Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): role of neural and circulating catecholamines

2006 ◽  
Vol 291 (3) ◽  
pp. R711-R718 ◽  
Author(s):  
Erik Sandblom ◽  
Michael Axelsson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Blood Volume ◽  
Body Mass ◽  
Venous Capacitance ◽  
Moderate Hypoxia ◽  
Rainbow Trout Oncorhynchus Mykiss

Central venous blood pressure (Pven) increases in response to hypoxia in rainbow trout ( Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including Pven, dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (PWO2 = ∼9 kPa), where PWO2 is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80–100, 90–110, and 100–120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure Pven during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by α-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80–100% blood volume, whereas vascular capacitance decreased significantly at 90–110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, Pven always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an α-adrenergic mechanism with both humoral and neural components.

Venous hemodynamic responses to acute temperature increase in the rainbow trout (Oncorhynchus mykiss)

2007 ◽  
Vol 292 (6) ◽  
pp. R2292-R2298 ◽  
Author(s):  
Erik Sandblom ◽  
Michael Axelsson
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Temperature Increase ◽  
Venous Return ◽  
Filling Pressure ◽  
Venous Capacitance ◽  
Cardiac Filling Pressure ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Cardiac Filling

Many ectotherms regularly experience considerable short-term variations in environmental temperature, which affects their body temperature. Here we investigate the cardiovascular responses to a stepwise acute temperature increase from 10 to 13 and 16°C in rainbow trout ( Oncorhynchus mykiss). Cardiac output increased by 20 and 31% at 13 and 16°C, respectively. This increase was entirely mediated by an increased heart rate (fH), whereas stroke volume (SV) decreased significantly by 20% at 16°C. The mean circulatory filling pressure (MCFP), a measure of venous capacitance, increased with temperature. Central venous pressure (Pven) did not change, whereas the pressure gradient for venous return (MCFP-Pven) was significantly increased at both 13 and 16°C. Blood volume, as measured by the dilution of 51Cr-labeled red blood cells, was temperature insensitive in both intact and splenectomized trout. This study demonstrates that venous capacitance in trout decreases, but cardiac filling pressure as estimated by Pven does not change when cardiac output increases during an acute temperature increase. SV was compromised as fH increased with temperature. The decreased capacitance likely serves to prevent passive pooling of blood in the venous periphery and to maintain cardiac filling pressure and a favorable pressure gradient for venous return.

Cardiovascular effects of hypercarbia in rainbow trout (Oncorhynchus mykiss): a role for externally oriented chemoreceptors

2001 ◽  
Vol 204 (1) ◽  
pp. 115-125 ◽  
Author(s):  
J.E. McKendry ◽  
S.F. Perry
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Systemic Resistance ◽  
Rainbow Trout Oncorhynchus Mykiss

In situ and in vivo experiments were performed on rainbow trout (Oncorhynchus mykiss) to examine (i) the direct effect of CO(2) on the systemic vasculature and (ii) the influence of internal versus external hypercapnic acidosis on cardiovascular variables including blood pressure, cardiac output and systemic vascular resistance. Results from in situ saline-perfused trunk preparations indicated that CO(2) (0.6, 1.0 or 2.0% CO(2)) elicited a significant vasodilation, but only in the presence of pre-existing humoral adrenergic tone. In the absence of pre-existing vascular tone, CO(2) was without effect on systemic resistance. In contrast, hypercarbia in vivo triggered a statistically significant increase in systemic resistance (approximately 70 %) that was associated with elevated ventral aortic (approximately 42 %) and dorsal aortic (approximately 43 %) blood pressures and with a significant bradycardia (approximately 12 %); cardiac output was not significantly affected. To determine the potential roles of internal versus external chemoreceptors in mediating the cardiovascular responses to hypercarbia, experiments were performed to elevate the endogenous arterial partial pressure of CO(2) (Pa(CO2)) without an accompanying increase in external P(CO2) (Pw(CO2)). In one series, trout were given a bolus injection of the carbonic anhydrase inhibitor acetazolamide (30 mg kg(−1)) to inhibit CO(2) excretion, and thus raise Pa(CO2), 5–7 h prior to being exposed to an acute increase in Pw(CO2) (maximum Pw(CO2)=6.3+/−0.4 mmHg; 1 mmHg=0.133 kPa). Despite a marked increase in Pa(CO2) (approximately 7 mmHg) after injection of acetazolamide, there was no increase in dorsal aortic blood pressure (P(DA)) or systemic resistance (R(S)). The ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 35 %). A second series of experiments used a 5–7 h period of exposure to hyperoxia (Pw(O2)=643+/−16 mmHg) to establish a new, elevated baseline Pa(CO2) (7.8+/−1.1 mmHg) without any change in Pw(CO2). Despite a steadily increasing Pa(CO2) during the 5–7 h of hyperoxia, there was no associated increase in P(DA) or R(S). Ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 150 %). Plasma adrenaline levels were increased significantly during exposure to hypercarbia and, therefore, probably contributed to the accompanying cardiovascular effects. These findings demonstrate that the cardiovascular effects associated with hypercarbia in rainbow trout are unrelated to any direct constrictory effects of CO(2) on the systemic vasculature and are unlikely to be triggered by activation of internally oriented receptors. Instead, the data suggest that the cardiovascular responses associated with hypercarbia are mediated exclusively by externally oriented chemoreceptors.

