Respiratory Mechanics In Rats Research Articles

Respiratory Muscle Training Improves Chemoreflex Response, Heart Rate Variability, and Respiratory Mechanics in Rats With Heart Failure

BackgroundThe aim of the present report was to evaluate respiratory muscle training (RMT) effects on hemodynamic function, chemoreflex response, heart rate variability, and respiratory mechanics in rats with heart failure (HF rats). MethodsWistar rats were divided into 4 groups: sedentary–sham (Sed-Sham, n = 8), respiratory muscle trained–sham (RMT-Sham, n = 8), sedentary-HF (Sed-HF, n = 8) and respiratory muscle trained–HF (RMT-HF, n = 8). Animals were submitted to an RMT protocol performed 30 minutes per day, 5 days per week for 6 weeks, whereas the sedentary animals did not exercise. ResultsIn HF rats, RMT promoted the reduction of left ventricular end-diastolic pressure, right ventricular hypertrophy, and pulmonary edema. Moreover, RMT produced a reduction in pressure response during chemoreflex activation, sympathetic modulation, and sympathetic vagal balance in addition to an increase in parasympathetic modulation. Also after RMT, HF rats demonstrated a reduction in respiratory system resistance, tissue resistance, Newtonian resistance, respiratory system compliance, and quasistatic compliance. ConclusionsThese findings suggested that 6 weeks of RMT in HF rats promoted beneficial adaptations in hemodynamics, autonomic function, and respiratory mechanics and attenuated pressure response evoked by chemoreflex activation in HF rats.

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

ABSTRACTObjectiveTo 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.

Respiratory muscle training improves hemodynamics, autonomic function, baroreceptor sensitivity, and respiratory mechanics in rats with heart failure

Respiratory muscle training (RMT) improves functional capacity in chronic heart-failure (HF) patients, but the basis for this improvement remains unclear. We evaluate the effects of RMT on the hemodynamic and autonomic function, arterial baroreflex sensitivity (BRS), and respiratory mechanics in rats with HF. Rats were assigned to one of four groups: sedentary sham (n = 8), trained sham (n = 8), sedentary HF (n = 8), or trained HF (n = 8). Trained animals underwent a RMT protocol (30 min/day, 5 day/wk, 6 wk of breathing through a resistor), whereas sedentary animals did not. In HF rats, RMT had significant effects on several parameters. It reduced left ventricular (LV) end-diastolic pressure (P < 0.01), increased LV systolic pressure (P < 0.01), and reduced right ventricular hypertrophy (P < 0.01) and pulmonary (P < 0.001) and hepatic (P < 0.001) congestion. It also decreased resting heart rate (HR; P < 0.05), indicating a decrease in the sympathetic and an increase in the vagal modulation of HR. There was also an increase in baroreflex gain (P < 0.05). The respiratory system resistance was reduced (P < 0.001), which was associated with the reduction in tissue resistance after RMT (P < 0.01). The respiratory system and tissue elastance (Est) were also reduced by RMT (P < 0.01 and P < 0.05, respectively). Additionally, the quasistatic Est was reduced after RMT (P < 0.01). These findings show that a 6-wk RMT protocol in HF rats promotes an improvement in hemodynamic function, sympathetic and vagal heart modulation, arterial BRS, and respiratory mechanics, all of which are benefits associated with improvements in cardiopulmonary interaction.

The Effect of NG-Nitro-L-Arginine Methyl Ester, a Nitric Oxide Synthase Inhibitor, on Respiratory Mechanics in Rats

Background: Data describing the inhibitory effects of nitric oxide synthase (NOS) on respiratory mechanics are conflicting, and no data are available concerning possible effects on the viscoelasticity of the respiratory system, on the inspiratory work of breathing (WOB) or on respiratory system hysteresis. Objectives: The aim of this study was to measure the effects of NOS inhibition by N^G-nitro-L-arginine methyl ester (L-NAME) on respiratory mechanics in normal anesthetized rats. Methods: Using the end-inflation occlusion method, it was possible to quantify the ohmic and viscoelastic airway resistance and elastance of the respiratory system. Ohmic resistance is the normalized-to-flow pressure dissipation due to viscous forces opposing the airflow in the airways, as predicted by the Poiseuille law. Viscoelastic resistance is the normalized-to-flow pressure dissipation due to the resistance of respiratory system tissue to deformation during inflation, which is recovered after the arrest of the inspiratory flow (stress relaxation). The inspiratory WOB, its elastic and resistive components, and hysteresis were also calculated. Results:L-NAME induced an increment in the ohmic airway resistance and in the resistive ohmic inspiratory WOB. The viscoelastic resistance due to stress relaxation and the elastic properties of the respiratory system were not modified, and no effect was detected on the related components of the inspiratory WOB and on hysteresis. Conclusions: NO acts in normal rats to reduce the ohmic component of airway resistance, decreasing the ohmic inspiratory WOB. The elastic and viscoelastic components are unaltered. Hysteresis is also unaltered, suggesting that NO has negligible effects on alveolar surfactant activity.

