Chronic heart failure modifies respiratory mechanics in rats: a randomized controlled trial

Abstract

ObjectiveTo analyze respiratory mechanics and hemodynamic alterations in an experimental model of chronic heart failure (CHF) following myocardial infarction.MethodTwenty-seven male adult Wistar rats were randomized to CHF group (n=12) or Sham group (n=15). Ten weeks after coronary ligation or sham surgery, the animals were anesthetized and submitted to respiratory mechanics and hemodynamic measurements. Pulmonary edema as well as cardiac remodeling were measured.ResultsThe CHF rats showed pulmonary edema 26% higher than the Sham group. The respiratory system compliance (Crs) and the total lung capacity (TLC) were lower (40% and 27%, respectively) in the CHF rats when compared to the Sham group (P<0.01). There was also an increase in tissue resistance (Gti) and elastance (Hti) (28% and 45%, respectively) in the CHF group. Moreover, left ventricular end-diastolic pressure was higher (32 mmHg vs 4 mmHg, P<0.01), while the left ventricular systolic pressure was lower (118 mmHg vs 130 mmHg, P=0.02) in the CHF group when compared to the control. Pearson’s correlation coefficient showed a negative association between pulmonary edema and Crs (r=–0.70, P=0.0001) and between pulmonary edema and TLC (r=–0.67, P=0.0034). Pulmonary edema correlated positively with Gti (r=0.68, P=0.001) and Hti (r=0.68, P=0.001). Finally, there was a strong positive relationship between pulmonary edema and heart weight (r=0.80, P=0.001).ConclusionRats with CHF present important changes in hemodynamic and respiratory mechanics, which may be associated with alterations in cardiopulmonary interactions.

Diaphragm weakness and proteomics (global and redox) modifications in heart failure with reduced ejection fraction in rats

“…These contradictory findings are difficult to reconcile, as there is not a consistent pattern among studies showing atrophy or lack thereof. However, two interesting aspects to consider from our current findings are: first, the presence of atrophy without statistically significant contractile dysfunction in moderate HFrEF and second, the absence of diaphragm fiber hypertrophy in rats with severe HFrEF, where lowered respiratory system compliance (54,55) and elevated ventilation (56) increase work of breathing. One possibility is that a threshold of inflammatory or neurohumoral signaling may have been met to induce atrophy, but not to elicit contractile dysfunction in moderate HFrEF.…”

Can diaphragmatic breathing modify chest wall volumes during inspiratory loaded breathing in patients with heart failure?

“…We can hypothesize that it can also be related to lung properties changes previously reported in patients and animals with HF. 35,36 To the best of our knowledge, this was the first study to evaluate chest wall volumes during ILB associated with diaphragmatic breathing in patients with heart failure. One of the limitations was the absence of a randomization between the ILB and ILB di conditions and, therefore, it is not possible to exclude the learning effect during ILB di .…”

Exercise training to reduce sympathetic nerve activity in heart failure patients. A systematic review and meta-analysis

“… 8 The pathophysiology is characterized by an imbalance in the autonomic control of the cardiovascular system, with a predominance of sympathetic nervous systems and inhibition of parasympathetic nervous systems. 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 This imbalance promotes the activation of renin–angiotensin system and mechanisms associated with myocardial remodeling, which worse the disease prognosis and increases patient mortality rates. 11 , 12 , 13 , 14 …”