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Validation of Evans Blue inhibits Compound 48/80 induced inflammation in hypertension rat models
Author(s) -
Lue ShengI,
Lu Tzongshi,
Fu YawSyan
Publication year - 2018
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.2018.32.1_supplement.847.12
Subject(s) - extravasation , medicine , inflammation , blood pressure , evans blue , hemodynamics , pathophysiology , analysis of variance , mean arterial pressure , endocrinology , pathology , heart rate
Background Hypertension (HT) is a multifactorial cardiovascular disorder involves in variety genetic and environmental factors, and it is a major risk factor for cardiovascular disease. In order to study the pathophysiology of HT, the proper robust and reproducible experimental animal models are required. Phase‐1 hypertension (P1‐HT) is the beginning stage of high blood pressure (BP). The ideal P1‐HT animal model should have human‐like cardiovascular anatomy, hemodynamics, and physiology that includes genetic and non‐genetic models. Moreover, inflammation responses may cause plasma leakage and affect BT readings in experimental animals. Among current HT rat 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 inflammatory mediators' effects and responses in correlation with BP readings among current commercial available SD/SHR rats and our new breeding P1‐HT rat to further calibrating BP readings in variety rat HT models. Methods Histamine, Capsaicin, Compound 48/80 or Substance P were administered into the femoral vein of rats individually to induce inflammation and vascular dysfunction. Then we analyzed mean arterial pressure (MAP) 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 BP changes in substance P induced neurogenic inflammation but positive linear regression in compound 48/80 induced immunogenic inflammation. In addition, pretreated with Evans blue dye could inhibit compound 48/80 induced extensive plasma extravasation, mast cell degranulation, and edema significantly. In addition, our data show significant variation BP readings among neurogenic and immunogenic inflammation induced BP changes in different rat HT models. Conclusion Our data shows for the first time that methodical variations observed among normal and hypertensive animals, can potentially translate into differential BP patterns, which can be falsely taken to generate significant biological bias. Our study therefore highlights the pivotal need in interpretation of BP data using different HT rat models in the study. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .