1. Pulmonary hypertension impairs vasomotor function in rat diaphragm arterioles.
- Author
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Schulze KM, Horn AG, Muller-Delp JM, White ZJ, Hall SE, Medarev SL, Weber RE, Poole DC, Musch TI, and Behnke BJ
- Subjects
- Animals, Female, Arterioles physiopathology, Disease Models, Animal, Vasodilator Agents pharmacology, Endothelium, Vascular physiopathology, Vasoconstriction, Monocrotaline toxicity, Rats, Rats, Sprague-Dawley, Vasodilation, Hypertension, Pulmonary physiopathology, Hypertension, Pulmonary chemically induced, Hypertension, Pulmonary etiology, Diaphragm physiopathology, Diaphragm blood supply
- Abstract
Pulmonary hypertension (PH) is a chronic, progressive condition in which respiratory muscle dysfunction is a primary contributor to exercise intolerance and dyspnea in patients. Contractile function, blood flow distribution, and the hyperemic response are altered in the diaphragm with PH, and we sought to determine whether this may be attributed, in part, to impaired vasoreactivity of the resistance vasculature. We hypothesized that there would be blunted endothelium-dependent vasodilation and impaired myogenic responsiveness in arterioles from the diaphragm of PH rats. Female Sprague-Dawley rats were randomized into healthy control (HC, n = 9) and monocrotaline-induced PH rats (MCT, n = 9). Endothelium-dependent and -independent vasodilation and myogenic responses were assessed in first-order arterioles (1As) from the medial costal diaphragm in vitro. There was a significant reduction in endothelium-dependent (via acetylcholine; HC, 78 ± 15% vs. MCT, 47 ± 17%; P < 0.05) and -independent (via sodium nitroprusside; HC, 89 ± 10% vs. MCT, 66 ± 10%; P < 0.05) vasodilation in 1As from MCT rats. MCT-induced PH also diminished myogenic constriction (P < 0.05) but did not alter passive pressure responses. The diaphragmatic weakness, impaired hyperemia, and blood flow redistribution associated with PH may be due, in part, to diaphragm vascular dysfunction and thus compromised oxygen delivery which occurs through both endothelium-dependent and -independent mechanisms., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)
- Published
- 2024
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