Novel Porcine Model of Acute Severe Cardiogenic Shock Developed by Upper-Body Hypoxia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023884%3A_____%2F16%3A%230007010" target="_blank" >RIV/00023884:_____/16:#0007010 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68407700:21460/16:00305992 RIV/00216208:11110/16:10329184

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Novel Porcine Model of Acute Severe Cardiogenic Shock Developed by Upper-Body Hypoxia

Popis výsledku v původním jazyce

Despite the urgent need for experimental research in the field of acute heart failure and, particularly cardiogenic shock, currently there are only limited options in large animal models enabling research using devices applied to human subjects. The majority of available models are either associated with an unacceptably high rate of acute mortality or are incapable of developing sufficient severity of acute heart failure. The objective of our research was to develop a novel large animal model of acute severe cardiogenic shock. Advanced left ventricular dysfunction was induced by global myocardial hypoxia by perfusing the upper body (including coronary arteries) with deoxygenated venous blood. The model was tested in 12 pigs: cardiogenic shock with signs of tissue hypoxia developed in all animals with no acute mortality. Cardiac output decreased from a mean ( SD) of 6.61 1.14 l/min to 2.75 0.63 l/min, stroke volume from 79.7 9.8 ml to 25.3 7.8 ml and left ventricular ejection fraction from 61.2 4.3 % to 17.7 4.8 % (P 0.001 for all comparisons). In conclusion, the porcine model of acute cardiogenic shock developed in the present study may provide a basis for studying severe left ventricular dysfunction, low cardiac output and hypotension in large animals. The global myocardial hypoxia responsible for the decrease in cardiac contractility was not associated with acute death in this model.

Název v anglickém jazyce

Novel Porcine Model of Acute Severe Cardiogenic Shock Developed by Upper-Body Hypoxia

Popis výsledku anglicky

Despite the urgent need for experimental research in the field of acute heart failure and, particularly cardiogenic shock, currently there are only limited options in large animal models enabling research using devices applied to human subjects. The majority of available models are either associated with an unacceptably high rate of acute mortality or are incapable of developing sufficient severity of acute heart failure. The objective of our research was to develop a novel large animal model of acute severe cardiogenic shock. Advanced left ventricular dysfunction was induced by global myocardial hypoxia by perfusing the upper body (including coronary arteries) with deoxygenated venous blood. The model was tested in 12 pigs: cardiogenic shock with signs of tissue hypoxia developed in all animals with no acute mortality. Cardiac output decreased from a mean ( SD) of 6.61 1.14 l/min to 2.75 0.63 l/min, stroke volume from 79.7 9.8 ml to 25.3 7.8 ml and left ventricular ejection fraction from 61.2 4.3 % to 17.7 4.8 % (P 0.001 for all comparisons). In conclusion, the porcine model of acute cardiogenic shock developed in the present study may provide a basis for studying severe left ventricular dysfunction, low cardiac output and hypotension in large animals. The global myocardial hypoxia responsible for the decrease in cardiac contractility was not associated with acute death in this model.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FA - Kardiovaskulární nemoci včetně kardiochirurgie

OECD FORD obor

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Projekt

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Návaznosti

N - Vyzkumna aktivita podporovana z neverejnych zdroju

Rok uplatnění

2016

Kód důvěrnosti údajů

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

Název periodika

Physiological Research

ISSN

0862-8408

e-ISSN

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Svazek periodika

65

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

5

Strana od-do

711-715

Kód UT WoS článku

000386685600018

EID výsledku v databázi Scopus

2-s2.0-84997531320