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窒息和失血诱发新生猪心搏骤停后的心肌损伤。

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

机构信息

Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University of Ulm, Ulm, Germany.

Department of Pediatrics and Adolescent Medicine, Division of Neonatology and Pediatric Critical Care, Ulm University, Ulm, Germany.

出版信息

Pediatr Res. 2019 Dec;86(6):709-718. doi: 10.1038/s41390-019-0505-6. Epub 2019 Jul 23.

DOI:10.1038/s41390-019-0505-6
PMID:31336381
Abstract

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.

摘要

背景

新生儿窒息是围产期和产后的严重且常见的挑战。

方法

44 头新生仔猪经历窒息和出血(AH),随后通过输血或晶体液复苏。在这项研究中,随机选择了 15 头仔猪(血液组 n = 9,生理盐水组 n = 6,平均年龄 31 小时)。在自主循环恢复后 4 小时,采集心脏组织和血液。分析心脏脂肪酸结合蛋白(HFABP)、心肌肌钙蛋白 I(TnI)水平和补体系统的激活情况。进行连接蛋白 43(Cx43)和补体 C5a 受体 1(C5aR1)的组织学染色。

结果

AH 后,两组的心肌肌钙蛋白 I 和 HFABP 均升高,表明心脏受损。血液输注组观察到全身补体系统的激活和血浆中细胞外组蛋白的出现。AH 后 Cx43 从闰盘转移到细胞质。两组的心肌糖原浓度均降低。血液输注后,左心室的 C5aR1 明显减少,心脏损伤评分明显升高。

结论

AH 导致心脏发生变化,特别是 Cx43 和糖原储备发生变化,同时还伴有局部炎症。

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