The control of blood pressure during external hypercapnia in the rainbow trout (Oncorhynchus mykiss)

1999 ◽  
Vol 202 (16) ◽  
pp. 2177-2190 ◽  
Author(s):  
S.F. Perry ◽  
R. Fritsche ◽  
T.M. Hoagland ◽  
D.W. Duff ◽  
K.R. Olson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Central Venous ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Blood Pressures

Adult freshwater rainbow trout (Oncorhynchus mykiss) were exposed acutely (approximately 20 min) in a stepwise manner to increasing levels of environmental carbon dioxide ranging between 1.7 and 9.0 mmHg (0.23-1.2 kPa). Experiments were performed to examine, for the first time, the influence of hypercapnic acidosis on aspects of cardiovascular physiology including blood pressure, cardiac output and vascular resistance. Fish displayed dose (water CO(2) partial pressure) -dependent increases in ventral aortic (13–39 %) and dorsal aortic (17–54 %) blood pressures that reflected marked increases in systemic vascular resistance (16–78 %); branchial vascular resistance was unaffected by hypercapnia. At the highest level of hypercapnia (9.0 mmHg), central venous pressure was significantly elevated by 54 %. Although cardiac output remained constant, heart rate was significantly lowered by 4–7 beats min(−)(1) at the two highest levels of hypercapnia. To determine whether the cardiovascular responses to hypercapnia were being blunted by the stepwise increase in external P(CO2), a separate group of fish was exposed directly to a single step of hypercapnia (water P(CO2) 8.0 mmHg). The cardiovascular responses were similar to those exhibited by the more gradually exposed fish except that central venous pressure did not increase and the extent of the bradycardia was greater (13 beats min(−)(1)). After confirming the effectiveness of yohimbine in blocking the vasoconstrictory (α)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (α)-adrenoreceptor stimulation in promoting the cardiovascular responses during hypercapnia. Prior treatment of fish with yohimbine prevented the increased blood pressures and systemic vascular resistance during hypercapnia but did not influence the CO(2)-induced bradycardia. Plasma levels of catecholamines did not change during hypercapnia, and therefore the stimulation of the systemic (α)-adrenoreceptors presumably reflected increased sympathetic nerve activity. To determine whether the cardiovascular changes elicited by hypercapnia were related to acidosis-induced hypoxaemia, fish were exposed to hypoxia in a stepwise manner (water P(O2) 65–151 mmHg). The cardiovascular responses to hypoxia were markedly different from those to hypercapnia and consisted of pronounced increases in systemic and branchial vascular resistance, but only at the most severe level of hypoxia; ventral and dorsal aortic pressures were unaffected. The differences between the responses to hypercapnia and hypoxia, coupled with the smaller reductions in blood oxygen content during hypercapnia, support the hypothesis that the cardiovascular responses to CO(2) are direct and are unrelated to hypoxaemia.

