AFRICA Cardiovascular Journal of Africa • SAHS Biennial Congress 2024 32 POSTER PRESENTATION Submission ID: 1642 Introduction Hypertension causes structural remodelling of the myocardium, which often results in left ventricular (LV) dysfunction. Systemic inflammation contributes to LV systolic and diastolic dysfunction. The compounding effect of inflammation on hypertension-induced LV dysfunction is uncertain. This study investigated the short- and long-term effects of acute exposure to lipopolysaccharide (LPS) on LV structure and function in a hypertensive rat model. Methods Wistar-Kyoto (WKY, n=36) and spontaneously hypertensive rats (SHR, n=38) were divided into control or LPS groups, receiving a single dose of saline or 1 mg/kg LPS, respectively. The rats were further divided into the short-term group, which were terminated 24 hours after injections, or the long-term group, which were terminated 6 weeks after injections. LV geometry, systolic and diastolic functions were determined using conventional and speckle tracking echocardiography. Serum interleukin (IL)-1β concentrations were determined using an ELISA and LV collagen content was determined with histology. A two-way ANOVA was used to determine group differences. Pearson’s correlation was used to determine associations. Results In the short-term groups, LPS increased serum IL-1β concentration and impaired LV systolic and diastolic function in SHR and WKY rats compared to the rats in the respective control groups. In the short term, LPS administration worsened LV systolic and diastolic dysfunction in SHR compared to the WKY rats. In the long term, there were no significant LPS-induced effects on any LV function markers. Hypertension resulted in increased heart weight and impaired LV systolic function in SHR compared to WKY rats. In the presence of hypertension, LPS administration increased collagen volume and worsened LV systolic dysfunction. Conclusion In conclusion, acute LPS exposure induced short- and long-term cardiac structural changes and LV systolic and diastolic dysfunction, which were worsened in rats predisposed to hypertension. Name: Presenting Author Information Article Category Abstract Title Integrated Molecular Physiology Research Initiative, School of Physiology, University of the Witwatersrand 1616188@students.wits.ac.za English Abstract Students - Currently enrolled postgraduate students LPS-induced inflammation worsens cardiac dysfunction in a hypertensive model Author Affiliation: Email: Kealeboga M Fako Science Theme Basic Authors Name & Surname Title Expertise Affiliation Email Country Kealeboga M Fako Ms Cardiovascular diseases Integrated Molecular Physiology Research Initiative, School of Physiology, University of the Witwatersrand 1616188@students.wits.ac.za South Africa Tiiso T Maluleke Ms Cardiovascular diseases Integrated Molecular Physiology Research Initiative, School of Physiology, University of the Witwatersrand Tiiso.Maluleke@wits.ac.za South Africa Leandrie Pienaar Ms Neurosciences Integrated Molecular Physiology Research Initiative, School of Physiology, University of the Witwatersrand 1836318@students.wits.ac.za South Africa Frederic S Michel Associate Professor Cardiovascular diseases Integrated Molecular Physiology Research Initiative, School of Physiology, University of the Witwatersrand Frederic.Michel@wits.ac.za South Africa Aletta ME Millen Associate Professor Inflammation noncommunicable diseases Integrated Molecular Physiology Research Initiative, School of Physiology, University of the Witwatersrand Aletta.Millen@wits.ac.za South Africa
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