A Reductive Metabolic Switch Protects Infants with Transposition of Great Arteries Undergoing Atrial Septostomy against Oxidative Stress

Transposition of the great arteries (TGA) is one of the most common cyanotic congenital heart diseases requiring neonatal surgical intervention. Parallel circulations that result in impaired cerebral oxygen delivery already in utero may lead to brain damage and long-term neurodevelopmental delay. Balloon atrial septostomy (BAS) is often employed to mix deoxygenated and oxygenated blood at the atrial level. However, BAS causes a sudden increase in arterial blood oxygenation and oxidative stress. We studied changes in oxygen saturation as well as metabolic profiles of plasma samples from nine newborn infants suffering from TGA before and until 48 h after undergoing BAS. The plasma metabolome clearly changed over time and alterations of four metabolic pathways, including the pentose phosphate pathway, were linked to changes in the cerebral tissue oxygen extraction. In contrast, no changes in levels of lipid peroxidation biomarkers over time were observed. These observations suggest that metabolic adaptations buffer the free radical burst triggered by re-oxygenation, thereby avoiding structural damage at the macromolecular level. This study enhances our understanding of the complex response of infants with TGA to changes in oxygenation induced by BAS.

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Importance of Cardiac Murmur in Diagnosing Congenital Heart Disease in Neonatal Period

Bangladesh Journal of Child Health ◽

10.3329/bjch.v32i1.6008 ◽

1970 ◽

Vol 32 (1) ◽

pp. 17-20

Author(s):

Md Mahbubul Hoque ◽

Jotsna Ara Begum ◽

Rawshan Jahan ◽

MAK Azad Chowdhury ◽

Manzoor Hussain

Keyword(s):

Heart Disease ◽

Congenital Heart ◽

Septal Defect ◽

Heart Diseases ◽

Gas Analysis ◽

Heart Murmur ◽

Cardiac Murmur ◽

Transposition Of Great Arteries ◽

Arterial Blood ◽

Careful Clinical Examination

Introduction: Congenital heart diseases (CHD) are serious problem of perinatology, occur in 8/1000 live birth. Approximately one third of these neonates require intervention in the first month of life. Clinical features of CHD vary according to type of lesion. Presence or absence of a murmur does not assure either the presence or absence of significant CHD. This study was conducted to determine the clinical and echocardiographic evaluation of neonate with heart murmur and contribution of neonatal examination especially presence or absence of cardiac murmur in the detection of CHD. Method: The study was carried out in Special Care Baby Unit of Dhaka Shishu Hospital during the period from January 2004 to December 2004. Neonates having heart murmur or when there were some clues to doubt CHD like cyanosis, respiratory distress, heart failure, persistent low partial pressure of oxygen(PaO2) in arterial blood gas analysis were underwent echocardiography. CHD were classified according to the structural defect with the echocardiographic findings. Results: Total 812 neonates were admitted during one year period. Heart murmurs were found in 33 cases. Out of 33 cases 15 (45.45%) had CHD confirmed by echocardiography. Another 7 neonates were found to have CHD without murmur after echocardiography. In total 22 (2.7%) neonates had CHD. Pattern of CHD were Ventricular Septal Defect (VSD), Atrial Septal Defect (ASD), Transposition of Great Arteries (TGA), Tetralogy of Fallot (TOF) and Complex cyanotic heart disease. Conclusion: Infant with CHD may present with or without murmur. Careful clinical examination is mandatory in the initial evaluation of neonates to identify CHD. The infant having suggestive features for CHD with or without murmur should undergone echocardiography, so that appropriate intervention and counseling can be done. Key words: neonates; murmur; CHD. DOI: 10.3329/bjch.v32i1.6008 Bangladesh Journal of Child Health 2008; Vol.32(1): 17-20

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The Effects of Vibroacoustically Induced Microvibrations on Arterial Blood Pressure and Oxidative Stress in Rats

