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RESEARCH PRODUCT
The Adult Sprague-Dawley Sugen-Hypoxia Rat Is Still "the One:" A Model of Group 1 Pulmonary Hypertension: Reply to Le Cras and Abman
Harm Jan BogaardXiao-qing SunKetul R ChaudharyMaximilian AckermannMaximilian AckermannDuncan J. StewartMark P. KühnelDanny JonigkGeorg HansmannEkaterina Legchenkosubject
Pulmonary and Respiratory MedicineEmphysema0303 health sciencesIndolesbusiness.industryHypertension PulmonaryHypoxia (medical)Critical Care and Intensive Care Medicinemedicine.diseasePulmonary hypertensionRatsSprague dawleyRats Sprague-Dawley03 medical and health sciences0302 clinical medicine030228 respiratory systemAnesthesiaCorrespondenceMedicineAnimalsPyrrolesmedicine.symptombusinessHypoxia030304 developmental biologydescription
To the editor: Kojonazarov et al. recently reported severe emphysema in the SU5416/Hypoxia (SuHx) rat model of pulmonary hypertension (1). The authors found that adult male Wistar Kyoto (WKY) rats had increased air-to-tissue ratio as judged by non-gated in vivo micro-computed tomography (CT), and an increased mean linear intercept (MLI) as surrogate of emphysema (1, 2). Le Cras and Abman now responded to the Kojonazarov report by underlining the “important role of the developmental timing of disrupted VEGF signaling” (3). They cite earlier studies conducted on the ovine fetus showing that VEGF inhibition caused vascular remodeling, reduction in vascular/airway growth, and neonatal pulmonary hypertension at birth (4). Although SU5416 is known to induce emphysema in rats housed in room air at Denver altitude (1609m altitude) (5, 6), we contended in our response letter (11) that, at least in male Sprague Dawley (SD) rats, the combination of VEGFR inhibition and hypoxia does not lead to any biologically relevant emphysema or other significant parenchymal lung disease (7) but to pulmonary arterial hypertension (PAH) due to severe angioproliferative remodeling (7, 8).
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2020-03-01 |