Kentucky State University

Poster Title

Characterization of Cardiac Inflammatory-Fibrotic Responses in Angiotensin II-Exposed APOE-/- & APOE/GV SPLA2 Mice Following Treatment with Angiotensin II or Aldosterone Receptor Antagonists

Institution

Kentucky State University

Abstract

Angiotensin II and aldosterone antagonist receptor drugs have been reported to influence the development of fibrosis and collagen production in cardiac tissues from the development of hypertension. To test this hypothesis, APOE mice-models were infused Angiotensin II through osmotic pumps to produce hypertensive-induced changes in cardiac fibrotic connective tissue. This study investigated the affects of Angiotensin II receptor blocker LosartinTM, as well as the aldosterone receptor antagonist EplerenoneTM on the Angiotensin II-induced changes in cardiac fibrotic tissues, while saline-infused APOE mice served as control models. Subsequent of the 7 days of administration of antagonist receptor drugs, heart tissue from the control and treated groups were prepared for microscopic computation of cardiac collagen deposition in the heart wall at the level of the papillary muscles. Gomori trichrome and picrosirius red staining techniques were utilized to perform microscopic histochemical collagen comparisons between the treatment and control groups. Following statistical analysis of the assessed percentages of the collagen production in the control and treatment groups, it was determined that the LosartanTM group of mice had the least amount of abnormal collagen production within the cardiac tissue, showing that the drug significantly slowed fibrosis and produced fibrotic tissue material compared to the other treated group. The EperloneTM treatment group showed lesser microscopic evidence of collagen production, which did not necessarily mean that the drug did not work to reverse the fibrotic buildup, but may potentially require a longer duration than 7 days to fully produce its effect on damaged area. Observation and quantification of the amount of collagen present in the hearts of the various mice treatment and control groups assisted in determining the prominent antagonistic receptor drug which limited the inflammatory response within the 7 day study.

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Characterization of Cardiac Inflammatory-Fibrotic Responses in Angiotensin II-Exposed APOE-/- & APOE/GV SPLA2 Mice Following Treatment with Angiotensin II or Aldosterone Receptor Antagonists

Angiotensin II and aldosterone antagonist receptor drugs have been reported to influence the development of fibrosis and collagen production in cardiac tissues from the development of hypertension. To test this hypothesis, APOE mice-models were infused Angiotensin II through osmotic pumps to produce hypertensive-induced changes in cardiac fibrotic connective tissue. This study investigated the affects of Angiotensin II receptor blocker LosartinTM, as well as the aldosterone receptor antagonist EplerenoneTM on the Angiotensin II-induced changes in cardiac fibrotic tissues, while saline-infused APOE mice served as control models. Subsequent of the 7 days of administration of antagonist receptor drugs, heart tissue from the control and treated groups were prepared for microscopic computation of cardiac collagen deposition in the heart wall at the level of the papillary muscles. Gomori trichrome and picrosirius red staining techniques were utilized to perform microscopic histochemical collagen comparisons between the treatment and control groups. Following statistical analysis of the assessed percentages of the collagen production in the control and treatment groups, it was determined that the LosartanTM group of mice had the least amount of abnormal collagen production within the cardiac tissue, showing that the drug significantly slowed fibrosis and produced fibrotic tissue material compared to the other treated group. The EperloneTM treatment group showed lesser microscopic evidence of collagen production, which did not necessarily mean that the drug did not work to reverse the fibrotic buildup, but may potentially require a longer duration than 7 days to fully produce its effect on damaged area. Observation and quantification of the amount of collagen present in the hearts of the various mice treatment and control groups assisted in determining the prominent antagonistic receptor drug which limited the inflammatory response within the 7 day study.