Key result
Pulmonary hypertension in a rat model impairs muscle oxygenation during the rest-to-contractions transition.
Why the study?
To investigate whether peripheral skeletal muscle aberrations in oxygen delivery-to-utilization matching and vascular control contribute to exercise intolerance in pulmonary hypertension, and whether nitric oxide attenuates these decrements.
Does pulmonary hypertension impair skeletal muscle oxygen delivery-to-utilization matching during contractions in a rat model?
Population
21 male Sprague-Dawley rats administered monocrotaline to induce pulmonary hypertension, compared with healthy controls
Comparison
MCT-induced pulmonary hypertension vs healthy controls under control (SNP-) and NO-donor (SNP+) conditions
Design
Preclinical animal study
Authors
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Peripheral dysfunction may contribute to PH exercise intolerance; leaves open human translation.
Does pulmonary hypertension impair skeletal muscle oxygen delivery-to-utilization matching during contractions in a rat model?
p-value: p=<0.05
In a rat model of pulmonary hypertension, skeletal muscle oxygenation is impaired during the rest-to-contractions transition, suggesting peripheral vascular dysfunction contributes to exercise intolerance.
Schulze et al. (2021) studied Pulmonary hypertension (n=21). Monocrotaline (MCT) and sodium nitroprusside (SNP) vs. Healthy controls was evaluated on O2 partial pressure in the interstitial space in the spinotrapezius muscle at rest and during contractions (p=<0.05). In a rat model of pulmonary hypertension, muscle oxygenation was significantly impaired across the rest-to-contractions transition compared to healthy controls (P<0.05).
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