Early effects of right ventricular volume overload on ventricular performance and β-adrenergic signaling

Autor: Ashish S. Shah, R.Eric Lilly, B. Zane Atkins, Jonathan A. Hata, Walter J. Koch, Oliver Tai, Donald D. Glower, Alan P. Kypson
Jazyk: angličtina
Předmět:
Pulmonary and Respiratory Medicine
medicine.medical_specialty
Ventricular Dysfunction
Right

Hemodynamics
030204 cardiovascular system & hematology
Contractility
03 medical and health sciences
Dogs
0302 clinical medicine
Tricuspid Valve Insufficiency
GTP-Binding Proteins
Internal medicine
Receptors
Adrenergic
beta

Ventricular Pressure
medicine
Animals
Neuropeptide Y
cardiovascular diseases
Kinase activity
030304 developmental biology
Analysis of Variance
0303 health sciences
Tricuspid valve
biology
business.industry
Myocardium
Fissipedia
Stroke Volume
Stroke volume
biology.organism_classification
medicine.anatomical_structure
Endocrinology
Linear Models
Ventricular pressure
Cardiology
cardiovascular system
Surgery
business
Cardiology and Cardiovascular Medicine
Adenylyl Cyclases
Signal Transduction
Zdroj: The Journal of Thoracic and Cardiovascular Surgery. (2):342-349
ISSN: 0022-5223
DOI: 10.1067/mtc.2000.107278
Popis: Objective: Right ventricular dysfunction is a poorly understood but persistent clinical problem. This study was undertaken to evaluate ventricular performance and β-adrenergic receptor signaling in a tricuspid regurgitation model of right ventricular overload. Methods: Seventeen dogs were chronically instrumented with epicardial dimension transducers. By means of the shell-subtraction model, right ventricular pressure-volume relationships were evaluated in normal and right ventricular overload states. Right ventricular chamber performance was quantified by the stroke work at an end-diastolic volume relationship. Results: Right ventricular volume overload caused a 28% ± 11% and 31% ± 9% decline in chamber performance acutely and at 1 week, respectively, whereas end-diastolic volume increased from 45 ± 21 to 60 ± 30 mL ( P =.019). β-Adrenergic receptor signaling in myocardial samples was assessed, examining adenylyl cyclase and G-protein–coupled receptor kinase activity. Stimulated adenylyl cyclase activity significantly decreased, and G-protein–coupled receptor kinase activity significantly increased in both left and right ventricular samples caused by increased levels of β-adrenergic receptor kinase 1. No change in β-adrenergic receptor density was seen at 1 week. Conclusions: Early right ventricular overload is associated with impaired right ventricular chamber contractility, dilation, and, importantly, a biventricular alteration of β-adrenergic receptor signaling. (J Thorac Cardiovasc Surg 2000;119:342-9)
Databáze: OpenAIRE