title: Increased systemic vascular resistance in Atlantic salmon, Salmo salar L., affected with amoebic gill disease.
abstract: Previous investigations into the pathophysiology of amoebic gill disease (AGD) have suggested that there are probable cardiovascular effects associated with this disease. In the present study Atlantic salmon, Salmo salar L., were experimentally infected by cohabitation with diseased individuals. Two commonly used vasodilators, sodium nitroprusside (SNP) and captopril, the angiotensin-converting enzyme (ACE) inhibitor, were used as tools to investigate possible vasoconstriction and/or renin-angiotensin system (RAS) dysfunction in AGD-affected animals. Within the SNP trial, results showed that AGD-affected fish exhibited lowered cardiac output (Q), lowered cardiac stroke volume (V(S)) and a significantly elevated systemic vascular resistance (R(S)) compared with non-affected naïve counterparts. These effects were totally abolished following SNP administration (40 microg kg(-1)), however significant cardiovascular effects associated with SNP were not observed. Within the captopril trial, where AGD-affected fish were more diseased compared with the SNP trial, a significant hypertension was observed in AGD-affected fish. Captopril administration (10(-4) mol L(-1) at 1 mL kg(-1)) resulted in a significant drop in dorsal aortic pressure (P(DA)) for both AGD-affected and naïve control fish. In terms of peak individual responses, captopril administration effectively lowered P(DA) in both AGD-affected and naïve control groups equally. The drop in P(DA) following SNP administration however was significantly greater in AGD-affected fish potentially suggesting disease-related vasoconstriction. The lack of significant cardiovascular effects directly associated with both SNP and captopril administrations possibly relate to the 6 h recovery period following surgical procedures. However, while variable, these results do suggest that there are significant cardiovascular effects including vasoconstriction and hypertension associated with AGD.
authors.affiliation: School of Aquaculture, Tasmanian Aquaculture and Fisheries Institute and Cooperative Research Centre for Sustainable Aquaculture of Finfish, University of Tasmania, Launceston, Tasmania, Australia.
authors.forename: M J
authors.initials: MJ
authors.lastname: Leef
authors.forename: J V
authors.initials: JV
authors.lastname: Hill
authors.forename: J O
authors.initials: JO
authors.lastname: Harris
authors.forename: M D
authors.initials: MD
authors.lastname: Powell
mesh_terms: D000562:Amebiasis / Q000469:parasitology / Q000503:physiopathology / Q000662:veterinary*; D016841:Amoebida / Q000472:pathogenicity; D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001774:Blood Chemical Analysis; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000008:administration & dosage / Q000494:pharmacology; D002302:Cardiac Output / Q000187:drug effects; D002319:Cardiovascular System / Q000187:drug effects / Q000503:physiopathology; D005393:Fish Diseases / Q000469:parasitology / Q000503:physiopathology*; D005398:Fisheries; D005880:Gills / Q000469:parasitology*; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology; D020317:Salmo salar / Q000469:parasitology*; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D002216:Captopril