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

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Abstract

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 PaO ₂ 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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Use of dexmedetomidine as a sedative and analgesic agent in critically ill adult patients: a meta-analysis.

Jen A. Tan, Kwok M Ho (2010)

To assess the effects of using dexmedetomidine as a sedative and analgesic agent on length of intensive care unit (ICU) stay, duration of mechanical ventilation, risk of bradycardia, and hypotension in critically ill adult patients. Two researchers searched MEDLINE, EMBASE, and the Cochrane controlled trial register independently for randomized controlled trials comparing dexmedetomidine with a placebo or an alternative sedative agent, without any language restrictions. A total of 2,419 critically ill patients from 24 trials were subject to meta-analysis. Dexmedetomidine was associated with a significant reduction in length of ICU stay [weighted mean difference -0.48 days, 95% confidence interval (CI) -0.18 to -0.78 days, P = 0.002], but not duration of mechanical ventilation, when compared with an alternative sedative agent. There was, however, significant heterogeneity in these two outcomes between the pooled studies. Dexmedetomidine was associated with increased risk of bradycardia requiring interventions in studies that used both a loading dose and maintenance doses >0.7 microg kg(-1) h(-1) [relative risk (RR) 7.30, 95% CI 1.73-30.81, P = 0.007]. Risks of hypotension requiring interventions (RR 1.43, 95% CI 0.78-2.6, P = 0.25), delirium (RR 0.79, 95% CI 0.56-1.11, P = 0.18), self-extubation, myocardial infarction, hyperglycemia, atrial fibrillation, and mortality were not significantly different between dexmedetomidine and traditional sedative and analgesic agents. Significant heterogeneity existed between the pooled studies. The limited evidence suggested that dexmedetomidine might reduce length of ICU stay in some critically ill patients, but the risk of bradycardia was significantly higher when both a loading dose and high maintenance doses (>0.7 microg kg(-1) h(-1)) were used.

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W Karzai, Konrad Schwarzkopf (2009)

When switching from two-lung to one-lung ventilation (OLV), shunt fraction increases, oxygenation is impaired, and hypoxemia may occur. Hypoxemia during OLV may be predicted from measurements of lung function, distribution of perfusion between the lungs, whether the right or the left lung is ventilated, and whether the operation will be performed in the supine or in the lateral decubitus position. Hypoxemia during OLV may be prevented by applying a ventilation strategy that avoids alveolar collapse while minimally impairing perfusion of the dependent lung. Choice of anesthesia does not influence oxygenation during clinical OLV. Hypoxemia during OLV may be treated symptomatically by increasing inspired fraction of oxygen, by ventilating, or by using continuous positive airway pressure in the nonventilated lung. Hypoxemia during OLV may be treated causally by correcting the position of the double-lumen tube, clearing the main bronchi of the ventilated lung from secretions, and improving the ventilation strategy.

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Rho-kinase mediates hypoxia-induced downregulation of endothelial nitric oxide synthase.

Masao Takemoto, Jianxin Sun, Junko Hiroki … (2002)

Hypoxia-induced pulmonary hypertension is a major cause of morbidity and mortality. Hypoxia induces pulmonary vasoconstriction, in part, by decreasing endothelial nitric oxide synthase (eNOS) expression. The mechanism by which hypoxia decreases eNOS expression is not known but may involve Rho-kinase-induced actin cytoskeletal changes in vascular endothelial cells. To determine whether hypoxia regulates eNOS expression through Rho-kinase, we exposed human saphenous and pulmonary artery endothelial cells to hypoxia (3% O2) with and without a Rho-kinase inhibitor, hydroxyfasudil (0.1 to 100 micromol/L), for various durations (0 to 48 hours). Hypoxia increased Rho-kinase expression and activity by 50% and 74%, decreased eNOS mRNA and protein expression by 66+/-3% and 57+/-5%, and inhibited eNOS activity by 48+/-9%. All of these effects of hypoxia on eNOS were reversed by cotreatment with hydroxyfasudil. Furthermore, inhibition of Rho by Clostridium botulinum C3 transferase or Rho-kinase by overexpression of dominant-negative Rho-kinase reversed hypoxia-induced decrease in eNOS expression. Indeed, disruption of the actin cytoskeleton, the downstream target of Rho-kinase, by cytochalasin D also upregulated eNOS expression. Hypoxia reduced eNOS mRNA half-life from 22+/-2 to 13+/-2 hours, which was reversed by cotreatment with hydroxyfasudil. However, neither hypoxia nor hydroxyfasudil had any effects on eNOS gene transcription. These results indicate that hypoxia-induced decrease in eNOS expression is mediated by Rho-kinase and suggest that Rho-kinase inhibitors may have therapeutic benefits in patients with hypoxia-induced pulmonary hypertension.

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Author and article information

Journal

Journal ID (nlm-ta): Mediators Inflamm

Journal ID (iso-abbrev): Mediators Inflamm

Journal ID (publisher-id): MI

Title: Mediators of Inflammation

Publisher: Hindawi Publishing Corporation

ISSN (Print): 0962-9351

ISSN (Electronic): 1466-1861

Publication date (Print): 2015

Publication date (Electronic): 26 July 2015

Volume: 2015

Electronic Location Identifier: 238041

Affiliations

¹Department of Anesthesiology, First Affiliated Hospital, Yangtze University, Jingzhou 434000, China

²Department of Anesthesiology, Wuhan University Renmin Hospital, Wuhan 430060, China

³Department of Cardiothoracic Surgery, Fifth Affiliated Hospital of Zunyi Medical College, Zhuhai 519100, China

⁴Department of Anesthesiology, The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China

⁵Department of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong 524001, China

⁶Department of Anesthesiology, The University of Hong Kong, Hong Kong

⁷Department of Anesthesiology, Guangdong No. 2 Provincial People's Hospital, Guangdong Provincial Emergency Hospital, Guangzhou, Guangdong 510317, China

Author notes

*Zhengyuan Xia: zhengyuan_xia@ 123456yahoo.com and

*Xiaoshan Xiao: gd177mzk@ 123456163.com

Academic Editor: Huang-Ping Yu

Article

DOI: 10.1155/2015/238041

PMC ID: 4529970

PubMed ID: 26273134

SO-VID: e35d8a08-5b6c-4abb-88ed-2e9f0d2d95e0

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 7 January 2015

Date accepted : 13 February 2015

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