Early inflammatory response during the development of right ventricular heart failure in a rat model.
OBJECTIVE
Inflammatory activation plays an important role in the pathogenesis and progression of left ventricular (LV) heart failure. In right ventricular (RV) heart failure, little is known about the role of inflammatory activation. We aimed to study the role of inflammatory activation in RV heart failure by serial monitoring during disease progression.


RESULTS
Right ventricular heart failure was induced in male Wistar rats by intraperitoneal injection of monocrotaline (MCT). Two groups were studied: MCT-treated rats (MCT-rats), and age-matched controls (CON-rats). Serial echocardiography and in vivo 67-Gallium ((67)Ga) scintigraphy were performed. Local inflammation in the RV was assessed by (i) ex vivo semi-quantitative (67)Ga autoradiography, (ii) immunohistochemistry of myeloperoxidase (MPO), a marker of neutrophil activity, and (iii) mRNA assays of tumour necrosis factor-alpha (TNF-alpha). In MCT-rats, (67)Ga scintigraphy showed increased myocardial uptake which started during the early stages of RV disease. (67)Ga autoradiography revealed that this increased (67)Ga uptake occurred in the RV and inter-ventricular septum, but not in the LV. The stage-dependent increases of in vivo (67)Ga RV myocardial uptake were paralleled by increases in mRNA gene expression for TNF-alpha in RV, and increased MPO staining in RV.


CONCLUSIONS
Development and progression of RV heart failure is associated with an early increase in RV inflammation. (67)Ga scintigraphy may be used for the serial assessment of inflammation and monitoring of disease progression in RV heart failure.
Campian
Maria E
ME
Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Meibergdreef 9, Amsterdam 1105 AZ, The Netherlands.
Hardziyenka
Maxim
M
de Bruin
Kora
K
van Eck-Smit
Berthe L F
BL
de Bakker
Jacques M T
JM
Verberne
Hein J
HJ
Tan
Hanno L
HL
D000818:Animals; D001345:Autoradiography; D004195:Disease Models, Animal; D018450:Disease Progression; D005710:Gallium Radioisotopes; D020869:Gene Expression Profiling; D006333:Heart Failure / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D017380:Hypertrophy, Right Ventricular / Q000097:blood; D007120:Immunochemistry; D007249:Inflammation / Q000209:etiology*; D008297:Male; D016686:Monocrotaline / Q000009:adverse effects; D009206:Myocardium / Q000378:metabolism; D018375:Neutrophil Activation / Q000502:physiology; D009195:Peroxidase / Q000378:metabolism; D011877:Radionuclide Imaging; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D018497:Ventricular Dysfunction, Right / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging
D005710:Gallium Radioisotopes; D014409:Tumor Necrosis Factor-alpha; D016686:Monocrotaline; D009195:Peroxidase