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ORIGINAL ARTICLE
Year : 2022  |  Volume : 22  |  Issue : 1  |  Page : 23-28

Resuscitation of hemorrhagic shock using normal saline does not damage the glycocalyx in the immediate resuscitation phase


1 Department of Child Health, Faculty of Medicine, Cipto Mangunkusumo Hospital, Universitas Indonesia, Jakarta, Indonesia
2 Department of Veterinary Clinic Reproduction and Pathology, Division of Veterinary Surgery and Radiology, Faculty of Veterinary Medicine, Bogor Agricultural University, Bogor, Indonesia
3 Department of Nutrition, Universitas Indonesia, Jakarta, Indonesia
4 Department of Biochemistry and Molecular Biology, Universitas Indonesia, Jakarta, Indonesia
5 Department of Physiology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia
6 Department of Child Health, North Sumatera University Hospital, Faculty of Medicine North Sumatera University, Medan, Indonesia

Correspondence Address:
Dr. Antonius Hocky Pudjiadi
Jl. Salemba Raya No. 6, Jakarta
Indonesia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2452-2473.336100

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OBJECTIVES: The objectives were to study the effect of aggressive resuscitation using normal saline on hemodynamics, serum atrial natriuretic peptide (ANP), syndecan-1 (marker of endothelial glycocalyx shedding), and extravascular lung water index (ELWI) following hemorrhagic shock. METHODS: Eleven male piglets (Sus scrofa) underwent blood drawing to create 20% drop in mean arterial pressure (MAP). Two-phase resuscitation was performed: Phase 1 using normal saline of an equal volume of blood drawn to create shock and Phase 2 using 40 ml/kg BW of normal saline to simulate hypervolemia and hemodilution. Heart rate, MAP, cardiac index (CI), systemic vascular resistance index, oxygen delivery (DO2), global end-diastolic volume index, ELWI, hemoglobin (Hb), lactate, ANP, and syndecan-1 at each phase and up to 60 min following Phase 2 resuscitation were recorded. RESULTS: Phase 2 resuscitation significantly decreased Hb concentration (P = 0.006), however, DO2 was maintained (P = 1.000). CI increased from shock to Phase 1 (P = 0.029) and further increase in Phase 2 resuscitation (P = 0.001). Overall, there was a transient increase of ANP following Phase 1 resuscitation, from 85.20 ± 40.86 ng/L at baseline to 106.42 ± 33.71 ng/L (P = 0.260). Serum syndecan-1 and ELWI change at all phases were not significant. CONCLUSIONS: We demonstrate compensatory protective mechanism despite overzealous fluid resuscitation. Compensatory increased CI despite decreased Hb maintained DO2. In the absence of inflammation, serum ANP did not increase significantly, no glycocalyx shedding occurred, subsequently no change in ELWI. We show that factors other than volume overload are more dominant in causing glycocalyx shedding.


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