MECHANICAL PERFORMANCE OF AN IN SITU PERFUSED HEART FROM THE TURTLE CHRYSEMYS SCRIPTA DURING NORMOXIA AND ANOXIA AT 5 C AND 15 C

1994 ◽  
Vol 191 (1) ◽  
pp. 207-229 ◽  
Author(s):  
A Farrell ◽  
C Franklin ◽  
P Arthur ◽  
H Thorarensen ◽  
K Cousins

We developed an in situ perfused turtle (Chrysemys scripta) heart preparation to study its intrinsic mechanical properties at 5°C and 15°C using normoxic and anoxic perfusion conditions. The in situ preparation proved durable and stable. At 15°C and a spontaneous heart rate of 23.4 beats min-1, maximum stroke volume was 2.54 ml kg-1 body mass, maximum cardiac output was 62.5 ml min-1 kg-1 and maximum cardiac myocardial power output was 1.50 mW g-1 ventricular mass. There was good agreement between these values and those previously obtained in vivo. Furthermore, since the maximum stroke volume observed here was numerically equivalent to that observed in ventilating C. scripta in vivo, it seems likely that C. scripta has little scope to increase stroke volume to a level much beyond that observed in the resting animal through intrinsic mechanisms alone. The ability of the perfused turtle heart to maintain stroke volume when diastolic afterload was raised (homeometric regulation) was relatively poor. At 5°C, the spontaneous heart rate (8.1 beats min-1) was threefold lower and homeometric regulation was impaired, but maximum stroke volume (2.25 ml kg-1) was not significantly reduced compared with the value at 15°C. The significantly lower maximum values for cardiac output (18.9 ml min-1 kg-1) and power output (0.39 mW g-1 ventricular mass) at 5°C were largely related to pronounced negative chronotropy with only a relatively small negative inotropy. Anoxia had weak negative chronotropic effects and marked negative inotropic effects at both temperatures. Negative inotropy affected pressure development to a greater degree than maximum flow and this difference was more pronounced at 5°C than at 15°C. The maximum anoxic cardiac power output value at 15°C (0.77 mW g-1 ventricular mass) was not that different from values previously obtained for the performance of anoxic rainbow trout and hagfish hearts. In view of this, we conclude that the ability of turtles to overwinter under anoxic conditions depends more on their ability to reduce cardiac work to a level that can be supported through glycolysis than on their cardiac glycolytic potential being exceptional.

1982 ◽  
Vol 60 (12) ◽  
pp. 3165-3171 ◽  
Author(s):  
A. P. Farrell ◽  
K. MacLeod ◽  
W. R. Driedzic

The preparation of the in situ heart was accomplished without any physical disturbance to the heart. The heart generated an intrinsic rhythm which was steady throughout the experiment and apparently was derived from the sinoatrial pacemaker. The power output developed by the in situ heart at physiological preloads and after loads was comparable to in vivo values. The effect of increasing preload (0 to 3 cmH2O) was a fourfold increase in stroke volume with little or no change in heart rate. When after load was changed (25 to 45 cmH2O) heart rate was unchanged and stroke volume was usually maintained. As a consequence, cardiac output was maintained by intrinsic factors alone at a higher work load. Epinephrine (10−9 to 10−5 M) in the perfusate produced relatively weak positive chronotropic and inotropic effects. The increase in cardiac output produced by epinephrine was small compared with the intrinsic changes evoked when preload was raised.


1996 ◽  
Vol 199 (2) ◽  
pp. 401-405 ◽  
Author(s):  
M Johnsson ◽  
M Axelsson ◽  
W Davison ◽  
M Forster ◽  
S Nilsson

The portal heart of the New Zealand hagfish (Eptatretus cirrhatus) was perfused in situ. Stroke volume, cardiac output and power output increased in response to increased preload, in accordance with Starling's law of the heart. A positive chronotropic effect was found when the input pressure increased from 0.05 to 0.1 kPa. Increased afterload decreased stroke volume and cardiac output. Power output peaked at an output pressure of 0.22 kPa, after which it decreased. There was no change in heart rate in response to increased afterload. In unanaesthetized resting animals, the pressure in the supraintestinal vein, which supplies the portal heart, ranged from 0.025 to 0.07 kPa (mean 0.040±0.005 kPa). The beta-adrenoceptor antagonist sotalol did not affect the response to different input and output pressures. Sotalol produced a significant decrease in heart rate and abolished the pressure-sensitive increase in heart rate. Bolus injections of adrenaline produced a transient increase in portal heart rate. The negative chronotropic response to sotalol and the response to adrenaline indicate the presence of an endogenous beta-adrenergic tonus on the portal heart.


