chronic obstructive pulmonary disease and time trends.

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