Bulk and Regional Diaphragm Blood Flow during Chemical Hyperpnea in Pulmonary Hypertensive Rats
Introduction: Pulmonary hypertension (PH) is a disease characterized by increased pulmonary arterial pressures, impaired gas exchange, dyspnea, and diaphragmatic dysfunction. Specifically, in PH, the diaphragm displays impaired contractility, vascular dysfunction, and blood flow redistribution toward less mechanically advantageous regions such as the ventral costal and crural diaphragm at rest and during submaximal exercise. While diaphragm blood flow is not a limitation to maximal exercise in health, whether it limits diaphragm function in PH is unknown. We hypothesize that, during chemically induced hyperpnea:1) diaphragm blood flow will be lower in PH rats compared with healthy controls due to vasodilatory impairments in the diaphragm vasculature, and 2) in PH, blood flow will be redistributed toward less mechanically advantageous regions of the diaphragm. Methods: Female Sprague-Dawley rats were randomized into healthy or monocrotaline-induced PH groups. Fluorescent microspheres were used to determine bulk and regional diaphragm blood flow at rest and during hypoxic-hypercapnic gas inhalation (10% O 2 -8% CO 2 ). RESULTS AND CONCLUSIONS: Our results demonstrate that, during chemically-induced hyperpnea, diaphragm blood flow was higher in PH compared with healthy controls (483 ± 39 vs. 360 ± 72 ml/min/100g; P=0.025), and that less efficient regions of the diaphragm (ventral costal and crural) supported greater perfusion in PH. These results are consistent with previous findings at rest and during submaximal exercise in PH, which may help explain diaphragmatic weakness and dyspnea across a range of ventilatory demands in PH. National Institute on Aging 1R15AG078060 (BJB and DCP) NIH NHLBI Ruth L. Kirschstein National Research Service Awards 1F31HL167618-02 (AGH) and 1F31HL170643-02 (KMS) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Authors
- David C. Poole (ORCID: https://orcid.org/0000-0003-2441-3793)
- Kiana M. Schulze (ORCID: https://orcid.org/0000-0001-6467-5179)
- Bradley J. Behnke (ORCID: https://orcid.org/0000-0002-8928-928X)
- Andrew G. Horn (ORCID: https://orcid.org/0000-0003-4435-4022)
- Timothy I. Musch (ORCID: https://orcid.org/0000-0003-1599-1751)
- Ramona E. Weber (ORCID: https://orcid.org/0000-0001-5110-270X)
- Carl J. Ade (ORCID: https://orcid.org/0000-0002-1837-2342)
- Britton Scheuermann
Institutions
- Kansas State University (US)
Publication Details
- Journal
- Physiology
- Published
- 2025-05-01
- DOI
- https://doi.org/10.1152/physiol.2025.40.s1.1656
- Primary Topic
- Neuroscience of respiration and sleep
- Type
- article
- Field-Weighted Citation Impact
- 0.00