Simple model of pulmonary hypertension secondary to left heart pressure overload induced by partial intravascular occlusion of the ascending aorta

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F24%3A10481962" target="_blank" >RIV/00216208:11130/24:10481962 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/24:10481962 RIV/00023884:_____/24:00009854

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=q~FRMGOPQx" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=q~FRMGOPQx</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1152/ajplung.00243.2023" target="_blank" >10.1152/ajplung.00243.2023</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Simple model of pulmonary hypertension secondary to left heart pressure overload induced by partial intravascular occlusion of the ascending aorta

Popis výsledku v původním jazyce

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 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&lt;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 precapillary vascular segment and of 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.

Název v anglickém jazyce

Simple model of pulmonary hypertension secondary to left heart pressure overload induced by partial intravascular occlusion of the ascending aorta

Popis výsledku anglicky

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 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&lt;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 precapillary vascular segment and of 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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2024

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

American Journal of Physiology - Lung Cellular and Molecular Physiology

ISSN

1040-0605

e-ISSN

1522-1504

Svazek periodika

327

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

"L371"-"L381"

Kód UT WoS článku

001313860400004

EID výsledku v databázi Scopus

2-s2.0-85203204319