American Society of Hirudotherapy

Effect of hirudin on arterialized venous flap survival in rabbits

Research article published in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (2021)

Last Updated: June 18, 2026Reviewed by: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Preclinical (animal)Salivary PharmacologyClinical TrialsDrug DevelopmentLiu J et al. · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2021

Abstract

Arterialized venous flap (AVF) is limited in clinical application because its survival remains inconsistent and its exact survival mechanism is still unclear. Hirudin is an effective thrombin specific inhibitor, which is isolated from the salivary gland secretions of the leech. Our study evaluated the impact of hirudin on the viability of AVFs in rabbits. Thirty-six rabbits were randomly divided into three groups: sham group (physiological perfusion), control group (AVF), and hirudin group (AVF + hirudin). In hirudin group, 20 antithrombin units (ATU) hirudin (2.5 ml) were injected into each flap. In sham group and control group, the same amount of normal saline was injected into each flap. Status of flap survival, water content, vascular perfusion, histopathology, expression of CD34, VEGF, eNOS and HIF-1α were analyzed in each group. Analysis of oxidative stress was performed by measuring the activity of superoxide dismutase (SOD) and malondialdehyde (MDA). Compared with flaps in sham group with physiological perfusion mode, results of survival rate, perfusion status, SOD activity, expression of CD34, VEGF, and eNOS of AVFs in control group were significantly lower, while water content, MDA level and expression of HIF-1α were higher. The flap condition of AVFs injected with hirudin in hirudin group was improved significantly, and the results were similar to sham group. Our findings revealed that hirudin can effectively improve survival of AVF.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal Article
Indexed MeSH termsAnimalsFibrinolytic AgentsGraft SurvivalHirudinsMaleMalondialdehydeOxidative StressRabbitsSuperoxide DismutaseSurgical Flaps

Summary

Arterialized venous flap (AVF) is limited in clinical application because its survival remains inconsistent and its exact survival mechanism is still unclear.

Why This Matters for Hirudotherapy

This study examined the effect of hirudin — a thrombin-specific inhibitor isolated from leech salivary gland secretions — on the survival of arterialized venous flaps (AVFs) in a rabbit model, assessing flap viability, vascular perfusion, histopathology, angiogenic and oxidative stress markers (CD34, VEGF, eNOS, HIF-1α, SOD, MDA), and tissue water content across sham, control, and hirudin-treated groups. It is directly relevant to ASH's domain because it demonstrates that a key bioactive component of the leech salivary secretome can improve compromised tissue flap survival, with the hirudin-treated flaps showing restored perfusion, angiogenic marker expression, and antioxidant status approaching those of sham controls. The mechanistic pathways illuminated — anticoagulation coupled with modulation of oxidative stress and angiogenesis — are central to understanding leech-derived therapeutics. However, this is an animal model study using injected purified hirudin rather than live hirudotherapy, and findings in rabbits may not directly translate to human reconstructive outcomes.

Citation

Effect of hirudin on arterialized venous flap survival in rabbits.

Liu J et al. · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2021

Added to ASH library: March 18, 2026 · Site last updated: June 18, 2026

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