Respiratory, Ventilatory, and Cardiovascular Responses to Experimental Anaemia in the Starry Flounder, Platichthys Stellatus

1979 ◽  
Vol 82 (1) ◽  
pp. 139-162
Author(s):  
CHRIS M. WOOD ◽  
B. R. McMAHON ◽  
D. G. MCDONALD

Unrestrained, quiescent starry flounder maintained approximately normal levels of O2 uptake in the face of severe experimental anaemia. At haematocrits above about 5 %, the only major compensation was a reduction in venous O2 tension which lowered venous saturation and thereby kept a constant difference between arterial and venous O2 contents. Below a haematocrit of about 5 %, this difference decreased, and many additional compensations were invoked, including increases in ventilation, expired O2 tension, arterial O2 tension, and cardiac output, and decreases in systemic vascular resistance and blood pH. All changes could be reversed by restoration of haematocrit. Exercise performance and post-exercise changes in blood pH and lactate differed only slightly between anaemic and normal flounder. In wild flounder, anaemia commonly occurs and apparently only causes death at the haematocrit value (about 5 %) below which most major compensations are implemented. The respiratory strategy of the flounder during anaemia is compared with that of the rainbow trout.

1977 ◽  
Vol 69 (1) ◽  
pp. 173-185
Author(s):  
C. M. Wood ◽  
B. R. McMahon ◽  
D. G. McDonald

Exhausting activity results in a marked and immediate drop in blood pH which gradually returns to normal over the following 6h. The acidosis is caused largely by elevated Pco2 levels, which vary inversely with pH. Blood lactate concentration increases slowly, reaching a maximum at 2--4h post-exercise, and contributes significantly to the acidosis only late in the recovery period. The slow time course of lactic acid release into the blood permits temporal separation of the peak metabolic acidosis from the peak respiratory acidosis. Evidence is presented that a metabolic acid other than lactic also makes a modest contribution to the pH depression during the recovery period.


2001 ◽  
Vol 204 (1) ◽  
pp. 115-125 ◽  
Author(s):  
J.E. McKendry ◽  
S.F. Perry

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.


2018 ◽  
Vol 120 (11) ◽  
pp. 1201-1216 ◽  
Author(s):  
Achraf Ammar ◽  
Stephen J. Bailey ◽  
Hamdi Chtourou ◽  
Khaled Trabelsi ◽  
Mouna Turki ◽  
...  

AbstractThe functional significance of pomegranate (POM) supplementation on physiological responses during and following exercise is currently unclear. This systematic review aimed (i) to evaluate the existing literature assessing the effects of POM supplementation on exercise performance and recovery; exercise-induced muscle damage, oxidative stress, inflammation; and cardiovascular function in healthy adults and (ii) to outline the experimental conditions in which POM supplementation is more or less likely to benefit exercise performance and/or recovery. Multiple electronic databases were used to search for studies examining the effects of POM intake on physiological responses during and/or following exercise in healthy adult. Articles were included in the review if they investigated the effects of an acute or chronic POM supplementation on exercise performance, recovery and/or physiological responses during or following exercise. The existing evidence suggests that POM supplementation has the potential to confer antioxidant and anti-inflammatory effects during and following exercise, to improve cardiovascular responses during exercise, and to enhance endurance and strength performance and post-exercise recovery. However, the beneficial effects of POM supplementation appeared to be less likely when (i) unilateral eccentric exercise was employed, (ii) the POM administered was not rich in polyphenols (<1·69 g/l) and (iii) insufficient time was provided between POM-ingestion and the assessment of physiological responses/performance (≤1 h). The review indicates that POM has the potential to enhance exercise performance and to expedite recovery from intensive exercise. The findings and recommendations from this review may help to optimise POM-supplementation practice in athletes and coaches to potentially improve exercise-performance and post-exercise recovery.


2008 ◽  
Vol 33 (2) ◽  
pp. 246-253 ◽  
Author(s):  
Jessica M. Scott ◽  
Ben T.A. Esch ◽  
Sarah-Jane C. Lusina ◽  
Donald C. McKenzie ◽  
Michael S. Koehle ◽  
...  

We tested the hypothesis that following an acute bout of exercise cardiovascular and cerebrovascular responses to lower-body negative pressure (LBNP) would be altered due to post-exercise hypotension (PEH). Ten healthy, male, endurance-trained athletes (mean age ± SD = 29.6 ± 5) were assessed for cardiovascular and cerebrovascular responses to LBNP following acute bouts of interval and continuous exercise. Mean arterial pressure (MAP), cardiac output, total peripheral resistance, heart rate variability, and total cerebral oxygen index were determined during a baseline LBNP session. These indices were also determined during two other LBNP sessions: following an acute bout of interval exercise, and following an acute bout of continuous exercise. Compared with baseline, MAP was reduced after both exercise conditions, similar to values previously reported (10 mmHg; p < 0.05 vs. pre-exercise). Total peripheral resistance was significantly reduced following both exercise bouts, and heart rate was significantly increased post-exercise (rest: 59.6 ± 11.2; interval: 77.8 ± 12.8; continuous: 80.3 ± 15.2 beats·min–1). Both cardiac output and stroke volume responses to LBNP following exercise were not altered when compared with baseline measurements. Tissue oxygenation during –40 mmHg (interval: 74.31% ± 7.82% vs. continuous: 69.13% ± 5.23%) was significantly lower than during normobaric pressure (interval: 77.14% ± 1.30% vs. continuous: 74.41% ± 0.94%). It appears from these observations that although young, endurance-trained males experience PEH following acute bouts of interval or continuous exercise, this hypotension does not alter the cardiovascular and cerebrovascular responses to a moderate orthostatic stress.


