scholarly journals Seawater acclimation affects cardiac output and adrenergic control of blood pressure in rainbow trout (Oncorhynchus mykiss)—implications for salinity variations now and in the future

2018 ◽  
Vol 6 (1) ◽  
Author(s):  
Erika Sundell ◽  
Daniel Morgenroth ◽  
Jeroen Brijs ◽  
Andreas Ekström ◽  
Albin Gräns ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Adrenergic Control ◽  
The Future ◽  
Seawater Acclimation ◽  
Salinity Variations

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.

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.

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.

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.

Effects of gastric distension on the cardiovascular system in rainbow trout (Oncorhynchus mykiss)

2008 ◽  
Vol 294 (5) ◽  
pp. R1648-R1656 ◽  
Author(s):  
Henrik Seth ◽  
Erik Sandblom ◽  
Susanne Holmgren ◽  
Michael Axelsson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Gastrointestinal Tract ◽  
Arterial Pressure ◽  
Oncorhynchus Mykiss ◽  
Vascular Resistance ◽  
Stomach Wall ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Chemical Stimuli

When animals feed, blood flow to the gastrointestinal tract increases to ensure an adequate oxygen supply to the gastrointestinal tissue and an effective absorption of nutrients. In mammals, this increase depends on the chemical properties of the food, as well as, to some extent, on the mechanical distension of the stomach wall. By using an inflatable nitrile balloon positioned in the stomach, we investigated the cardiovascular responses to mechanical stretch of the stomach wall in rainbow trout ( Oncorhynchus mykiss). Distension with a volume equivalent to a meal of 2% of the body mass increased dorsal aortic blood pressure by up to 29%, and central venous blood pressure increased transiently nearly fivefold. The increase in arterial pressure was mediated by an increased vascular resistance of both the systemic and the intestinal circulation. Cardiac output, heart rate, and stroke volume (SV) did not change, and only transient changes in gut blood flow were observed. The increase in arterial pressure was abolished by the α-adrenergic antagonist prazosin, indicating an active adrenergic vasoconstriction, whereas the venous pressor response could be the consequence of a passive increase in intraperitoneal pressure. Our results show that mechanical distension of the stomach causes an instantaneous increase in general vascular resistance, which may facilitate a redistribution of blood to the gastrointestinal tract when chemical stimuli from a meal induce vasodilation in the gut circulation. The normal postprandial increase in gut blood flow in teleosts is, therefore, most likely partly dependent on mechanical stimuli, as well as on chemical stimuli.

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.

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