1991 ◽  
Vol 332 (1264) ◽  
pp. 191-198 ◽  

Scaling of heart ventricle mass and body mass in the haemoglobinless Antarctic fish Chionodraco hamatus Lönnberg shows a relationship similar to those reported for other ‘cardiomegalic ’ icefish ( Chaenocephalus aceratus and Channichthys rhinoceratus ). An in vitro preparation of the heart of C. hamatus was set up to investigate the mechanical performance of this heart at different preloads and afterloads. It appears that this heart is well adapted to working within a range of preloads varying from —0.07 to —0.04 kPa, while it is unable to sustain increases of afterloads higher than 3.0 kPa. As in other teleosts, heart rate is unaffected by changes in preload and afterload. Increase in temperature from 0.5 to 5.8 °C affects heart rate whereas stroke volume is unaffected. On the whole, the in vitro data are similar to those in vivo measured in another icefish, C. aceratus and show that the heart of C. hamatus works as a typical volume pump. This is discussed in relation to both the structural constraints related to the cardiac design of this icefish and the biology of this unique vertebrate.


1988 ◽  
Vol 137 (1) ◽  
pp. 287-301 ◽  
Author(s):  
M. Axelsson

The nervous regulation of heart rate and stroke volume in the Atlantic cod Gadus morhua was investigated both in vivo, during rest and exercise, and in vitro. The cholinergic and adrenergic influences on the heart were estimated in experiments with injections of atropine and sotalol. At rest the cholinergic and adrenergic tonus on the heart were 38% and 21%, respectively (ratio 1.81:1). At the end of an exercise period, the cholinergic tonus had decreased to 15% but the adrenergic tonus had increased to 28% (ratio 0.54:1). The results suggest that variation of the cholinergic tonus on the heart is a major factor in the regulation of the heart rate. In one group of fish, cardiac output was also measured, allowing calculation of stroke volume. Cardiac output increased significantly during exercise, and this effect persisted in the presence of both atropine and sotalol, although the increase in heart rate was reduced or abolished. The persisting increase in cardiac output during exercise is due to an increase in stroke volume, reflecting a Starling relationship. In the presence of the adrenergic neurone-blocking agent bretylium, a positive inotropic effect on isolated, paced atrial and ventricular strips was observed. In the atrial preparations the effect persisted after 24 h. The effect was prevented by pretreatment with sotalol or cocaine, but potentiated by phentolamine pretreatment. This shows that bretylium exerts its neurone-blocking action after being taken up into the adrenergic nerves, and suggests that the positive inotropic effect of bretylium observed in vivo is due to release of endogenous catecholamines. The concentration-response curves for adrenaline on isolated spontaneously beating atrial preparations showed that the concentrations of catecholamines necessary to produce appreciable effects on the heart are higher than the concentrations found in cod plasma during ‘stress’ situations (handling and exhaustive swimming).


2002 ◽  
Vol 205 (13) ◽  
pp. 1881-1888 ◽  
Author(s):  
Jason M. Blank ◽  
Jeffery M. Morrissette ◽  
Peter S. Davie ◽  
Barbara A. Block

SUMMARYTuna are endothermic fish with high metabolic rates, cardiac outputs and aerobic capacities. While tuna warm their skeletal muscle, viscera, brain and eyes, their hearts remain near ambient temperature, raising the possibility that cardiac performance may limit their thermal niches. We used an in situ perfused heart preparation to investigate the effects of acute temperature change and the effects of epinephrine and extracellular Ca2+ on cardiac function in yellowfin tuna (Thunnus albacares). Heart rate showed a strong temperature-dependence, ranging from 20 beats min-1 at 10 °C to 109 beats min-1 at 25 °C. Maximal stroke volume showed an inverse temperature-dependence,ranging from 1.4 ml kg-1 at 15 °C to 0.9 ml kg-1 at 25 °C. Maximal cardiac outputs were 27 ml kg-1 min-1at 10 °C and 98 ml kg-1 min-1 at 25 °C. There were no significant effects of perfusate epinephrine concentrations between 1 and 100 nmoll-1 at 20 °C. Increasing extracellular Ca2+ concentration from 1.84 to 7.36 mmoll-1 at 20°C produced significant increases in maximal stroke volume, cardiac output and myocardial power output. These data demonstrate that changes in heart rate and stroke volume are involved in maintaining cardiac output during temperature changes in tuna and support the hypothesis that cardiac performance may limit the thermal niches of yellowfin tuna.


