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Vida, Vladimiro (2008) The effects of basic-FGF in an animal model of acute mechanically induced right ventricular hypertrophy. [Tesi di dottorato]

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Abstract (inglese)

Introduction
Several studies have been conducted to analyse the morphological and physiological causes of the systemic right ventricle failure in patients with corrected transposition of the great arteries of in patients with complete transposition of the great arteries who underwent an atrial switch procedure (according to Mustard or Senning). Even if an impaired myocardial flow reserve of the right ventricle has been advocated as the possible cause for myocardial failure, the definitive and true history of the right ventricle supporting systemic pressure in humans is not as yet known, and very few is its structural adaptation to the new workload
In a previous study, we have created an animal model of acute increased after-load of the right ventricle by banding the main pulmonary trunk we showed a significant increase of the RV interstitial fibrosis together with a decreased micro-vascular density.
With this concept in mind we hypothized that increasing the vascular support to the right ventricular myocardium, by a continuous infusion of basic fibroblast growth factor, during induced ventricular hypertrophy could probably modify the myocardial adaptation to the increased workload hampering the development of interstitial fibrosis.
Methods
A rat model of mechanical-induced right ventricle (RV) hypertrophy was used in this study. Pressure-overload hypertrophy was achieved by banding the main pulmonary artery in 10 week-old Lewis/HanHsd rats and was maintained for 30 days. Some of the rats had also an additional implantation of an osmotic pump that released basic Fibroblastic Growth Factor for during the banding. Once the hearts were harvested, they were weighed and processed to evaluate right ventricular: 1) free wall thickness, 2) myocyte diameter, 3) percentage of RV interstitial fibrosis and 4) capillary density.
Results
Seventeen rats were considered for the analysis including: 1) rats who underwent pulmonary artery banding group (PAB), 2) rats who underwent pulmonary artery banding and continuous infusion of bFGF (PAB-bFGF), 3) rats who underwent sham operation (SO), 4) rats who underwent sham operation and continuous infusion of bFGF (SO-bFGF).
The RV free wall thickness was significantly increased in PAB and PAB-bFGF rats if compared to SO rats. There was no significant increase of RV thickness between PAB and PAB-bFGF rats and also between SO and SO-bFGF rats.
The myocyte diameter was significantly higher in PAB-bFGF rats if compared to PAB rats, SO and SO-bFGF rats. No difference was detected between PAB-bFGF rats and both sham operated groups.
The percentage of interstitial fibrosis was significantly higher in PAB rats if compared to PAB-bFGF, SO and S0-bFGF rats. However also in PAB-bFGF rats the percentage of fibrosis was significantly higher than SO and SO-bFGF rats. No pathological fibrosis has been detected in SO and SO-bFGF rats.
The number of capillaries per 100 ?m2 was significantly higher in PAB-bFGF rats if compared to PAB rats. However the capillary density in PAB-bFGF was still lower than in SO rats.
Of note that the number of capillaries per 100 ?m2 was also significantly higher in SO-bFGF rats if compared to SO rats. This data showed the effects of bFGF also in normal heart tissue.
Conclusion
This experimental study demonstrates that subcutaneous infusion with osmotic pumps is a valid and reproducible method to deliver bFGF to heart tissue. The bFGF increases the vascular support to right ventricular myocardium, reducing the degree of interstitial fibrosis and the degree of compensatory hyperthrophy.

Abstract (italiano)

