Histopathological Alterations in the Kidney Tissue Following Topical Ankaferd Hemostat Application in a Rat Renal Injury Model


KARAKOÇ D., Akar E., AKSU S., ÜNER A., ÖZDEMİR A., HAMALOĞLU E., ...More

UHOD-ULUSLARARASI HEMATOLOJI-ONKOLOJI DERGISI, vol.22, no.4, pp.275-281, 2012 (Peer-Reviewed Journal) identifier identifier

  • Publication Type: Article / Article
  • Volume: 22 Issue: 4
  • Publication Date: 2012
  • Doi Number: 10.4999/uhod.11047
  • Journal Name: UHOD-ULUSLARARASI HEMATOLOJI-ONKOLOJI DERGISI
  • Journal Indexes: Science Citation Index Expanded, Scopus, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.275-281

Abstract

Ankaferd Blood Stopper (ABS) is a novel topical hemostatic agent. ABS has been approved in Turkey for clinical hemorrhages, when the conventional control of bleeding by ligature and/or conventional hemostatic measures is ineffective. ABS has many cellular effects and could modulate numerous hemostatic proteins at the tissue and blood. ABS-induced formation of the protein network with vital erythroid aggregation covers the entire physiological hemostatic process. The aim of this study was to assess histopathological alterations due to topical ABS administration at the renal tissue level. Thirty-six Wistar rats weighing 70 to 80 gm were included into the study. The rats were divided into two groups as "the ABS-applied group" (ABS-G) and "the control group" (C-G). The animals in both groups were then again divided into the three subgroups of "postoperative (Postop.) 60th minutes", "Postop. 48th hours", and "Postop. 15th day". Therefore, there were six rats in each of the subgroups at the end of the analyses. The standard renal injury sites in the rats of ABS-G were applied 2 ml. of topical ABS, whereas 2 ml. of topical saline was applied to the renal injury sites of the rats in the C-G group. We detected significant erythrocyte aggregation and the accumulation of siderophages in the kidney tissue just after 60 minutes of ABS application persisting over 15 days. Our results indicated red blood cell accumulation and siderophages following the use of ABS are compatible with the suggested 'mechanism-of-action' of ABS that ABS-induced formation of the protein network with vital erythroid aggregation covers the entire physiological hemostatic process. Further experimental search is needed to find out the molecules inside the ABS protein library leading to the ABS-induced aggregation at the renal tissue level.