Cardiac physiology in tunas. I. In vitro perfused heart preparations from yellowfin and skipjack tunas

1992 ◽  
Vol 70 (6) ◽  
pp. 1200-1210 ◽  
Author(s):  
A. P. Farrell ◽  
P. S. Davie ◽  
C. E. Franklin ◽  
J. A. Johansen ◽  
R. W. Brill
Keyword(s):  
Cardiac Output ◽  
Coronary Circulation ◽  
Perfusion Pressure ◽  
Yellowfin Tuna ◽  
Skipjack Tuna ◽  
Perfused Heart ◽  
Pressure Flow ◽  
Ventricular Mass

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.

Effects of acute temperature change, in vivo and in vitro, on the acid–base status of blood from yellowfin tuna (Thunnus albacares)

1992 ◽  
Vol 70 (4) ◽  
pp. 654-662 ◽  
Author(s):  
Richard W. Brill ◽  
Peter G. Bushnell ◽  
David R. Jones ◽  
Manabu Shimizu
Keyword(s):  
Ion Exchange ◽  
Exchange Rates ◽  
Temperature Change ◽  
Yellowfin Tuna ◽  
Thunnus Albacares ◽  
Skipjack Tuna ◽  
Acid Base ◽  
System Temperature

In most fishes, blood acid–base regulation following a temperature change involves active adjustments of gill ion-exchange rates which take hours or days to complete. Previous studies have shown that isolated blood from skipjack tuna, Katsuwonus pelamis, and albacore, Thunnus alalunga, had rates of pH change with temperature (in the open system) equivalent to those necessary to retain net protein charge in vivo (≈ −0.016 ΔpH∙ °C−1). It was postulated that this is due to protons leaving the hemoglobin combining with plasma bicarbonate [Formula: see text], which is removed as gaseous CO2, and that this ability evolved so that tunas need not adjust gill ion-exchange rates to regulate blood pH appropriately following ambient temperature changes. We reexamined this phenomenon using blood and separated plasma from yellowfin tuna, Thunnus albacares. Unlike previous studies, our CO2 levels (0.5 and 1.5% CO2) span those seen in yellowfin tuna arterial and venous blood. Various bicarbonate concentrations [Formula: see text] were obtained by collecting blood from fully rested as well as vigorously exercised fish. We use our in vitro data to calculate basic physiochemical parameters for yellowfin tuna blood: nonbicarbonate buffering (β), the apparent first dissociation constant of carbonic acid (pKapp), and CO2 solubility (αCO2). We also determined the effects of acute temperature change on arterial pH, [Formula: see text], and partial pressures of O2 and CO2in vivo. The pH shift of yellowfin tuna blood subjected to a closed-system temperature change did not differ from previous studies of other teleosts (≈ −0.016 ΔpH∙ °C−1). The pH shift in blood subjected to open-system temperature change was Pco2 dependent and lower than that in skipjack tuna or albacore blood in vitro, but identical with that seen in yellowfin tuna blood in vivo. However, pH adjustments in vivo were caused by changes in both [Formula: see text] and Pco2. The exact mechanisms responsible for these changes remain to be elucidated.

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
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Power Output ◽  
Mechanical Performance ◽  
Perfused Heart ◽  
Inotropic Effects ◽  
Ventricular Mass

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.

Collateral influence on pressure-flow characteristics of coronary circulation

1989 ◽  
Vol 257 (3) ◽  
pp. H717-H725 ◽  
Author(s):  
K. W. Scheel ◽  
H. Mass ◽  
S. E. Williams
Keyword(s):  
Coronary Circulation ◽  
Perfusion Pressure ◽  
Isolated Heart ◽  
Flow Characteristics ◽  
Positive Pressure ◽  
Circumflex Artery ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Heart Preparation ◽  
Collateral Vessels

