Impact of elevated water temperature and zatebradine-induced bradycardia on cardiovascular function in male and female rainbow trout


Meeting Abstract

P3.10  Saturday, Jan. 5  Impact of elevated water temperature and zatebradine-induced bradycardia on cardiovascular function in male and female rainbow trout. GAMPERL, A./Kurt**; SWAFFORD, Brenda/L; RODNICK, Kenneth/J; Memorial Univ. of Newfoundland; Idaho State Univ.; Idaho State Univ. rodnkenn@isu.edu

Questions still remain about the regulation of cardiovascular function in teleosts, including under what conditions and to what extent sex differences influence cardiac performance. This study examined the in vivo relationship between heart rate (FH), stroke volume (Vs) and cardiac output (Q) in sexually immature, rainbow trout Oncorhynchus mykiss: 1) when trout were challenged with an increase in water temperature from 14 to 24�C at 2�C/h; and 2) following a 50% reduction in FH at 24�C, achieved by the administration of the bradycardic agent zatebradine (total dose 2 mg/kg). All fish were fitted with Doppler flow probes around the ventral aorta for the recording of cardiac variables (FH, Vs and Q), and a dorsal aortic cannula for drug injection and blood pressure recording. In vivo FH increased in a linear fashion with temperature; from ~ 60 bpm at 14�C to ~ 130 bpm at 24�C in both males (n = 9) and females (n = 9). In contrast, Q peaked between 22 and 24�C, and the relative increase in Q was significantly greater in males [2.3 � 0.3 V (mean � SE) at 14�C versus 4.5 � 0.8 V at 24�C] as compared with females [2.0 � 0.2 V at 14�C versus 3.5 � 0.4 V at 24�C]. At 24�C, zatebradine treatment halved heart rate in both sexes, and yet Q was maintained within 10% of pretreatment values. Overall, these results: 1) indicate that sedentary male trout are better able to maintain stroke volume at high temperatures/heart rates than female trout, despite both sexes being capable of cardiac autoregulation; 2) support recent in vivo data for Atlantic cod challenging whether temperature and heart rate negatively influence teleost stroke volume/ventricular inotropy as has been shown in vitro. Supported by NSF grant IOB-517669.

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