Early Cardiac Injury in Acute Respiratory Distress Syndrome: Comparison of Two Experimental Models
Autor: | Daniel Čierny, Pavol Mikolka, P Kosutova, J Kopincova, Andrea Calkovska, Marian Adamkov, Daniela Mokra, M Kolomaznik, Sona Balentova |
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Rok vydání: | 2021 |
Předmět: |
Male
medicine.medical_specialty ARDS Necrosis Physiology Apoptosis Inflammation 030204 cardiovascular system & hematology Hypoxemia 03 medical and health sciences 0302 clinical medicine Internal medicine medicine Animals Respiratory system Respiratory Distress Syndrome Lung biology business.industry Lung Injury Articles General Medicine medicine.disease Troponin Meconium Aspiration Syndrome Disease Models Animal Oxidative Stress medicine.anatomical_structure Heart Injuries 030228 respiratory system biology.protein Cardiology Female Creatine kinase Rabbits medicine.symptom business Biomarkers |
Zdroj: | Physiol Res |
ISSN: | 1802-9973 0862-8408 |
Popis: | Acute respiratory distress syndrome (ARDS) is characterized by diffuse lung damage, inflammation, oedema formation, and surfactant dysfunction leading to hypoxemia. Severe ARDS can accelerate the injury of other organs, worsening the patient´s status. There is an evidence that the lung tissue injury affects the right heart function causing cor pulmonale. However, heart tissue changes associated with ARDS are still poorly known. Therefore, this study evaluated oxidative and inflammatory modifications of the heart tissue in two experimental models of ARDS induced in New Zealand rabbits by intratracheal instillation of neonatal meconium (100 mg/kg) or by repetitive lung lavages with saline (30 ml/kg). Since induction of the respiratory insufficiency, all animals were oxygen-ventilated for next 5 h. Total and differential counts of leukocytes were measured in the arterial blood, markers of myocardial injury [(troponin, creatine kinase - myocardial band (CK-MB), lactate dehydrogenase (LD)] in the plasma, and markers of inflammation [tumour necrosis factor (TNF)α, interleukin (IL)-6], cardiovascular risk [galectin-3 (Gal-3)], oxidative changes [thiobarbituric acid reactive substances (TBARS), 3-nitrotyrosine (3NT)], and vascular damage [receptor for advanced glycation end products (RAGE)] in the heart tissue. Apoptosis of heart cells was investigated immunohistochemically. In both ARDS models, counts of total leukocytes and neutrophils in the blood, markers of myocardial injury, inflammation, oxidative and vascular damage in the plasma and heart tissue, and heart cell apoptosis increased compared to controls. This study indicates that changes associated with ARDS may contribute to early heart damage what can potentially deteriorate the cardiac function and contribute to its failure. |
Databáze: | OpenAIRE |
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