CARDIOVASCULAR RESPONSES TO SCYLIORHININ I AND II IN THE RAINBOW TROUT, ONCORHYNCHUS MYKISS, IN VIVO AND IN VITRO

1994 ◽  
Vol 191 (1) ◽  
pp. 155-166 ◽  
Author(s):  
J Kagstrom ◽  
M Axelsson ◽  
S Holmgren
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Initial Decrease

Changes in cardiac output, heart rate, dorsal aortic blood pressure and coeliac artery blood flow were measured in unrestrained rainbow trout, Oncorhynchus mykiss, following injections of the elasmobranch tachykinins scyliorhinin I and II. The resistance in the coeliac vascular bed and the total systemic vasculature were calculated from blood pressure and flow. In addition, isolated tails were perfused to investigate the effect of the peptides on the somatic vasculature. Scyliorhinin I (SCY I) produced a biphasic change in the coeliac vascular resistance: an initial decrease was followed by an increase. The decrease in coeliac vascular resistance was accompanied by a decrease in the total systemic vascular resistance, leading to an increased cardiac output. The ensuing increase in coeliac vascular resistance caused a slight increase in blood pressure. In the perfused tail, SCY I produced a marked increase in the somatic vascular resistance. Scyliorhinin II (SCY II) decreased the systemic vascular resistance, causing an increase in cardiac output. SCY II also caused a late increase in the coeliac vascular resistance, which led to hypertension and bradycardia. In vitro, SCY II produced a biphasic response in which an initial decrease in the somatic resistance was followed by a larger increase. The results demonstrate that exogenous SCY I and II are vasoactive peptides that act by different mechanisms in the rainbow trout cardiovascular system. Their actions also differ from the actions of substance P previously observed in the cod, Gadus morhua, and possibly involve a neural reflex.

How the efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle changes with cycle frequency

2002 ◽  
Vol 205 (5) ◽  
pp. 697-706 ◽  
Author(s):  
Claire L. Harwood ◽  
Iain S. Young ◽  
John D. Altringham
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Cardiac Muscle ◽  
Power Output ◽  
Energy Cost ◽  
Total Efficiency ◽  
Ventricular Muscle ◽  
Cycle Frequency ◽  
Rainbow Trout Oncorhynchus Mykiss

SUMMARYDifferent species of animals require different cardiac performance and, in turn, their cardiac muscle exhibits different properties. A comparative approach can reveal a great deal about the mechanisms underlying myocardial contraction. Differences in myocardial Ca2+ handling between fish and mammals suggest a greater energy cost of activation in fish. Further, while there is considerable evidence that heart rate (or cycle frequency) should have a profound effect on the efficiency of teleost cardiac muscle, this effect has been largely overlooked. We set out to determine how cycle frequency affects the power output and efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle and to relate this to the heart’s function in life. We measured power output and the rate of oxygen consumption (V̇O2) and then calculated efficiency over a physiologically realistic range of cycle frequencies.In contrast to mammalian cardiac muscle, in which V̇O2 increases with increasing heart rate, we found no significant change in V̇O2 in the teleost. However, power output increased by 25 % as cycle frequency was increased from 0.6 to 1.0 Hz, so net and total efficiency increased. A maximum total efficiency of 20 % was achieved at 0.8 Hz, whereas maximum power output occurred at 1.0 Hz. We propose that, since the heart operates continuously, high mechanical efficiency is a major adaptive advantage, particularly at lower heart rates corresponding to the more commonly used slower, sustainable swimming speeds. Efficiency was lower at the higher heart rates required during very fast swimming, which are used during escape or prey capture.If a fixed amount of Ca2+ is released and then resequestered each time the muscle is activated, the activation cost should increase with frequency. We had anticipated that this would have a large effect on the total energy cost of contraction. However, since V̇O2 remains constant, less oxygen is consumed per cycle at high frequencies. We suggest that a constant V̇O2 would be observed if the amount of activator Ca2+ were to decrease with frequency. This decrease in activation energy is consistent with the decrease in the systolic intracellular Ca2+ ([Ca2+]i) transient with increasing stimulation frequency seen in earlier studies.

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia

1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Plasma Catecholamines ◽  
Central Blood Volume ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

Cholecystokinin as a regulator of cardiac function and postprandial gastrointestinal blood flow in rainbow trout (Oncorhynchus mykiss)

2010 ◽  
Vol 298 (5) ◽  
pp. R1240-R1248 ◽  
Author(s):  
Henrik Seth ◽  
Albin Gräns ◽  
Michael Axelsson
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Direct Effect ◽  
Flow Profile ◽  
Subsequent Increase ◽  
Physiological Concentration ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Gastrointestinal Blood Flow

