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Spontaneous hypertension induced pulmonar and diaphragm disorders in rats (856.11)
Author(s) -
Souza Pamella,
Flues Karin,
De Moraes Wilson,
Santos Fernando,
Ferreira Janaina,
Medeiros Alessandra,
De Angelis Katia,
Irigoyen Maria Cláudia
Publication year - 2014
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.28.1_supplement.856.11
Subject(s) - medicine , cardiology , blood pressure , diaphragm (acoustics) , ventilation (architecture) , ventricle , endocrinology , respiratory system , mechanical engineering , physics , acoustics , loudspeaker , engineering
Hypertension induces modifications of standard rhythm breathing. However, the interaction of these effects with the cardiopulmonary and diaphragm morphological changes is not well known. We evaluated the influence of high blood pressure (BP) on cardiovascular modulation, chemoreflex sensitivity, right ventricle (RV) function, arterial blood gases and pulmonary morphometric parameters in rats. We also evaluated the diaphragm muscle profile in response to possible ventilator alterations. Hypertension adversely changed arterial blood gases patterns (pH, pO 2 , HCO 3 , SpO 2 ) and the autonomic cardiovascular modulation (systolic BP variance, low frequency band and pulse interval variance), as well exacerbated chemoreflex pressor response and increased RV end diastolic pressure. We observed that SHRs present higher lung to body weight index, arterial lumen to wall ratio (lung arteries), and collagen deposition compared to aged matched Wistar rats. The SHR diaphragm muscle showed increase in type I cross‐sectional fiber (CSA) (16%) and reduction in type II CSA area (41%), increased activity of the ubiquitin proteasome system and lipid peroxidation, with no differences between groups in the analysis of ubiquitinated proteins and misfolded proteins. In conclusion, hypertension induced cardiopulmonary morphometric and functional compensatory/adverse alterations associated with diaphragm fiber type changes and protein degradation. These data suggest a possible adaptation in ventilatory pattern as an attempt to improve ventilatory endurance and prevent the development of fatigue and muscle weakness.