Control of the systemic heart and the portal heart of Myxine glutinosa

1996 ◽  
Vol 199 (6) ◽  
pp. 1429-1434 ◽  
Author(s):  
M Johnsson ◽  
M Axelsson

The effects of preload and afterload on the performance of the systemic heart of the hagfish Myxine glutinosa were investigated before and during sotalol treatment using an in situ perfusion technique. Elevation of input pressure (preload) increased flow by means of increased stroke volume and heart rate in accordance with Starling's law of the heart, while increased output pressure (afterload) decreased flow mainly because of decreased stroke volume. Treatment with the beta-adrenoceptor antagonist sotalol did not change the quality of the responses to increased preload or afterload, although power output decreased by 40 % and flow rate was reduced by 35 % mainly due to a decrease in heart rate. Isolated preparations of the systemic heart and the portal heart provided information on the chronotropic effects of different agonists and antagonists. Both the systemic heart and the portal heart were insensitive to adrenergic and cholinergic agonists, adrenocorticotropic hormone and the cholinoceptor antagonist atropine. Sotalol treatment lowered the rate of spontaneous contractions by 30 % in the systemic heart preparation and by 21 % in the portal heart preparation. This study has given further evidence for the existence of a tonic beta-adrenoceptor stimulation of the hagfish systemic heart and portal heart, and demonstrated the importance of that stimulation in maintaining systemic heart performance.

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 69 (7) ◽  
pp. 1822-1828 ◽  
Author(s):  
Peter S. Davie ◽  
Anthony P. Farrell

An isolated preparation of the heart of the spiny dogfish, Squalus acanthias, was developed that allowed control of filling and output pressures and perfusion of the coronary arteries. Cardiac output and stroke volume, but not frequency, were dependent upon atrial filling pressure. The mean maximum cardiac power output of 1.76 mW/g ventricle mass was achieved at high stroke volumes and moderate output pressures (29 cmH2O). When stroke volume was set at half of its measured maximum, increases in output pressure did not affect stroke volume up to pressures near 46 cmH2O, at which point cardiac power output was 1.4 mW/g ventricle mass. In the absence of coronary perfusion, hypoxic perfusion of the heart lumen reduced maximum power output by 38% at 58 ± 3.4 torr and by 64% at 7.7 ± 0.8 torr. Perfusion of the coronary circulation with air-saturated saline or red cell suspensions had no effect on hearts pumping air-saturated saline or hypoxic [Formula: see text] saline, but significantly increased the maximum power output of the hearts pumping severely hypoxic [Formula: see text] saline.


1990 ◽  
Vol 68 (4) ◽  
pp. 792-798 ◽  
Author(s):  
Robert E. Shadwick ◽  
Ronald K. O'Dor ◽  
John M. Gosline

We investigated the cardiorespiratory performance of the squid Loligo opalescens at rest and during jet locomotion while tethered in an aquarium or while swimming in a Brett respirometer at speeds ranging from 0.05 to 0.6 m∙s−1. Simultaneous records of systemic heart rate and ventilatory frequency at each swimming speed were used with data for oxygen consumption to calculate the cardiac output and stroke volume. For a squid of mean weight 0.03 kg and length 0.18 m the resting heart rate averaged 60/min, the ventilatory rate was 26/min, and the calculated stroke volume was 0.05 mL (0.9 mL∙g heart−1) at 12 °C. During exercise the increased oxygen demand was accommodated by increases in both heart rate and stroke volume of almost 100% at the critical swimming speed of about 0.34 m∙s−1. Concomitant increases in the ventilation rate (350%) and ventilatory volume (500%) due to the requirements of jet locomotion were much greater than needed to deliver oxygen to the gills. At rest the oxygen extraction from the respiratory stream was 11%, and this declined to 5% at the critical swimming speed. The possibility that mechanical coupling of the circulatory and respiratory pumps may occur during jet swimming is examined.


1994 ◽  
Vol 186 (1) ◽  
pp. 269-288 ◽  
Author(s):  
C. Franklin ◽  
M. Axelsson

An in situ perfused crocodile (Crocodylus porosus) heart preparation was developed to investigate the effects of input and output pressure on cardiac dynamics and to determine the conditions that lead to a right-to-left cardiac shunt. The pericardium was kept intact, both the left and right atria were perfused and all three outflow tracts (right aortic, left aortic and pulmonary) were cannulated, enabling pressures and flows to be monitored. The perfused heart preparation had an intrinsic heart rate of 34 beats min-1 and generated a physiological power output. Both the left and right sides of the heart were sensitive to filling pressure. Increasing the filling pressure to both atria resulted in an increase in stroke volume and cardiac output (Frank­Starling effect). Increasing the filling pressure to the right atrium also had a positive chronotropic effect. Large right ventricular stroke volumes initiated a right-to-left shunt, despite the left aorta having a pressure 1.5 kPa higher than the pulmonary output pressure. The left ventricle was able to maintain its output and stroke volume up to an output pressure of approximately 8 kPa. However, the right ventricle was significantly weaker. Right ventricular output and stroke volume showed a marked decrease when the output pressure was increased above 5 kPa. A right-to-left shunt occurred when pulmonary output pressure was increased. Surprisingly, a shunt occurred into the left aorta before the pressure in the pulmonary artery became greater than that in the left aorta. Once the pressure in the pulmonary artery exceeded the left aortic pressure, pulmonary artery flow ceased and right ventricular output was solely via the left aorta. A right-to-left shunt could also be initiated by increasing the filling pressure to the left atrium.