We have studied the potential role of CCK as a regulator/modulator of the postprandial increase in gastrointestinal blood flow. Rainbow trout ( Oncorhynchus mykiss ) were instrumented with pulsed Doppler flow probes to measure the effects of CCK on cardiac output and gastrointestinal blood flow. Furthermore, vascular preparations were used to study the direct effects of CCK on the vessels. In addition, we used in situ perfused hearts to further study the effects of CCK on the cardiovascular system. When the sulfated form of CCK-8 was injected at a physiological concentration (0.19 pmol/kg) in vivo, there was a significant increase in the gastrointestinal blood flow (18 ± 4%). This increase in gastrointestinal blood flow was followed by a subsequent increase in cardiac output (30 ± 6%). When the dose was increased to 0.76 pmol/kg, there was only a 14 ± 6% increase in gastrointestinal blood flow; possibly due to a dose-dependent increase in the gill vascular resistance as previously reported or a direct effect on the heart. Nevertheless, CCK did not affect the isolated vessel preparations, and thus, it seems unlikely that CCK has a direct effect on the blood vessels of the second or third order. CCK did, however, have profound effects on the dynamics of the heart, and without a change in cardiac output, there was a significant increase in the amplitude (59 ± 4%) and rate (dQ/d t: 55 ± 4%; -dQ/d t: 208 ± 49%) of the phasic flow profile. If and how this might be coupled to a postprandial gastrointestinal hyperemia remains to be determined. We conclude that CCK has the potential as a regulator of the postprandial gastrointestinal blood flow in fish and most likely has its effect by inducing a gastrointestinal hyperemia. The mechanism by which CCK acts is at present unknown.

Tissue and whole-body extracellular, red blood cell and albumin spaces in the rainbow trout as a function of time: a reappraisal of the volume of the secondary circulation

1998 ◽  
Vol 201 (9) ◽  
pp. 1381-1391 ◽  
Author(s):  
P G Buschnell ◽  
D J Conklin ◽  
D W Duff ◽  
K R Olson
Keyword(s):  
Rainbow Trout ◽  
Blood Volume ◽  
Body Mass ◽  
Extracellular Fluid ◽  
Secondary Circulation ◽  
Whole Body ◽  
Secondary System ◽  
Tissue Mass ◽  
Tissue Samples ◽  
Rainbow Trout Oncorhynchus Mykiss

[58Co]EDTA, [51Cr]RBC and [125I]albumin spaces in the whole body and 28 tissue samples were examined at timed intervals over 16 h in rainbow trout Oncorhynchus mykiss. [58Co]EDTA space (which approximates extracellular fluid volume; ECF) in fins, skin, gallbladder and eye are reported for the first time. After a 16 h equilibration, ECF volume was large (376-726 microl g-1 wet tissue mass) in kidney, swimbladder, skin and fins, moderate (219-313 microl g-1 wet tissue mass) in stomach, skull, spleen, liver, intestine, gills, eye and cecum, and small (53-181 microl g-1 wet tissue mass) in red muscle, fat, brain, gallbladder and white muscle. Whole-body ECF was 387+/-10.6 microl g-1 (mean +/- s.e.m.; N=11). [51Cr]RBC space relative to [58Co]EDTA space was large in spleen, liver, intestine and gill, and low in skin, fins, stomach and skull. Whole-body [51Cr]RBC space was 9.9+/-0.6 microl g-1 body mass (N=17). Blood volume calculated from [51Cr]RBC space at 16 h and a dorsal aortic hematocrit of 24.5 % was 40.4 microl g-1 body mass. Whole-body [125I]albumin space at 16 h was 118.0+/-7.4 microl g-1 body mass (N=6), which resulted in an estimated blood volume of 156. 6 microl g-1 body mass, nearly four times that estimated from the [51Cr]RBC space. Tissue hematocrits, calculated from [125I]albumin and [51Cr]RBC spaces, were significantly lower than dorsal aortic hematocrit in all tissues except spleen, kidney and liver. [58Co]EDTA and [51Cr]RBC spaces reached equilibrium in nearly all tissues within 1 h, whereas [125I]albumin continued to accumulate in many tissues up 24 h. The disparity between [125I]albumin distribution kinetics compared with the kinetics of [58Co]EDTA and [51Cr]RBC distribution, as well as the accumulation of [125I]albumin in tissues not known to have a secondary circulation, indicates that [125I]albumin is a poor marker of plasma volume in trout and that previous studies based on [125I]albumin clearance from the plasma have overestimated both the volume and the turnover rate of the secondary system. Revised estimates of secondary circulation volume, based on [58Co]EDTA distribution rate, indicate that it is no more than 10-20 % of the volume of the primary circulation. &lt;P&gt;

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