CARDIOVASCULAR FUNCTION IN SALMO SALAR WITH INFECTIOUS SALMON ANAEMIA (ISA): PUTATIVE ROLE OF NITRIC OXIDE

• Main Author: Gattuso A
• Other Authors: The Pennsylvania State University CiteSeerX Archives
• Format: Text
• Language: English
• Subjects: Salmo salar
• Online Access: http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.493.1994; http://www-heb.pac.dfo-mpo.gc.ca/congress/2000/papers/cardiopdf/gattuso.pdf

In higher vertebrates, particulary in mammals, a depressed myocardial contraction during sepsis or exposure to bacterial endotoxin (EDTX) has been documented (Parrillo, 1993). Recent studies have shown that alterations in transduction pathways in cardiac myocytes during sepsis or after exposure to cytokines involve NO (Kelly et al., 1996). Under these conditions there is often an induction of a calcium-independent NO synthase (iNOS or NOS2), whose role could be important in the determination of myocardial dysfunction. One cardiac action of NO can be via the Starling mechanism, as shown in the isolated ejecting guinea pig heart, in which basal intracardiac production of NO increased preload-induced rises in cardiac output (Prendergast et al., 1997). Our aim was to investigate in ISA salmon the potential role of NO-transduction pathway in the determinism of cardiac dysfunction and to provide some information on the time course of heart dysfunction during the infection. We have studied the chronology of cardiac impairment from the time of the virus administration to the time of the typical pathological features at the peak of the desease. Salmon hearts (13 from control group and 30 from infected group) were isolated from specimens of Salmo salar (weighing 79,41 ±1,73 g; mean value ±S.E.M.) and connected to the perfusion apparatus. Experiments were carried out at