Simple model of pulmonary hypertension secondary to left heart pressure overload induced by partial intravascular occlusion of the ascending aorta
Language English Country United States Media print-electronic
Document type Journal Article
Grant support
13-01710S
Grantová Agentura České Republiky (GAČR)
17-11223S
Grantová Agentura České Republiky (GAČR)
210216
Grantová Agentura, Univerzita Karlova (GA UK)
- Keywords
- group 2 pulmonary hypertension, heart failure with preserved ejection fraction, left ventricle pressure overload, pulmonary hypertension due to left heart disease, rat model,
- MeSH
- Aorta * physiopathology pathology MeSH
- Pulmonary Artery physiopathology pathology MeSH
- Vascular Resistance MeSH
- Hypertrophy, Right Ventricular physiopathology etiology MeSH
- Rats MeSH
- Disease Models, Animal * MeSH
- Hypertension, Pulmonary * physiopathology etiology MeSH
- Rats, Sprague-Dawley MeSH
- Rats, Wistar MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Pulmonary hypertension is a group of diseases characterized by elevated pulmonary artery pressure and pulmonary vascular resistance with significant morbidity and mortality. The most prevalent type is pulmonary hypertension secondary to left heart disease (PH-LHD). The available experimental models of PH-LHD use partial pulmonary clamping by technically nontrivial open-chest surgery with lengthy recovery. We present a simple model in which the reduction of the cross-sectional area of the ascending aorta is achieved not by external clamping but by partial intravascular obstruction without opening the chest. In anesthetized rats, a blind polyethylene tubing was advanced from the right carotid artery to just above the aortic valve. The procedure is quick and easy to learn. Three weeks after the procedure, left heart pressure overload was confirmed by measuring left ventricular end-diastolic pressure by puncture (1.3 ± 0.2 vs. 0.4 ± 0.3 mmHg in controls, mean ± SD, P < 0.0001). The presence of pulmonary hypertension was documented by measuring pulmonary artery pressure by catheterization (22.3 ± 2.3 vs. 16.9 ± 2.7 mmHg, P = 0.0282) and by detecting right ventricular hypertrophy and increased muscularization of peripheral pulmonary vessels. Contributions of a precapillary vascular segment and vasoconstriction to the increased pulmonary vascular resistance were demonstrated, respectively, by arterial occlusion technique and by normalization of resistance by a vasodilator, sodium nitroprusside, in isolated lungs. These changes were comparable, but not additive, to those induced by an established pulmonary hypertension model, chronic hypoxic exposure. Intravascular partial aortic obstruction offers an easy model of pulmonary hypertension induced by left heart disease that has a vasoconstrictor and precapillary component.NEW & NOTEWORTHY We present a new, simple model of a clinically important type of pulmonary hypertension, that induced by left heart failure. Left ventricular pressure overload is induced in rats by inserting a blinded cannula into the ascending aorta via carotid artery access. This partial intravascular aortic obstruction, which does not require opening of the chest and prolonged recovery, causes pulmonary hypertension, which has a precapillary and vasoconstrictor as well as a vascular remodeling component.
Department of Cardiology Na Homolce Hospital Prague Czech Republic
Department of Pathophysiology 2nd Faculty of Medicine Charles University Prague Czech Republic
Department of Physiology 2nd Faculty of Medicine Charles University Prague Czech Republic
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