Tissue damage in the heart after cardiac arrest induced by asphyxia and hemorrhage in newborn pigs

Asphyxia of newborns is a severe and frequent challenge of the peri- and postnatal period. Forty-four neonatal piglets underwent asphyxia and hemorrhage (AH), followed by resuscitation with blood or crystalloid transfusion. In this study, 15 piglets (blood n = 9, NaCl n = 6, mean age 31 h) were rand...

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Bibliographic Details
Published in:Pediatric research 2019-12, Vol.86 (6), p.709-718
Main Authors: Weber, Birte, Mendler, Marc Robin, Lackner, Ina, Pressmar, Jochen, Haffner-Luntzer, Melanie, Höfler, Severin, Braun, Christian Karl, Hummler, Helmut, Schwarz, Stephan, Kalbitz, Miriam
Format: Article
Language:English
Subjects:
Blood transfusions
Cardiac arrest
Heart
Heart attacks
Hemorrhage
Hypoxia
Tissues
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Summary:Asphyxia of newborns is a severe and frequent challenge of the peri- and postnatal period. Forty-four neonatal piglets underwent asphyxia and hemorrhage (AH), followed by resuscitation with blood or crystalloid transfusion. In this study, 15 piglets (blood n = 9, NaCl n = 6, mean age 31 h) were randomly chosen. Four hours after return of spontaneous circulation, heart tissue and blood were collected. Analyses of heart fatty acid binding protein (HFABP), cardiac troponin I (TnI) levels, and activation of the complement system were performed. Histological staining for connexin 43 (Cx43) and complement C5a receptor 1 (C5aR1) was performed. Following AH, systemic elevation of cardiac TnI and HFABP revealed cardiac damage in both groups. Systemic activation of the complement system and the appearance of extracellular histones in plasma of the blood transfusion group were observed. The Cx43 was translocated from the intercalated discs to the cytosol after AH. Cardiac glycogen concentration was reduced in both groups. A significant reduction of C5aR1 in the left ventricle and a significant elevation of the heart injury score were investigated after blood transfusion. AH leads to alteration of the heart, particularly in Cx43 and glycogen reserves, as well as local inflammation.
ISSN:0031-3998
1530-0447
DOI:10.1038/s41390-019-0505-6