1995 ◽  
Vol 269 (4) ◽  
pp. R914-R922 ◽  
Author(s):  
K. Kamimura ◽  
H. Nishimura ◽  
J. R. Bailey

Several avian species show elevated blood pressure (BP) and spontaneous atherogenesis in the aorta and other large arteries. The BP appears to be influenced by age, sex (higher in males), environment, and diet in some species. We reported previously that mean aortic pressure and heart rate, but not plasma renin activity (PRA), of conscious female domestic fowl were markedly reduced by propranolol. In the present study, we aimed to determine in conscious roosters whether 1) hypotension evoked by atenolol or practolol, which selectively inhibit cardiac beta-receptors in mammals, is more potent than that evoked by propranolol, and 2) the renin-angiotensin (ANG) system and/or catecholamines are involved in beta-adrenoceptor antagonist-induced hypotension. Mean arterial pressure (171.2 +/- 3.5 mmHg) and heart rate (281 +/- 4 beats/min) of chronically cannulated roosters (n = 38) were markedly reduced by acute infusion or repeated injections (14 days) of propranolol, atenolol, or practolol, but not by SQ-14,225 (ANG-converting enzyme inhibitor) or [Sar1, Thr8]ANG II (nonselective ANG receptor antagonist). None of the beta-adrenoceptor blockers, however, showed cardioselectivity. The resting PRA of conscious roosters (1.27 +/- 0.09 ng.ml-1.h-1, n = 38) was low and did not change significantly after chronic or acute treatment with beta-adrenoceptor blockers except for a slight decrease induced by practolol. PRA increased after SQ-14,225. The plasma levels (pg/ml) of norepinephrine (701.9 +/- 76.0), epinephrine (337.2 +/- 57.1), and dopamine (299.1 +/- 39.0) of conscious roosters were further increased by propranolol. Practolol also increased dopamine significantly.(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 198 (12) ◽  
pp. 2509-2518 ◽  
Author(s):  
M Axelsson ◽  
C Franklin

An in situ perfused crocodile (Crocodylus porosus) heart preparation was used to examine the mechanical responses of the heart to increases in adrenaline concentration, to a decrease in oxygen tension and to opening of the pericardium. Starling and power curves were constructed before and after these experimental manipulations. Increasing adrenaline concentration in the perfusate from 5 nmol l-1 to 0.5 µmol l-1 produced a significant increase in heart rate and a decrease in stroke volume, leaving cardiac output unchanged. With maximal adrenergic stimulation, the left ventricle was able to generate greater power outputs at high right aortic output pressures; however, the right ventricle showed a decrease in performance with increasing output pressure. Decreasing the PO2 of the perfusate to 10 kPa resulted in a significant bradycardia. Both the flow and pressure-generating capabilities of the perfused heart preparation were reduced, although the heart was able to maintain low work levels at this PO2. Opening the pericardium permitted greater movement/expansion of the cardiac chambers and resulted in an increase in heart rate. Higher flows were generated at low filling pressures during the input pressure challenge as a result of an increase in the sensitivity of the Starling response.


1974 ◽  
Vol 48 (s2) ◽  
pp. 65s-67s ◽  
Author(s):  
C. F. George ◽  
P. J. Lewis ◽  
J. A. Steiner ◽  
C. T. Dollery

1. The effects of propranolol and R03-4787, a new beta-adrenoceptor antagonist with a partial agonist activity, have been studied in a blind, cross-over comparison with placebo. 2. In ten patients who completed the study, the two drugs produced a similar reduction in blood pressure; the reduction in heart rate with propranolol was significantly(P0.001)greater than that produced by R03-4787. 3. Plasma renin activity averaged 4.13 ± 1.37 ng h−1ml−1 on placebo, fell to 3.64 ± 1.47 ng h−1ml−1 on propranolol and to 2.50 ± 1.39 ngh−1ml−1 on R03-4787. 4. No correlation was demonstrable between the log plasma concentration of either propranolol or R03-4787 and change in blood pressure.


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.


1989 ◽  
Vol 4 (2) ◽  
pp. 173-185
Author(s):  
Yasuhiro YAMADA ◽  
Mika NAKAHARA ◽  
Kazuaki NAITO ◽  
Michihiro KOHNO ◽  
Minezo OTSUKA ◽  
...  

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