Serbian Journal of Experimental and Clinical Research ◽

10.2478/sjecr-2014-0011 ◽

2014 ◽

Vol 15 (2) ◽

pp. 83-88

Author(s):

Dusko Kornjaca ◽

Vladimir Zivkovic ◽

Nevena Barudzic ◽

Vladimir Jakovljevic ◽

Dragan Djuric

Keyword(s):

Oxidative Stress ◽

Arterial Pressure ◽

Systolic Arterial Pressure ◽

Control Group ◽

Oxidative Stress Markers ◽

Sound Waves ◽

Initial Value ◽

The Third ◽

Stress Markers ◽

Arterial Blood

ABSTRACT Vibroacoustics, a scientific field that has been intensively studied for the last thirty years, uses the properties of sound waves (infrasound, ultrasound, noise and music) to induce vibrations that, like a sound wave, may have both useful and harmful effects. Th e aim of this study was to examine the effects of vibroacoustically induced microvibrations on arterial blood pressure and markers of oxidative stress in the blood. Th e experiments were performed on Wistar male rats that had a 180-200 g body mass and were divided into control and experimental groups (6 rats in each). In the experimental group, microvibrations were induced using the Vitafon vibroacoustic apparatus (Vitafon, St. Petersburg, Russian Federation), which delivers sound waves of varying frequencies by a process called “phoning”. Up to 60 minutes of phoning time was delivered to the kidney and liver using 4 diff erent regimens that included a 5-minute stabilisation time; up to four 10-minute phoning regimens, with 5-minute breaks between each single regimen, at a 30 Hz-18000 kHz frequency range;, and 2.8 μm-12.3 μm microwave amplitudes. After the completion of a phoning regimen, animals were sacrificed and the oxidative stress markers were measured in blood samples (O2-, H2O2, nitrites, lipid peroxidation index, superoxide dismutase, catalase, and glutathione) and compared with the values of markers in the control group. Systolic arterial pressure was analysed after the acute application of up to four diff erent regimens of vibroacoustic microvibrations. Systolic arterial pressure decreased significantly during the administration of the second regimen in comparison to the control group. Systolic arterial pressure returned, almost completely, to the initial value after the administration of the third and fourth regimens. Th ere was no significant change in diastolic arterial pressure after the acute administration of up to four different regimens, although the pressure decreased slightly after the first and second regimens and returned to the initial value during the administration of the third and fourth regimens. Analysis of oxidative stress markers showed a statistically significant change in the catalase level. No statistically significant differences were found in the other oxidative stress markers analyzeanalysed. Further research is needed to clarify the physiological effects of low compared to high frequencies of vibroacoustically induced microvibrations and their possible therapeutic significance.

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Functional linkage as a direction for studies in oxidative stress: α-adrenergic receptorsThis review is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y10-013 ◽

2010 ◽

Vol 88 (3) ◽

pp. 220-232 ◽

Cited By ~ 12

Author(s):

Natalia Ziolkowski ◽

Ashok K. Grover

Keyword(s):