The effect of body warming on respiratory mechanics in rats

The temperature dependence of airway smooth muscle cells and alveolar surfactant activity, and of the elastin stress-strain relationship, suggests that body warming may affect respiratory mechanics in vivo, a possibility that has not yet been investigated. To examine this hypothesis, healthy rats were studied using the end-inflation occlusion method under control conditions and after an infrared lamp was used for body warming. Hysteresis areas, the inspiratory work of breathing, and its elastic and resistive components were also calculated. After body warming, static and dynamic elastance, ohmic airway resistance, mean value of hysteresis, the inspiratory work of breathing, and additional resistance due to pendelluft and stress relaxation were all decreased. These data suggest that body warming reduces the inspiratory work of breathing by improving the elastic and resistive mechanical properties of airways. This effect is evident even for limited temperature variations suggesting that it may occur in the event of spontaneous pathological conditions, such as fever.

The effect of experimental pleurodesis caused by aluminum hydroxide on lung and chest wall mechanics.

The aim of this study was to evaluate the effect of a chemical sclerosing agent, aluminum hydroxide, on pleural remodeling and on respiratory mechanics in rats. Saline (2 mL) or aluminum hydroxide [2 mL (0.15 g/mL)] was instilled intrapleurally in anesthetized male rats. The animals were studied 7 or 30 days after the instillation. Respiratory system, lung, and chest wall elastic, resistive, and viscoelastic/inhomogeneous pressures were measured by the end-inflation occlusion method. We studied the pleural remodeling process by means of semiquantitative analysis of the induced inflammation and quantitative analysis of the collagen extracellular matrix component. The effects on the underlying lung were analyzed morphometrically. Chest wall elastic and viscoelastic pressures increased after aluminum hydroxide instillation independent of time after instillation. Pleural inflammation was observed 7 days after instillation, while pleural adherence with a marked increase in the type I/type III collagen ratio was present 30 days after instillation. Histological examination demonstrated no differences in lung parenchyma among the groups. In conclusion, the present model describes the establishment of pleurodesis by aluminum hydroxide, which thwarts the normal chest wall mechanical profile without inducing any changes in the underlying lungs. The results were disclosed by both mechanical and morphological evaluation of the pleural remodeling.

Respiratory mechanics in rats anaesthetized with propofol

Respiratory mechanics in rats anaesthetized with propofol

Effects of prosthetic reconstruction of the abdominal wall on respiratory mechanics in rats

Respiratory mechanics and thoracoabdominal morphometry were determined in four sets of animal experiments before and after surgery. In group RRA the rectus abdominus muscles were removed; in RRAH rats the muscle resection was followed by lung hyperinflation; in PPM animals the defect was repaired by suturing a polypropylene mesh (Marlex ®); and in PPMH lung hyperinflation was performed after abdominal wall reconstruction. Lung and chest wall elastances, and chest wall viscoelastic/inhomogeneous pressures increased in RRA, RRAH and PPM groups. Static lung elastance was progressively smaller in the following order: RRA, PPM, and PPMH. In conclusion, removal of the rectus abdominus muscles and abdominal wall reconstruction could account for higher energy losses against viscoelastic and elastic forces acting on the chest wall, and these are related to a cephalad deviation of the diaphragm. Furthermore, hyperinflation reverses lung elastic modification after abdominal wall reconstruction with PPM, without beneficial effects in the presence of abdominal wall defect.

Effects of uni- and bilateral phrenicotomy on active and passive respiratory mechanics in rats

Eighteen spontaneously breathing anesthetized rats were selected to belong to three groups: control (C), unilateral (U), and bilateral phrenicotomy (B). Eight days after surgery, the passive and active mechanical properties of the respiratory system, the shape of the occlusion pressure wave, the decay of inspiratory muscle activity during expiration and control of breathing were analysed. Passive and active elastances increased significantly from C to U and from U to B. Passive and active time constants decreased either in uni- or bilateral phrenicotomies. Passive and active resistances remained unaltered. The intensity of respiratory drive increased from C to U and B. In conclusion, uni- and bilateral phrenicotomies increase the elastic load of the respiratory system, because of both its passive and active components, which raised the respiratory neuromuscular drive of the remaining muscles. Consequently, minute ventilation remained unchanged. The higher frequency was allowed for, by a shorter time constant of the respiratory system and by a faster decay of post-inspiratory muscle activity.