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Evaluation of biological and mechanical variations in hypertensive animal models
Author(s) -
Lue ShengI,
Ho Lilun,
Fu YawSyan,
Lu Tzongshi
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1011.14
Subject(s) - extravasation , evans blue , medicine , blood pressure , capsaicin , inflammation , pathophysiology , histamine , hemodynamics , animal studies , pharmacology , anesthesia , pathology , receptor
Background Hypertension (HT) is a multifactorial cardiovascular disorder that involves a variety of genetic and environmental factors. To properly study the pathophysiology of hypertension, robust and reproducible experimental animal models are required. The ideal HT animal model should have human‐like cardiovascular anatomy, hemodynamics, and physiology that includes genetic and non‐genetic models. Among these HT animal models, Spontaneously Hypertensive Rats (SHR) with both neural and vascular alterations is the most commonly used genetic HT animal model. In this study, we investigated methodical variations among current HT animal models. Methods Histamine, Capsaicin, C48/80 or Substance P were administered into the femoral vein of Sprague Dawley rats or SHR to induce endothelial dysfunction. We analyzed mean arterial pressure and analyze plasma extravasation using Evans Blue dye. One way ANOVA with Bonferroni correction, and linear regression were used for statistics. Statistical significances were set at a P< 0.05. Results Our data showed significant negative linear regression on the degree of plasma extravasation with blood pressure changes in neurogenic inflammation (Substance P) but positive linear regression in immunogenic inflammation (Histamine, Capsaicin, C48/80). In addition, Evans blue dye inhibited C48/80‐induccd extensive plasma extravasation, mast cell degranulation, and edema significantly. Conclusions We have observed significant variations among neurogenic and immunogenic inflammation induced blood pressure changes. Our data shows for the first time that methodical variations observed among animal models, can potentially translate into differential blood pressure patterns, which can be falsely taken to be biologically significant. Our study therefore highlights the pivotal need to carefully consider methodical approaches to animal models that report quantitative differences.