1992 ◽  
Vol 70 (6) ◽  
pp. 1200-1210 ◽  
Author(s):  
A. P. Farrell ◽  
P. S. Davie ◽  
C. E. Franklin ◽  
J. A. Johansen ◽  
R. W. Brill

An in situ heart preparation perfused with oxygenated saline was used to examine cardiac performance at 25 °C in yellowfin tuna (Thunnus albacares) and skipjack tuna (Katsuwonus pelamis). Heart rates (91–172 bpm in skipjack tuna and 101–157 bpm in yellowfin tuna) were comparable to those measured in vivo, and physiological stroke volumes were possible in yellowfin tuna with subambient filling pressures. In yellowfin tuna, maximum stroke volume and cardiac output were similar to the values obtained in vivo with spinally blocked animals; mean output pressures (up to 145 cmH2O, 1 cmH2O = 0.098 kPa) could exceed in vivo values without a major decrease in the resting cardiac output (homeometric regulation). In contrast, saline-perfused skipjack tuna hearts could not develop physiological output pressures without compromising cardiac output, with cardiac output being only 63% of the in vivo value at an output pressure near the in vivo ventral aortic pressure. The poor performance of the skipjack tuna heart is attributed to limited oxygen diffusion through the thicker walled ventricle. We conclude that the tuna heart is more dependent on its coronary circulation for normal function than the hearts of other fishes examined thus far. The coronary circulation was perfused with saline at various flow rates in isolated hearts from skipjack tuna to develop a pressure–flow relationship for the intact circulation. Coronary resistance reached a minimum of 24 cmH2O∙min∙g ventricular mass/mL at a flow rate of 2 mL/(min∙g ventricular mass) with perfusion pressure about 40 cmH2O. In vivo coronary blood flow was estimated from the pressure–flow relationship as 0.67 mL/(min∙g ventricular mass). Injections of adrenaline, noradrenaline, and phenylephrine into coronary circulation under constant flow conditions increased perfusion pressure, indicating the possibility of α-adrenergic vasoconstriction.


1989 ◽  
Vol 66 (2) ◽  
pp. 949-954 ◽  
Author(s):  
A. M. Rivera ◽  
A. E. Pels ◽  
S. P. Sady ◽  
M. A. Sady ◽  
E. M. Cullinane ◽  
...  

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.


1994 ◽  
Vol 266 (3) ◽  
pp. H1202-H1213 ◽  
Author(s):  
P. P. De Tombe ◽  
W. C. Little

Recent studies in isolated and in vivo canine hearts have suggested that the left ventricular end-systolic pressure (LVPes) of ejecting beats is the net result of a balance between positive and negative effects of ejection. At present, it is unknown whether these ejection effects are merely a ventricular chamber property or represent a fundamental myocardial property. Accordingly, we examined the effects of ejection in eight isolated rat cardiac trabeculae at the sarcomere level. We approximated in situ sarcomere shortening patterns using an iterative computer loading system. Six isovolumic contractions were compared with four ejecting contractions. The superfusing solution contained either 0.7 mM Ca2+ or 0.65 mM Sr2+ plus 0.15 mM Ca2+. With Ca2+, simulated LVPes ("LVP"es) of ejecting contractions was significantly lower than isovolumic "LVP"es (-5.3 +/- 5.6%), whereas with Sr2+, ejecting "LVP"es was significantly higher than isovolumic "LVP"es (+4.5 +/- 7.5%). Contraction duration and time to end systole were markedly prolonged in ejecting vs. isovolumic contractions with either Ca2+ or Sr2+. As a consequence, comparison of simulated LVP between ejecting and isovolumic beats throughout the contraction, i.e., at the same simulated LVV and time, revealed only a positive effect of ejection with either Ca2+ (+18.8 +/- 5.5%) or Sr2+ (+23.4 +/-9.3%). We conclude that both positive and negative effects of ejection are basic myocardial properties.


1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.


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