The purpose of this study was to determine the role of the coronary collateral circulation on the shape of the coronary pressure-flow (P-F) relationship and its effects on the pressure at zero flow (PZF) or pressure intercept. We investigated the P-F characteristics of the coronary circulation under two conditions. 1) To minimize the influence of collaterals, we measured coronary flow by timed collections of coronary sinus outflow in 15 dog hearts, as perfusion pressure to all vessels was varied; 2) to maximize the effect of collaterals, we measured circumflex artery flow in six dog hearts, as perfusion pressure to only the circumflex coronary artery was varied and the pressure in the remaining vessels was maintained constant. We used an isolated heart preparation in which ventricular chamber and venous outflow pressures equalled atmospheric pressure and the vessels were maximally dilated with adenosine. In the first condition, the P-F relationship was curvilinear with a PZF of 0 mmHg; in the second condition, the P-F relationship was curvilinear with a PZF of 16 +/- 2 mmHg, and flow was retrograde at pressures below PZF. We conclude that in both conditions the curvilinearity of the coronary P-F relationship was the result of nonlinear elastic properties of blood vessels, not requiring the “waterfall” concept to be invoked, and that in the second condition the influence of collateral vessels produced the positive pressure intercept.

EDRF as a possible mediator of sepsis-induced arteriolar dilation in skeletal muscle

1992 ◽  
Vol 262 (3) ◽  
pp. H880-H887 ◽  
Author(s):  
A. S. Lubbe ◽  
R. N. Garrison ◽  
H. M. Cryer ◽  
N. L. Alsip ◽  
P. D. Harris
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Output ◽  
Defense Mechanisms ◽  
Vascular Endothelial Cells ◽  
Early Period ◽  
Vascular Endothelial ◽  
Low Cardiac Output ◽  
E Coli

Vascular endothelial cells influence microvessel diameters in vivo and in vitro and participate in host-defense mechanisms during sepsis. We examined whether small arteriole dilation in skeletal muscle during high cardiac output bacteremia (HOB) and low cardiac output live Escherichia coli sepsis (LOS) is mediated by an endothelium-derived relaxing factor (EDRF). Local chemical blockade of EDRF by hydroquinone (HQ) substantially blunted acetylcholine-induced dilation of small arterioles. HQ also prevented large arteriole (55-135 microns) constriction and small arteriole (6-22 microns) dilation in the cremaster muscle of rats during HOB. In LOS, small arteriole dilation was also prevented by HQ but only during the early period when blood pressure was unchanged from baseline. HQ did not alter large arteriole constriction during LOS. We conclude that small arteriole vasodilation in skeletal muscle is mediated at least in part by EDRF during bacteremia. Because EDRF cannot mediate large arteriole constriction and because HQ blunted large arteriole constriction during HOB, we now suspect that HQ also interferes at least in part with some large arteriole vasoconstrictor mechanism, possibly leukotrienes or an endothelium-derived constricting factor, which mediates large arteriole constriction during HOB. Our data also suggest that large arteriole constriction during LOS is partly mediated by factors that are unaffected by HQ. The endothelium appears to play an important role in the microcirculatory responses of skeletal muscle to live E. coli sepsis through more than one mechanism.

Vascular Abnormalities and Pulmonary Hypertension in the Berkeley Sickle Mouse.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3185-3185
Author(s):  
David R. Archer ◽  
Shawn Elms ◽  
Joshua Boutwell ◽  
Jennifer Perry ◽  
Roy Sutliff
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Endothelial Dysfunction ◽  
Mouse Model ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
The Mean

