Gastric Bleeding Model

HuaTeng Biotech offers a high-fidelity preclinical Gastric Bleeding platform featuring both chemical-induced diffuse mucosal hemorrhage and precise, surgically/endoscopically driven acute focal bleeding.

Species & Strain
Sprague-Dawley (SD) / Wistar rats, New Zealand White rabbits, and Bama mini-pigs.
Model Description
Our platform accurately replicates human upper gastrointestinal bleeding scenarios, providing standard small-animal systems for pharmacological screening alongside large-animal (porcine) interventional suites. This platform is ideal for validating novel localized hemostatic powders, sprays, bio-adhesives, thermal ablation devices, and mechanical clipping systems under strict OECD GLP and AAALAC compliance.

Indication / Application

Preclinical validation of topical and systemic hemostatic agents, efficacy testing of endoscopic interventional devices (clips, bands, thermal probes), screening of gastroprotective formulations, and mechanistic evaluation of acute mucosal barrier defense.

 

Modeling Method

  1. Chemical Diffuse Bleeding Platform (Pharmacological Screening): Acute administration of absolute ethanol, indomethacin, or concentrated hydrochloric acid via oral gavage. This triggers rapid, widespread gastric mucosal denudation, vascular congestion, and multi-focal superficial gastric bleeding within hours.

  1. Surgical / Endoscopic Focal Bleeding Platform (Device Validation): Under general anesthesia and high-magnification or endoscopic visualization, a localized mucosal lesion or simulated ulcer is created via precise punch biopsy, Endoscopic Mucosal Resection (EMR), or controlled micro-scalpel incision into the submucosal arteriolar network of the gastric corpus or antrum, generating active, measurable focal bleeding.

 

Clinical Relevance

  • Interventional Translational Platform: For advanced device and biomaterial pipelines, our porcine gastric bleeding model provides exact human-scale anatomical access, gastric rugae architecture, and realistic blood flow pressures. This ensures high-fidelity translational data required for global regulatory submissions (FDA, NMPA, CE).

  • Pathological Homology: The chemical and surgical models closely simulate the rapid onset of clinical gastric ulcers, stress-induced mucosal disease (SRMD), and NSAID-induced bleeding complications, mirroring human physiological responses to gastric acid exposure and vascular injury.

 

Key Evaluation Endpoints

In Vivo / Interventional Evaluation

  • Hemostasis Kinetics (Gold Standard): Meticulous real-time recording of Time-to-Hemostasis (TTH), volume of blood loss, and incidence of delayed re-bleeding post-intervention.

  • Quantitative Endoscopic Scoring: Serial endoluminal tracking of the lesion site to score the severity of ongoing bleeding, clot stability, and mucosal healing over time.

  • Systemic Hemodynamic Stability: Continuous tracking of mean arterial pressure (MAP), heart rate, and shock index variations during acute bleeding episodes.

Biochemical & Hematological Profiling

  • Systemic Blood Loss Monitoring: Serial Complete Blood Count (CBC) tracking to evaluate hematocrit (Hct), hemoglobin (Hb) drops, and platelet consumption.

  • Coagulation Diagnostics: Real-time Thromboelastography (TEG) and activated partial thromboplastin time (aPTT) profiling to assess global clot structure and systemic clotting dynamics.

Histopathology & Biomaterial Characterization (Gold Standard)

  • Mucosal Healing & Lesion Indexing: Gross morphometric analysis and standard H&E staining to calculate the Gastric Ulcer Index (UI) and score the depth of tissue damage (mucosa, submucosa, or muscularis propria).

  • Interventional Interface Analysis: Specialized histopathology to evaluate the tissue-device interface, measuring the depth of thermal injury, mechanical tissue damage from clips, or the retention and biocompatibility of topical hemostatic polymers.

  • Inflammation & Remodeling Profiling: Masson’s Trichrome staining to monitor early collagen deposition, and IHC tracking for localized inflammatory cell infiltration (neutrophils, macrophages) and CD31-positive angiogenesis kinetics.

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