Oxidative Stress ◽

Protein Kinase ◽

Arterial Blood Flow ◽

Arterial Blood ◽

Functional Linkage ◽

Protein Kinase C Activity ◽

Downstream Effects ◽

Fine Regulation ◽

Health And Disease ◽

G Protein Coupled

The α-adrenergic receptors (adrenoceptors) are activated by the endogenous agonists epinephrine and norepinephrine. They are G protein-coupled receptors that may be broadly classified into α1 (subclasses α1A, α1B, α1D) and α2 (subclasses α2A, α2B, α2C). The α1-adrenoceptors act by binding to Gαq subunits of the G proteins, causing activation of phospholipase C (PLC). PLC converts phosphatidylinositol 4,5-bisphosphate into inositol trisphosphate (IP3) and diacylglycerol (DAG), which have downstream effects on cytosolic Ca2+ concentration. The α2-adrenoceptors bind to Gαi thus inhibiting adenylyl cyclase and decreasing cAMP levels. DAG alters protein kinase C activity and cAMP activates protein kinase A. The downstream pathways of the two receptors may also interact. Activation of α1- and α2-adrenoceptors in vascular smooth muscle results in vasoconstriction. However, the densities of individual receptor subclasses vary between vessel beds or between vessels of various sizes within the same bed. In vasculature, the densities of adrenoceptor subclasses differ between conduit arteries and arterioles. These differences, along with differences in coupling mechanisms, allow for fine regulation of arterial blood flow. This diversity is enhanced by interactions resulting from homo- and heterodimer formation of the receptors, metabolic pathways, and kinases. Reactive oxygen species generated in pathologies may alter α1- and α2-adrenoceptor cascades, change vascular contractility, or cause remodeling of blood vessels. This review emphasizes the need for understanding the functional linkage between α-adrenoceptor subtypes, coupling, cross talk, and oxidative stress in cardiovascular pathologies.

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Oxidative stress in patients on mechanical ventilation

Medicinski pregled ◽

10.2298/mpns0912578m ◽

2009 ◽

Vol 62 (11-12) ◽

pp. 578-581

Author(s):

Vesna Marjanovic ◽

Vidosava Djordjevic ◽

Goran Marjanovic

Keyword(s):

Oxidative Stress ◽

Mechanical Ventilation ◽

Head Injuries ◽

Lipid Peroxide ◽

Thiobarbituric Acid ◽

Lactic Dehydrogenase ◽

Lung Damage ◽

Thiobarbituric Acid Reactive Substances ◽

Acid Base Balance ◽

Arterial Blood

Introduction. The appearance and intensity of oxidative stress were analyzed in the course of mechanical ventilation and parameters that could point toward potential lung damage. Material and methods. In three time intervals on day 1, 3 and 7 of mechanical ventilation, parameters such as: triglycerides, cholesterol, lactate, serum lactic dehydrogenase, acid-base balance and lipid peroxidation products - thiobarbituric acid reactive substances, were followed in 30 patients with head injuries. Results. A decrease in the level of partial oxygen pressure (PaO2) (p<0.01) and PaO2/FiO2 index (p<0.05) in arterial blood was recorded on day 3 of mechanical ventilation. This was accompanied with an increase in alveolar-arterial difference (AaDO2) (p<0.05), thiobarbituric acid reactive substances (p<0.001) and lactic dehydrogenase (p<0.001) comparing to day 1 of mechanical ventilation. The patients with initial PaO2>120 mmHg, had significant increase of thiobarbituric acid reactive substances and AaDO2 (p<0.05) and fall of PaO2 (p<0.001) on day 3 of mechanical ventilation. Conclusion. Oxidative stress and lipid peroxide production are increased during third day of mechanical ventilation leading to disruption of oxygen diffusion through alveolar-capillary membrane and reduction of parameters of oxygenation.

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Psychological prognosis after newly diagnosed chronic conditions: socio-demographic and clinical correlates

International Psychogeriatrics ◽

10.1017/s1041610216001630 ◽

2016 ◽

Vol 29 (2) ◽

pp. 281-292 ◽

Cited By ~ 2

Author(s):

Ching-Ju Chiu ◽

Yu-Ching Hsu ◽

Shuo-Ping Tseng

Keyword(s):

