S169Abstracts / Comparative Biochemistry and Physiology, Part A 146 (2007) S165–S170

indicated that this control is of central importance indetermining seasonal changes in metabolic rate.

doi:10.1016/j.cbpa.2007.01.353

A11.12Seasonal acclimation in cardiac activity: Mammals vs. fish

S. Egginton, D. Hauton, H. Campbell, S. May, S. Young,(University of Birmingham)

The dominance of vagal tonus over cardiac sympathetic tone isaccentuated on acute cold exposure of mammals to a coretemperature of 25 °C, leading to a bradycardia appropriate forthe reduction in metabolic rate. When investigated by PowerSpectral Analysis, changes in heart rate variability (HRV) canbe seen as a decrease in the ratio of low frequency to highfrequency (LF:HF) power in rats. In hamsters this only occursafter a period of cold acclimation to an environmentaltemperature of 4 °C, whilst maintaining core temperature.Interestingly, despite ∼30% cardiac hypertrophy on chroniccold exposure, the power output of acclimated hamster hearts(either rate-pressure product, or dP/dt) is less than those fromeuthermic controls, although less temperature-sensitive. Accli-mation of common carp to similar environmental temperaturesleads to a commensurate drop in core temperature, with asimilar degree of cardiac hypertrophy. In this case, heart ratevaried directly with oxygen consumption, although HRdecreased and HRV increased in a non-linear manner between25 and 5 °C on chronic exposure. Interestingly, acute changes intemperature resulted in a decrease in vagal tone on warming, butno significant change on cooling. Pharmacological blockadeshows both chronic and acute responses to be dominated bycholinergic influences, with little role for adrenergic control.Supported by NERC.

doi:10.1016/j.cbpa.2007.01.354

A11.13Cold-induced cardiac hypertrophy does not preservecardiac performance

D. Hauton, S. Egginton, (University of Birmingham)

Cold acclimation of Golden hamsters led to cardiac hyper-trophy. Acute cold (25 °C) exposure of unpaced Langendorff-perfused hearts led to a decrease in heart rate (P<0.001) and forcontrol hearts led to a significant decrease in systolic pressure(P<0.01). Cold acclimation to 4 °C was without affect on heartrate for hearts perfused at either 25 °C or 37 °C. However, coldacclimation led to a preservation of systolic pressures followingacute cold exposure, whereas control hearts showed asignificant decrease in systolic pressure (P<0.01). For bothcontrol and cold-adapted hearts diastolic function was preservedwhen perfused at both 25 °C and 37 °C. Estimation of peak dP/

dt for cold-acclimated hearts revealed that cold-inducedhypertrophy led to a 75% reduction in dP/dt at both 25 °C(P<0.01) and 37 °C (P<0.01) when compared with controlhearts. Corresponding significant changes were also noted forrate-pressure product estimations. Interestingly, for coldacclimated hearts peak dP/dt and rate-pressure product wasachieved at double the ventricle volume recorded for controlhearts. Acute hypothermia led to a ∼66% decrease in coronaryflow for perfused control hearts, however, for cold-acclimatedhearts coronary flow was preserved under hypothermicconditions. These data indicate that cold acclimation of thehibernator heart may result in the preservation of developedpressures by the heart under hypothermic conditions, althoughthese hearts show poor contractile performance when comparedto control hearts. This may have implications for the transitionfrom hibernation to arousal.

doi:10.1016/j.cbpa.2007.01.355

A11.14Temperature acclimation modifies sinatrial pacemakermechanism of the trout heart

J. Haverinen, M. Vornanen, (University of Joensuu)

Acclimation to cold increases basal heart rate in rainbow trout(Oncorhynchus mykiss). This study tests the hypothesis thatthermal acclimation modifies pacemaker mechanism of the troutheart. To this end, action potentials (AP) were recorded in intactsinoatrial tissue and enzymatically isolated pacemaker cells oftrout acclimated at 4 °C (cold-acclimated, c.a.) or 18 °C (warm-acclimated, w.a.). With electrophysiological recordings theprimary pacemaker was located at the base of the sinoatrialvalve, and histological examination indicated a morphologicallydistinct ring of nodal tissue in this location. Intrinsic rate (APs/min) of the pacemaker was higher in c.a. (46±6) thanw.a. (38±3)(p<0.05) trout at 11 °C, and a similar difference was found inisolated pacemaker cells (44±6 vs. 38±6) (p<0.05). Inhibition ofsarcoplasmic reticulum (SR) with 10 μM ryanodine and 1 μMthapsigargin did not effect heart rate in either w.a. or c.a. trout.Half-maximal blockade of the delayed rectifier potassium current(IKr) with 0.1 μM E-4031 reduced heart rate more in w.a. (from45±1 to 24±5) than c.a. trout (from 56±3 to 48±2) (p<0.05).These findings indicate that thermal acclimation modifies pace-maker mechanism of the trout heart, and suggest that cold-induced increase in heart rate is at least partly due to high densityof the IKr in the c.a. trout, while contribution of SRCa2+ release tothermal compensation of heart rate is negligible.

doi:10.1016/j.cbpa.2007.01.356

A11.15Increased PRPC expression in human carotid artery lesions

P. Ethirajan, (Manchester Metropolitan University)