Abstract Clinically, pulmonary hypertension is a major risk factor for mortality in adults with sickle cell disease. Contributing factors probably include red cell hemolysis and vaso-occlusive injury with their associated oxidative and inflammatory stimuli. Previously, we have described RBC hemolysis and endothelial oxidative stress in the Berkeley sickle mouse model and extend those studies in this work to investigate cardiovascular and endothelial dysfunction. Eight to ten month old homozygous and hemizygous Berkeley sickle mice and C57BL/6 control mice were used for all aspects of these experiments. In vivo measurements of mean arterial pressure and right ventricular pressures were conducted in fully anesthetized mice using a pressure transducer inserted in the carotid and right ventricle respectively. Following in vivo readings hearts were excised for measurement of ventricular mass. The ascending aorta was removed and cut into 5 mm rings for in vitro studies of agonist- induced contractility and relaxation. The mean arterial pressure of the hemizygous sickle mice (70.6 ± 3.4) was significantly lower than the control mice (86.0 ± 3.1) and the mean arterial pressure of homozygous sickle mice (59.0 ± 2.2 mmHg) was significantly lower than the hemizygous and control mice (p≤0.05 and p≤0.001, respectively). The right ventricular pressure showed a trend that approached significance (p= 0.08) such that pressures in homozygous mice were ≥ than those in hemizygous which were ≥ than those in control mice. Increased basal cardiac output was suggested by significant left ventricular hypertrophy. In vitro examination of potassium chloride activation of voltage gated calcium channels showed no significant difference in sensitivity or maximal contraction. Similarly, there was no difference in sensitivity to the α1 agonist, phenylephrine. However, both hemi- and homozygous mice showed a significant reduction in maximal force of contraction (normalized to cross sectional area when compared to controls. Maximal acetylcholine induced relaxation of aortic rings was significantly reduced (p≤0.05) in homozygous sickle mice compared to controls. The same effect was not seen with sodium nitroprusside induced relaxation indicating that the acetylcholine effect was not due to effects on the smooth muscle but was endothelium-dependent. The Berkeley mouse model shows cardiac hypertrophy consistent with the increased cardiac output associated with chronic anemia and a reduced basal mean arterial blood pressure similar to that seen in humans. 8–10 month old mice have increased right ventricular pressure and RV mass indicative of pulmonary hypertension. Further endothelial dysfunction is characterized by a reduction in the maximal relaxation elicited by acetylcholine. Therefore, the Berkeley mouse is a good model for investigating sickle related endothelial dysfunction.

Mechanical performance of the isolated and perfused heart of the haemoglobinless Antarctic icefish Chionodraco hamatus (Lönnberg): effects of loading conditions and temperature

1991 ◽  
Vol 332 (1264) ◽  
pp. 191-198 ◽  
Keyword(s):  
Heart Rate ◽  
Mechanical Performance ◽  
Antarctic Fish ◽  
Structural Constraints ◽  
Heart Ventricle ◽  
Perfused Heart ◽  
Antarctic Icefish ◽  
Set Up

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.

Prostacyclin Release in the Coronary Circulation During Sustained Stimulation in In Vitro and in In Vivo Experimental Systems

1988 ◽  
Vol 59 (02) ◽  
pp. 180-185 ◽  
Author(s):  
M Prosdocimi ◽  
M Finesso ◽  
N Banzatto ◽  
A Zanetti ◽  
G de Gaetano ◽  
...  
Keyword(s):  
Coronary Circulation ◽  
Great Cardiac Vein ◽  
Experimental Systems ◽  
Perfused Hearts

SummaryProstacyclin release from rat isolated perfused hearts and from dog coronary circulation was studied by measuring immunoreac- tive 6-keto-PGFlalpha (6-keto-PGFla) in heart perfusate and in plasma obtained from the great cardiac vein respectively.

Novel catheterization technique for the in vivo measurement of pulmonary vascular responses in rats

1998 ◽  
Vol 274 (4) ◽  
pp. H1218-H1229 ◽  
Author(s):  
Albert L. Hyman ◽  
Qingzhong Hao ◽  
Allen Tower ◽  
Philip J. Kadowitz ◽  
Hunter C. Champion ◽  
...  
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Flow Curves ◽  
Pressure Flow ◽  
Flow Rates ◽  
Rat Lungs ◽  
Pulmonary Vasodilator ◽  
Catheterization Technique ◽  
Pulmonary Arterial