Depressive Symptoms ◽

Depressive Symptom ◽

Chronic Conditions ◽

Liver Diseases ◽

Lung Diseases ◽

Heart Diseases ◽

Psychological Burden ◽

Symptom Trajectories ◽

Physical Limitations ◽

Over Time

ABSTRACTBackground:This study was aimed toward discerning depressive symptom trajectories associated with different chronic conditions and toward finding modifiable factors associated with those trajectories.Methods:Data were drawn from the 1996–2007 Taiwan Longitudinal Study on Aging. Nine chronic conditions were selected, and mood trajectories were measured with the Center of Epidemiological Studies-Depression scale.Results:Among the nine chronic conditions we examined, four patterns of depressive symptom trajectories were identified: (1) elevated depressive symptoms and worsened over time after diagnosed with heart disease (n= 681), arthritis (n= 850), or hypertension (n= 1,207); (2) elevated depressive symptoms without worsening over time after diagnosed with stroke (n= 160), lung diseases (n= 432), gastric conditions (n= 691), or liver diseases (n= 234); (3) no elevated depressive symptoms after diagnosis but an increase in depressive symptoms over time for participants with diabetes (n= 499); and (4) no significant patterns after diagnosed with cancer (n= 57). Cumulative psychological burden over time was significant for participants with hypertension, diabetes, heart diseases, or arthritis. However, these effects disappeared after controlling for comorbidities and physical limitations. Moreover, psychiatric condition was found to play an important role in baseline depressive symptoms among participants diagnosed with lung diseases, arthritis, or liver diseases.Conclusions:Findings from this study provide information in addressing psychological burden at different times for different conditions. In addition, minimizing the incidence of comorbidities, physical limitations, or psychiatric conditions may have the prospective effect of avoiding the trend of increased depressive symptoms, especially when adults diagnosed with hypertension, diabetes, heart diseases, arthritis, lung diseases, arthritis, or liver diseases.

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Arterial Blood Oxygenation during and after Endotracheal Suctioning in the Apneic Patient

Anesthesiology ◽

10.1097/00000542-197002000-00005 ◽

1970 ◽

Vol 32 (2) ◽

pp. 114-118 ◽

Cited By ~ 26

Author(s):

Azmy R. Boutros

Keyword(s):

Blood Oxygenation ◽

Endotracheal Suctioning ◽

Arterial Blood

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Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat

AJP Renal Physiology ◽

10.1152/ajprenal.00252.2006 ◽

2007 ◽

Vol 292 (2) ◽

pp. F861-F867 ◽

Cited By ~ 17

Author(s):

Melvin R. Hayden ◽

Nazif A. Chowdhury ◽

Shawna A. Cooper ◽

Adam Whaley-Connell ◽

Javad Habibi ◽

...

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Systolic Blood Pressure ◽

Proximal Tubule ◽

Structural Damage ◽

Kidney Tissue ◽

Proximal Tubule Cell ◽

Ang Ii ◽

Sprague Dawley ◽

Sprague Dawley Rats

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5–8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT1R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6–7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-β-d-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and ×60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats ( P < 0.05) correlated strongly with albuminuria ( r2 = 0.83) and moderately with MDA ( r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats ( P < 0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-β-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.

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Abstract 5676: Elevated Oxidative Stress is Associated with Ventricular Fibrillation Episode in Patients with Brugada Syndrome without SCN5A Mutation

Circulation ◽

10.1161/circ.118.suppl_18.s_982-b ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Masamichi Tanaka ◽

Keiko Ohgou ◽

Koji Nakagawa ◽

Takeshi Tada ◽

Masato Murakami ◽

...

Keyword(s):

