scholarly journals INFLUENCE OF HYPOXIA AND ADRENALINE ADMINISTRATION ON CORONARY BLOOD FLOW AND CARDIAC PERFORMANCE IN SEAWATER RAINBOW TROUT (ONCORHYNCHUS MYKISS)

1994 ◽  
Vol 193 (1) ◽  
pp. 209-232 ◽  
Author(s):  
A Gamperl ◽  
A Pinder ◽  
R Grant ◽  
R Boutilier

To investigate the relationship between cardiac performance and coronary perfusion, cardiovascular variables (Q(dot), Vs, fh, Pda) and coronary blood flow (q·cor) were measured in rainbow trout (Oncorhynchus mykiss) (1.2­1.6 kg) before and after adrenergic stimulation (1.0 µg kg-1 adrenaline) under conditions of (1) normoxia, (2) hypoxia (approximate PwO2 12 kPa) and (3) 2.5 h after returning to normoxia. q·cor for resting fish under normoxic conditions was 0.14±0.02 ml min-1 kg-1 (approximately 0.85 % of Q(dot)). When exposed to hypoxia, although both resting Q(dot) and q·cor increased, q·cor increased to a greater degree (Q(dot) by 17 % and q·cor by 36 %). During hypoxia, maximum adrenaline-stimulated Q(dot) was comparable to that observed for normoxic fish. However, because Q(dot) was elevated in resting hypoxic fish, the capacity of hypoxic fish to increase Q(dot) above resting levels was 50 % lower than that measured in normoxic fish. Although maximum q·cor in adrenaline-injected hypoxic trout was greater than that measured in normoxic trout, post-injection increases in q·cor (above resting levels) were not different between the two groups. Two and a half hours after hypoxic exposure, resting Q(dot) was still elevated (11 %) above normoxic levels, and the ability to increase Q(dot) when adrenergically stimulated was not fully restored. These results suggest (1) that resting q·cor in salmonids is approximately 1 % of Q(dot), (2) that increases in q·cor may be important in maintaining cardiovascular performance during hypoxic conditions, (3) that interactions between alpha-adrenergic constriction and metabolically related vasodilation of the coronary vasculature are important in determining q·cor in fish, (4) that exposure of fish to moderate environmental hypoxia reduces the scope for adrenergically mediated increases in Q(dot), and (5) that periods of recovery in excess of several hours are required before cardiovascular performance returns to pre-hypoxic levels.

1995 ◽  
Vol 269 (5) ◽  
pp. R1258-R1266 ◽  
Author(s):  
A. K. Gamperl ◽  
M. Axelsson ◽  
A. P. Farrell

Previous studies have suggested that trout cardiac performance is highly dependent on coronary blood flow during periods of increased activity or hypoxia. To examine the relationship between coronary perfusion and cardiac performance in swimming trout, cardiac output (Q), coronary blood flow (qcor), and dorsal aortic blood pressure were measured in rainbow trout (Oncorhynchus mykiss) during normoxia and hypoxia (PO2 approximately 9 kPa). In normoxic trout, stepwise changes in cardiovascular variables were observed as the swimming speed was incrementally increased from 0.15 body lengths (bl)/s to 1.0 bl/s. At 1.0 bl/s, qcor and cardiac power output had both increased by approximately 110%, and coronary artery resistance (Rcor) had decreased by 40%. During hypoxia, resting qcor was 35% higher, and Rcor was 20% lower, compared with normoxic values. In hypoxic swimming trout, the maximum changes in qcor (155% increase) and Rcor (50% decrease) were recorded at 0.75 bl/s. In contrast, cardiac power output and Q increased by an additional 40 and 20%, respectively, as swimming speed was increased from 0.75 to 1.0 bl/s. The results indicate that 1) increases in qcor parallel changes in cardiac power output; 2) during hypoxia there are compensatory increases in cardiac performance and coronary perfusion; and 3) the scope for increasing qcor in swimming trout is approximately 150%. In addition, results from preliminary experiments suggest that beta-adrenergic, but not cholinergic, mechanisms are involved in the regulation of coronary blood flow during exercise.


2010 ◽  
Vol 298 (5) ◽  
pp. R1240-R1248 ◽  
Author(s):  
Henrik Seth ◽  
Albin Gräns ◽  
Michael Axelsson

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.


