Factors Regulating Isoprostane Formation <i>In Vivo</i>

Basu, Samar; Helmersson, Johanna

doi:10.1089/ars.2005.7.221

Cited by 109 publications

(102 citation statements)

References 129 publications

(170 reference statements)

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“…These studies support the concept that isoprostanes not only increase in models of ischemia-reperfusion but may also play a role in the pathophysiological sequelae of this injury [178].…”

Section: Cerebral Oxidative Nitrosative Inflammatory and Neurologicsupporting

confidence: 82%

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Miclescu¹

2010

Acta Anaesthesiol Scand

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Although survival rates are increasing, brain injury continues to be a leading cause of death after cardiac arrest (CA). Permanent brain damage after CA is determined by limited tolerance to ischemia from CA and cardiopulmonary resuscitation (CPR), as well as the unique cerebral response to reperfusion after return of spontaneous circulation (ROSC). A major pathway leading to neurotoxic cascade and neuronal injury after CA involves the increased presence of reactive oxygen and nitrogen species generated during ischemia and reperfusion. The magnitude of cerebral oxidative injury induced by free radicals increased with the duration of CA (Paper I). Nitric oxide (NO), a free radical responsible for the formation of reactive nitrogen species, is increased during global ischemia from CA and reperfusion (Paper IV). Hypothetically, the administration of a drug that counteracts the overproduction of NO and also acts as a scavenger of oxygen free radicals might be warranted in order to reduce the damage caused by nitrosative and oxidative stress. For these purposes we used methylene blue (MB), an old dye that has been used in medicine for almost half a century, and an experimental pig model of 20 min of ventricular fibrillation (VF) to reflect a clinical scenario of ischemia/reperfusion injury. Administration of MB added to a hypertonic-hyperoncotic solution (MBHSD) that was started during CPR and continued for 50 min after ROSC increased short-term survival by decreasing myocardial damage, as well as cerebral peroxidation and inflammatory injury (Paper II). Immunostaining of cerebral tissue collected at different time points after CA and ROSC (Paper IV) provided experimental evidence that cortical blood-brain barrier (BBB) disruption begins as early as during the initial phase of untreated as well as treated CA. The results indicated that MB administration reduced the neurologic injury and BBB disruption considerably, but did not reverse the ongoing detrimental processes. The demonstrated positive effects of MB were related to a decrease of nitrite/nitrate tissue content, and thus to a decrease of excess NO due to the MB inhibitory effects on NOS isoforms. A mixture of MB in hypertonic sodium lactate (MBL) was investigated to facilitate administration of MB in "the field." Based on findings that MBL cardio-and neuroprotective properties were similar to those of MBHSD, there is reason to believe that the use of MBL might be extended during ongoing CPR and after ROSC (Paper III). It would therefore make sense to try using MB as a pharmacological neuroprotectant during or after clinical CPR in order to expand the temporal therapeutic window before other measures for neuroprotection such as hypothermia are available. Keywords: Cardiac arrest, cardiopulmonary resuscitation, reperfusion injury, methylene blue, nitric oxide, nitric oxide synthases, blood-brain barrier

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“…These studies support the concept that isoprostanes not only increase in models of ischemia-reperfusion but may also play a role in the pathophysiological sequelae of this injury [178].…”

Section: Cerebral Oxidative Nitrosative Inflammatory and Neurologicsupporting

confidence: 82%

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Miclescu¹

2010

Acta Anaesthesiol Scand

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“…[113][114][115][116][117] Plasma levels as well as exhaled breath condensate were significantly higher when measured in the morning (i.e., after sleep) in patients with OSA compared to age-and weight-matched healthy obese subjects, while evening levels of 8-Isoprostanes were similar in both groups. 118 The positive correlation between morning levels of 8-isoprostane and AHI suggested an association between OSA and increased systemic and local levels of oxidative stress.…”

Section: Oxidative Stressmentioning

confidence: 95%

Obstructive Sleep Apnea and Kidney Disease: A Potential Bidirectional Relationship?

Abuyassin

Sharma

Ayas

et al. 2015

Journal of Clinical Sleep Medicine

114

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“…Reports have shown that F 2 -IsoPs are authentic, reliable biomarkers of lipid peroxidation and are useful in vivo indicators of oxidative stress in various clinical conditions, such as acute and chronic inflammation, ischemia/reperfusion injury, diabetes, and atherosclerosis (7,23,24,(63)(64)(65)(66)(67)(68). F 2 -IsoPs have also been used to assess in vivo oxidative response to various drugs, antioxidants, or dietary interventions for their free-radical-scavenging properties (7,23,24,(63)(64)(65)(66)(67)(68). Different methods for F 2 -IsoP quantification are available (23,68,69 ).…”

Section: Isoprostanesmentioning

confidence: 99%

Biomarkers of Oxidative Damage in Human Disease

et al. 2006

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Oxidative/nitrosative stress, a pervasive condition of increased amounts of reactive oxygen/nitrogen species, is now recognized to be a prominent feature of many acute and chronic diseases and even of the normal aging process. However, definitive evidence for this association has often been lacking because of recognized shortcomings with biomarkers and/or methods available to assess oxidative stress status in humans. Emphasis is now being placed on biomarkers of oxidative stress, which are objectively measured and evaluated as indicators of normal biological processes, pathogenic processes, or pharmacologic responses to therapeutic intervention. To be a predictor of disease, a biomarker must be validated. Validation criteria include intrinsic qualities such as specificity, sensitivity, degree of inter-and intraindividual variability, and knowledge of the confounding and modifying factors. In addition, characteristics of the sampling and analytical procedures are of relevance, including constraints and noninvasiveness of sampling, stability of potential biomarkers, and the simplicity, sensitivity, specificity, and speed of the analytical method. Here we discuss some of the more commonly used biomarkers of oxidative/nitrosative damage and include selected examples of human studies.

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Factors Regulating Isoprostane Formation In Vivo

Cited by 109 publications

References 129 publications

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Obstructive Sleep Apnea and Kidney Disease: A Potential Bidirectional Relationship?

Biomarkers of Oxidative Damage in Human Disease

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