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

Result code in 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>

Alternative codes found

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

Result on the web

<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>

Result language

angličtina

Original language name

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

Original language description

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.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30105 - Physiology (including cytology)

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

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

Publication year

2024

Confidentiality

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

Name of the periodical

American Journal of Physiology - Lung Cellular and Molecular Physiology

ISSN

1040-0605

e-ISSN

1522-1504

Volume of the periodical

327

Issue of the periodical within the volume

3

Country of publishing house

US - UNITED STATES

Number of pages

11

Pages from-to

"L371"-"L381"

UT code for WoS article

001313860400004

EID of the result in the Scopus database

2-s2.0-85203204319