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

• 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: Basic Science Article; Blood transfusions; Cardiac arrest; Heart; Heart attacks; Hemorrhage; Hypoxia; Medicine; Medicine & Public Health; Pediatric Surgery; Pediatrics; Tissues
• ISSN: 0031-3998; 1530-0447
• DOI: 10.1038/s41390-019-0505-6

Background Asphyxia of newborns is a severe and frequent challenge of the peri- and postnatal period. Methods 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. Results 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. Conclusion AH leads to alteration of the heart, particularly in Cx43 and glycogen reserves, as well as local inflammation.