Introduzione
Vari studi sono stati realizzati per analizzare le cause fisiologiche e morfologiche dello scompenso del ventricolo destro in posizione sistemica in pazienti affetti da cardiopatie complesse come la trasposizione corretta delle grandi arterie o da trasposizione completa delle grandi arterie dopo intervento di correzione fisiologica d’inversione atriale (secondo Mustard o Senning). Anche se è stato ipotizzato che la scarsa riserva vascolare miocardica possa essere la causa dello scompenso ventricolare destro, la vera storia naturale di un ventricolo destro che supporta la circolazione sanguigna sistemica negli esseri umani non è ancora ben conosciuta e ancor meno lo è il suo adattamento strutturale all’incremento di lavoro.
In uno studio precedente, dove è stato creato un modello animale di sovraccarico acuto del ventricolo destro mediante un bendaggio dell’arteria polmonare media, si è visto che vi era un significativo aumento della fibrosi interstiziale accompagnato da una diminuita densità capillare.
Partendo da questo presupposto, abbiamo ipotizzato che aumentando il supporto vascolare al miocardio ventricolare, mediante un’infusione continua di basic growth factor, durante un periodo di induzione dell’ipertrofia ventricolare, avremmo potuto modificare la risposta adattativa del miocardio all’aumentato post-carico, prevenendo la formazione di fibrosi interstiziale.
Materiali e Metodi
Per lo studio è stato utilizzato un modello di ipertrofia meccanicamente indotta del ventricolo destro. Il sovraccarico acuto del ventricolo destro è stato ottenuto mediante un bendaggio dell’arteria polmonare in ratti Lewis/HanHsd di 10 settimane ed è stato mantenuto per 30 giorni. Alcuni degli animali hanno ricevuto anche l’impianto di una pompetta osmotica per il rilascio continuo di basic Fibroblastic Growth Factor (bFGF) durante il periodo del bendaggio. Una volta prelevati, i cuori sono stati pesati e processati per valutare a livello del ventricolo destro: 1) lo spessore parietale, 2) il diametro miocitario, 3) la percentuale di fibrosi e 4) la densità capillare.
Risultati
Diciassette ratti sono stati valutati nello studio includendo: 1) ratti che hanno ricevuto il bendaggio dell’arteria polmonare (PAB), 2) ratti che hanno ricevuto il bendaggio dell’arteria polmonare e infusione continua di bFGF (PAB-bFGF), 3) ratti “sham operated” (SO)(ovvero ratti sottoposti alla stessa procedura chirurgica dei ratti PAB, tranne che per il bendaggio), 4) ratti “sham operated” infusione continua di bFGF (PAB-bFGF).
Lo spessore della parete libera del ventricolo destro era incrementato nei ratti PAB e PAB-bFGF se comparati ai ratti SO. Non c’è stata una diversità significativa di aumento dello spessore della parete del ventricolo destro tra ratti PAB e PAB-bFGF, e anche tra ratti SO e SO-bFGF.
Il diametro miocitario era significativamente maggiore in ratti PAB-bFGF se comparati a ratti PAB, SO e SO-bFGF. Non vi era differenza tra ratti PAB-bFGF ed entrambi i gruppi di ratti SO.
La percentuale di fibrosi era significativamente aumenta nei ratti PAB se comparati ai ratti PAB-bFGF, SO e S0-bFGF. Tuttavia, anche nei ratti PAB-bFGF la percentuale di fibrosi era significativamente più alta anche nei ratti SO e SO-bFGF. Non vi era una percentuale patologica di fibrosi nei ratti SO e SO-bFGF rats.
Il numero di capillari per 100 ?m2 era significativamente più alto nei ratti PAB-bFGF se comparati ai ratti PAB. Tuttavia la densità capillare era più bassa nei ratti PAB-bFGF rispetto ai ratti normali. Da notare che il numero di capillari 100 ?m2 era più alto anche nei ratti SO-bFGF se comparati ai ratti SO, evidenziando l’effetto del bFGF anche su tessuto cardiaco normale.
Conclusioni
Questo studio sperimentale ha evidenziato che l’infusione sottocutanea mediante pompette osmotiche è una metodologia valida e riproducibile per infondere bFGF con target il tessuto cardiaco. Il bFGF aumenta il supporto vascolare al miocardio ventricolare destro, riducendo il grado di fibrosi interstiziale e la risposta ipertrofica compensatoria.

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Tipo di EPrint:Tesi di dottorato
Relatore:Gaetano, Thiene
Correlatore:Giovanni, Stellin
Dottorato (corsi e scuole):Ciclo 21 > Scuole per il 21simo ciclo > SCIENZE MEDICHE, CLINICHE E SPERIMENTALI > SCIENZE CARDIOVASCOLARI
Data di deposito della tesi:31 Gennaio 2009
Anno di Pubblicazione:2008
Parole chiave (italiano / inglese):right ventricular hypertrophy fibroblatic growth factor acute mechanical ventricular overload
Settori scientifico-disciplinari MIUR:Area 06 - Scienze mediche > MED/11 Malattie dell'apparato cardiovascolare
Struttura di riferimento:Dipartimenti > pre 2012 - Dipartimento di Scienze Medico Diagnostiche e Terapie Speciali
Codice ID:1833
Depositato il:31 Gen 2009
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