Author(s):  
T.J. McArley ◽  
D. Morgenroth ◽  
L.A. Zena ◽  
A.E. Ekström ◽  
E. Sandblom

In fish, maximum O2 consumption rate (MO2max) and aerobic scope can be expanded following exhaustive exercise in hyperoxia; however, the mechanisms explaining this are yet to be identified. Here, in exhaustively exercised rainbow trout (Oncorhynchus mykiss), we assessed the influence of hyperoxia on MO2max, aerobic scope, cardiac function and blood parameters to address this knowledge gap. Relative to normoxia, MO2max was 33% higher under hyperoxia, and this drove a similar increase in aerobic scope. Cardiac output, due to increased stroke volume, was significantly elevated under hyperoxia at MO2max indicating hyperoxia released a constraint on cardiac contractility apparent with normoxia. Thus, hyperoxia improved maximal cardiac performance, thereby enhancing tissue O2 delivery and allowing a higher MO2max. Venous blood O2 partial pressure (PvO2) was elevated in hyperoxia at MO2max, suggesting a contribution of improved luminal O2 supply in enhanced cardiac contractility. Additionally, despite reduced haemoglobin and higher PvO2, hyperoxia treated fish retained a higher arterio-venous O2 content difference at MO2max. This may have been possible due to hyperoxia offsetting declines in arterial oxygenation known to occur following exhaustive exercise in normoxia. If this occurs, increased contractility at MO2max with hyperoxia may also relate to an improved O2 supply to the compact myocardium via the coronary artery. Our findings show MO2max and aerobic scope may be limited in normoxia following exhaustive exercise due to constrained maximal cardiac performance and highlight the need to further examine whether or not exhaustive exercise protocols are suitable for eliciting MO2max and estimating aerobic scope in rainbow trout.


2019 ◽  
Vol 189 (6) ◽  
pp. 757-769 ◽  
Author(s):  
Andreas Ekström ◽  
Albin Gräns ◽  
Erik Sandblom

Abstract Coronary perfusion and cardiac autonomic regulation may benefit myocardial oxygen delivery and thermal performance of the teleost heart, and thus influence whole animal heat tolerance. Yet, no study has examined how coronary perfusion affects cardiac output during warming in vivo. Moreover, while β-adrenergic stimulation could protect cardiac contractility, and cholinergic decrease in heart rate may enhance myocardial oxygen diffusion at critically high temperatures, previous studies in rainbow trout (Oncorhynchus mykiss) using pharmacological antagonists to block cholinergic and β-adrenergic regulation showed contradictory results with regard to cardiac performance and heat tolerance. This could reflect intra-specific differences in the extent to which altered coronary perfusion buffered potential negative effects of the pharmacological blockade. Here, we first tested how cardiac performance and the critical thermal maximum (CTmax) were affected following a coronary ligation. We then assessed how these performances were influenced by pharmacological cholinergic or β-adrenergic blockade, hypothesising that the effects of the pharmacological treatment would be more pronounced in coronary ligated trout compared to trout with intact coronaries. Coronary blockade reduced CTmax by 1.5 °C, constrained stroke volume and cardiac output across temperatures, led to earlier cardiac failure and was associated with reduced blood oxygen-carrying capacity. Nonetheless, CTmax and the temperatures for cardiac failure were not affected by autonomic blockade. Collectively, our data show that coronary perfusion improves heat tolerance and cardiac performance in trout, while evidence for beneficial effects of altered cardiac autonomic tone during warming remains inconclusive.


2009 ◽  
Vol 296 (2) ◽  
pp. R345-R352 ◽  
Author(s):  
Henrik Seth ◽  
Erik Sandblom ◽  
Michael Axelsson

Mechanical gastric distension induces a dorsal aortic pressor response in rainbow trout ( Oncorhynchus mykiss) with no change in gastrointestinal blood flow. To elucidate what role chemical stimuli from the digested food has on the postprandial cardiovascular response, a new method was developed to investigate the contribution of individual nutrient components. Three predigested experimental diets were injected directly into the proximal intestine of rainbow trout and cardiac output (CO), gut blood flow (Qcma), heart rate (HR), and stroke volume (SV) were recorded. Specific dynamic action (SDA) was estimated by measuring oxygen consumption. When a balanced diet (50% protein, 25% fat, 15% carbohydrate) was injected, Qcma and CO increased within 1 h by 45 and 27%, respectively. The response to a high-protein diet (70% protein, 5% fat, 15% carbohydrate) was quantitatively similar but delayed, with a maximal blood flow response after 2 h. With a high-lipid diet (60% fat, 15% protein, 15% carbohydrate), the peak increase in Qcma by 22% occurred after 30 min and thereafter declined rapidly. The SDA response (19%) to the balanced diet was temporally matched with the hyperemia. With a high-protein diet, the response is delayed and enlarged (34%) compared with the balanced diet. The high-lipid diet gave no significant SDA response. We conclude that the chemical composition of the food influences the postprandial hyperemia and the SDA, such that the components appear to work in a synergistic fashion. The present results also demonstrate that both redistribution of blood flow and an overall increase in CO contribute to the postprandial increase in gut blood flow in this species.


2008 ◽  
Vol 294 (5) ◽  
pp. R1648-R1656 ◽  
Author(s):  
Henrik Seth ◽  
Erik Sandblom ◽  
Susanne Holmgren ◽  
Michael Axelsson

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.


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jeroen Brijs ◽  
Michael Axelsson ◽  
Albin Gräns ◽  
Nicolas Pichaud ◽  
Catharina Olsson ◽  
...  

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