Oxidative Stress ◽

Risk Factor ◽

Ventricular Fibrillation ◽

Brugada Syndrome ◽

Endomyocardial Biopsy ◽

Heart Diseases ◽

Multivariable Analysis ◽

Pathophysiological Mechanism ◽

Normal Heart ◽

Scn5a Mutation

Background; Brugada Syndrome (BS) is a disease known to cause ventricular fibrillation (VF) with structurally normal heart. Gene mutation (i.e. SCN5A) has been proposed to be related to the development of BS and VF. However, the pathophysiological mechanism associated with VF development without SCN5A mutation has not been studied yet. Oxidative stress is a common disorder that is related to many heart diseases. We have previously demonstrated that oxidative stress is closely linked to the arrhythmic development. Accordingly, we examined 4-hydroxy-2-nonenal (HNE) modified protein, which is a common mediator of oxidative stress in the myocardium, and VF episodes in patients with BS. Methods; We collected sixty-eight BS patients that underwent right ventricular endomyocardial biopsy (66 males, 2 female; mean age 49.0±11.6 years old). VF was documented in 11 and SCN5A mutation was detected in 14 patients. Biopsy samples were processed for histology [Masson’s trichrome staining for fibrosis, immuno staining for CD45, CD68, and HNE modified protein]. All results from histology were compared with VF episodes. We also performed the analysis in VF patients with (n=14) or without SCN5A mutations (n=54). Results: HNE positive area was significantly larger in VF patients [VF(+): 16.3±10.5, VF(−): 9.3±5.7%: P=0.029]. All other parameters (fibrosis area, CD45, and CD68) were not different between the groups. In multivariable analysis, HNE positive area was most important risk factor of VF development in patients without SCN5A mutation (P=0.004). Conclusions ; These data suggested that oxidative stress is associated with VF development in BS patients, especially in patients without SCN5A mutation.

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Ventilator-induced diaphragm dysfunction in critical illness

Experimental Biology and Medicine ◽

10.1177/1535370218811950 ◽

2018 ◽

Vol 243 (17-18) ◽

pp. 1331-1339 ◽

Cited By ~ 3

Author(s):

Yung-Yang Liu ◽

Li-Fu Li

Keyword(s):

Oxidative Stress ◽

Mechanical Ventilation ◽

Muscle Atrophy ◽

Structural Damage ◽

Molecular Mechanisms ◽

Substantial Reduction ◽

Mechanical Stretch ◽

Janus Kinase ◽

Diaphragm Muscle ◽

Diaphragm Dysfunction

Mechanical ventilation is an essential intervention for intensive care unit patients with acute lung injury. However, the use of controlled mechanical ventilation in both animal and human models causes ventilator-induced diaphragm dysfunction, wherein a substantial reduction in diaphragmatic force-generating capacity occurs, along with structural injury and atrophy of diaphragm muscle fibers. Although diaphragm dysfunction, noted in most mechanically ventilated patients, is correlated with poor clinical outcome, the specific pathophysiology underlying ventilator-induced diaphragm dysfunction requires further elucidation. Numerous factors may underlie this condition in humans as well as animals, such as increased oxidative stress, calcium-activated calpain and caspase-3, the ubiquitin–proteasome system, autophagy–lysosomal pathway, and proapoptotic proteins. All these alter protein synthesis and degradation, thus resulting in muscle atrophy and impaired contractility and compromising oxidative phosphorylation and upregulating glycolysis associated with impaired mitochondrial function. Furthermore, infection combined with mechanical stretch may induce multisystem organ failure and render the diaphragm more sensitive to ventilator-induced diaphragm dysfunction. Herein, several major cellular mechanisms associated with autophagy, apoptosis, and mitochondrial biogenesis—including toll-like receptor 4, nuclear factor-κB, Src, class O of forkhead box, signal transducer and activator of transcription 3, and Janus kinase—are reviewed. In addition, we discuss the potential therapeutic strategies used to ameliorate ventilator-induced diaphragm dysfunction and thus prevent delay in the management of patients under prolonged duration of mechanical ventilation. Impact statement Mechanical ventilation (MV) is life-saving for patients with acute respiratory failure but also causes difficult liberation of patients from ventilator due to rapid decrease of diaphragm muscle endurance and strength, which is termed ventilator-induced diaphragmatic damage (VIDD). Numerous studies have revealed that VIDD could increase extubation failure, ICU stay, ICU mortality, and healthcare expenditures. However, the mechanisms of VIDD, potentially involving a multistep process including muscle atrophy, oxidative loads, structural damage, and muscle fiber remodeling, are not fully elucidated. Further research is necessary to unravel mechanistic framework for understanding the molecular mechanisms underlying VIDD, especially mitochondrial dysfunction and increased mitochondrial oxidative stress, and develop better MV strategies, rehabilitative programs, and pharmacologic agents to translate this knowledge into clinical benefits.

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