A novel cardiac catheterization technique was devised to investigate the pulmonary arterial pressure-blood flow relationship in intact spontaneously breathing rats (ISBR) under physiological conditions with constant left atrial pressure and controlled blood flow within the normal range. Observations using this new technique in vivo were contrasted with data derived with isolated perfused rat lungs in vitro. Unlike results in in vitro isolated perfused rat lungs, the pressure-flow curves in vivo were curvilinear, with pulmonary artery pressure increasing more rapidly at low pulmonary blood flows of 4–8 ml/min and less rapidly at higher flow rates. Pressure-flow curves were reproducible and were not altered by 1–1.5 h of arrested perfusion, cyclooxygenase blockade, or perfusion with aortic or mixed venous blood. In contrast to results in in vitro isolated perfused rat lungs, N G-nitro-l-arginine methyl ester (l-NAME) increased pulmonary arterial pressure at all but the lowest flow rates with a slight effect on the curvilinear pressure-flow relationship. l-NAME reversed pulmonary vasodilator responses to acetylcholine and bradykinin and enhanced the pulmonary vasodilator response to nitroglycerin. The present data suggest that actively induced pulmonary hypertension is under greater control by endothelium-derived relaxing factor (EDRF). Unlike previous results in in vitro perfused rat lungs, results in ISBR demonstrate that the pulmonary vasodilator response to adrenomedullin-(13—52) is not mediated by calcitonin gene-related peptide receptors, which are not coupled to the release of EDRF. These results indicate that this novel technique may provide a useful model for the study of the pulmonary circulation in the intact chest rat.

scholarly journals Paradoxical arteriole constriction compromises cytosolic and mitochondrial oxygen delivery in the isolated saline-perfused heart

2018 ◽  
Vol 315 (6) ◽  
pp. H1791-H1804 ◽  
Author(s):  
Abigail V. Giles ◽  
Junhui Sun ◽  
Armel N. Femnou ◽  
Sarah Kuzmiak-Glancy ◽  
Joni L. Taylor ◽  
...  
Keyword(s):  
Oxygen Delivery ◽  
Isolated Heart ◽  
Rabbit Heart ◽  
Reduced Form ◽  
Common Finding ◽  
Perfused Heart ◽  
Mitochondrial Redox State ◽  
Species Specific

The isolated saline-perfused heart is used extensively to study cardiac physiology. Previous isolated heart studies have demonstrated lower tissue oxygenation compared with in vivo hearts based on myoglobin oxygenation and the mitochondrial redox state. These data, consistent with small anoxic regions, suggest that the homeostatic balance between work and oxygen delivery is impaired. We hypothesized that these anoxic regions are caused by inadequate local perfusion due to a paradoxical arteriole constriction generated by a disrupted vasoregulatory network. We tested this hypothesis by applying two exogenous vasodilatory agents, adenosine and cromakalim, to relax vascular tone in an isolated, saline-perfused, working rabbit heart. Oxygenation was monitored using differential optical transmission spectroscopy and full spectral fitting. Increases in coronary flow over control with adenosine (27 ± 4 ml/min) or cromakalim (44 ± 4 ml/min) were associated with proportional spectral changes indicative of myoglobin oxygenation and cytochrome oxidase (COX) oxidation, consistent with a decrease in tissue anoxia. Quantitatively, adenosine decreased deoxymyoglobin optical density (OD) across the wall by 0.053 ± 0.008 OD, whereas the reduced form of COX was decreased by 0.039 ± 0.005 OD. Cromakalim was more potent, decreasing deoxymyoglobin and reducing the level of COX by 0.070 ± 0.019 OD and 0.062 ± 0.019 OD, respectively. These effects were not species specific, as Langendorff-perfused mouse hearts treated with adenosine demonstrated similar changes. These data are consistent with paradoxical arteriole constriction as a major source of regional anoxia during saline heart perfusion. We suggest that the vasoregulatory network is disrupted by the washout of interstitial vasoactive metabolites in vitro. NEW & NOTEWORTHY Regional tissue anoxia is a common finding in the ubiquitous saline-perfused heart but is not found in vivo. Noninvasive optical techniques confirmed the presence of regional anoxia under control conditions and demonstrated that anoxia is diminished using exogenous vasodilators. These data are consistent with active arteriole constriction, occurring despite regional anoxia, generated by a disrupted vasoregulatory network. Washout of interstitial vasoactive metabolites may contribute to the disruption of normal vasoregulatory processes in vitro.

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