Clinical and Experimental Hypertension (Apr 2021)

Echocardiographic follow-up to right ventricular modifications in secondary pulmonary hypertension to diabetes in rats

  • Gustavo López y López,
  • Ana Yessica Tepox Galicia,
  • Fausto Atonal Flores,
  • Jorge Flores Hernández,
  • Francisco Pérez Vizcaino,
  • Abel E. Villa Mancera,
  • García González Miguél,
  • Alejandro Reynoso Palomar

DOI
https://doi.org/10.1080/10641963.2020.1860077
Journal volume & issue
Vol. 43, no. 3
pp. 242 – 253

Abstract

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Clinical studies suggest that diabetes is a risk factor in the development of pulmonary arterial hypertension. The increase in blood pressure in the pulmonary area is characterized by the increase in the afterload and hypertrophy of the right ventricle. The objective of this study was to conduct a longitudinal follow-up of the morphological and functional changes in the right ventricle in a rat model with pulmonary arterial hypertension secondary to diabetes. Male Sprague Dawley rats were randomly divided into a control group (saline solution) and a diabetic group (60 mg/kg with streptozotocin). For 12 weeks, an echocardiography for longitudinal (in vivo) image analysis of the pulmonary pressure was performed at the same time as the evaluation of myocardial remodeling and right ventricular. After this period, the pulmonary pressure was measured by means of a pulmonary artery catheterization, and the presence of hypertrophy was determined by means of the Fulton index. The plasma concentration of brain natriuretic peptide was measured by means of the ELISA technique. It was found that the diabetic rats showed an increase in pressure in the pulmonary arteries, an increase in the Fulton index, and an increase in brain natriuretic peptide. The echocardiographic follow-up showed that the diabetic rats presented an increase in the pulmonary artery from the fourth week, while hypertrophy and right ventricular systolic dysfunction occurred until the twelfth week. In conclusion, pulmonary arterial hypertension induced by experimental diabetes generated hypertrophy and systolic dysfunction of the right ventricle.

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