Diaphragm hyperaemia and regional blood flow distribution are impaired with ageing, potentially consequent to altered vascular structure and/or diminished vasomotor function. Evidence from locomotory skeletal muscle suggests that age-related diaphragm vasomotor dysfunction may be related to a blunted endothelium-mediated vasodilatation, decreased nitric oxide (NO) bioavailability and/or augmented reactive oxygen species (ROS) generation. We hypothesized that, in the medial costal diaphragm with old age, there would be fewer feed arteries (FAs) and impaired vasomotor function, via endothelium-specific mechanisms, in first-order (1A) arterioles.
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