1987 ◽  
Vol 133 (1) ◽  
pp. 263-282 ◽  
Author(s):  
C. L. Milligan ◽  
C. M. Wood

In vitro, exogenous adrenaline reduced the Bohr and Root shifts caused by elevated PaCO2 and depressed plasma pH in rainbow trout blood, but not in starry flounder blood. In vivo immediately after exercise, plasma adrenaline (Ad) and noradrenaline (NAd) increased about 12-fold in rainbow trout. Associated with this catecholamine mobilization was a significant haemoconcentration, red blood cell (RBC) swelling and a reduction in RBC [NTP]; the latter was larger than that explained by cell swelling alone, indicating metabolic degradation of nucleoside triphosphate (NTP). RBC intracellular pH (pHi) fell only slightly after exercise (0.07 units) at 0 h, but was restored by 0.5 h in the face of a large plasma acidosis (0.4 units). [O2]/[Hb] fell significantly, but this decline may have been due in part to the significant reduction in PaO2. The reduction in [O2]/[Hb] was less than predicted from in vitro O2-dissociation curves at low (0.5 nmol l-1) catecholamine levels, but similar to that predicted at high (90 nmol l-1) catecholamine levels. In flounder, resting Ad and NAd levels were about 10 times those in trout and did not change significantly after exercise. As a consequence, there was no reduction in RBC [NTP], and RBC pHi fell significantly (0.10 units) after exercise in the face of a large plasma acidosis (0.4 units) and remained depressed until 4 h, although RBC swelling did occur. These factors in addition to the increased PaCO2 may have contributed to the reduction in arterial [O2]/[Hb], in the face of a constant PaO2. However, [O2]/[Hb] was restored to resting levels prior to the correction of RBC pHi and PaCO2. This, in conjunction with the observation that catecholamines did not affect the in vitro blood--O2 dissociation curve, suggests that additional factors may be involved in regulating O2 transport after exercise in flounder.


1999 ◽  
Vol 202 (16) ◽  
pp. 2177-2190 ◽  
Author(s):  
S.F. Perry ◽  
R. Fritsche ◽  
T.M. Hoagland ◽  
D.W. Duff ◽  
K.R. Olson

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.


1994 ◽  
Vol 191 (1) ◽  
pp. 155-166 ◽  
Author(s):  
J Kagstrom ◽  
M Axelsson ◽  
S Holmgren

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.


1979 ◽  
Vol 78 (1) ◽  
pp. 167-179
Author(s):  
CHRIS M. WOOD ◽  
B. R. McMAHON ◽  
D. G. McDONALD

A wide range of respiratory, ventilatory, and cardiovascular parameters have been recorded under completely resting conditions in the starry flounder (Platichthys stellatus), a generally inactive benthic teleost. The results differ in a number of important respects from those of a previous study on the same species. The present data have also been compared with those reported for the active pelagic rainbow trout (Salmo gairdnen) and for other teleost species. Of particular note in the flounder, relative to the trout, are low arterial and venous Poo2's, a low arterial-venous O2 content difference, a low transfer factor and high diffusion gradient for O2 across the gills, a high in vivo blood O2 affinity, a high cardiac output and stroke volume accompanied by a low peripheral vascular resistance, a low ventilation volume, a low ventilation-perfusion ratio, and a low capacity-rate ratio for O2 exchange at the gills. Parameters of CO2 transport and acidbase regulation appear conventional, though blood CO2 contents and lactate concentrations are low. The respiratory strategies of inactive versus active, and benthic versus pelagic teleosts are discussed. Note: Present address: Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario, Canada L8S 4K1.


2017 ◽  
Vol 312 (1) ◽  
pp. R31-R39 ◽  
Author(s):  
Jeroen Brijs ◽  
Erik Sandblom ◽  
Esmée Dekens ◽  
Joacim Näslund ◽  
Andreas Ekström ◽  
...  

Substantial increases in cardiac output (CO), stroke volume (SV), and gastrointestinal blood flow are essential for euryhaline rainbow trout ( Oncorhyncus mykiss) osmoregulation in seawater. However, the underlying hemodynamic mechanisms responsible for these changes are unknown. By examining a range of circulatory and cardiac morphological variables of seawater- and freshwater-acclimated rainbow trout, the present study revealed a significantly higher central venous pressure (CVP) in seawater-acclimated trout (~0.09 vs. −0.02 kPa). This serves to increase cardiac end-diastolic volume in seawater and explains the elevations in SV (~0.41 vs. 0.27 ml/kg) and CO (~21.5 vs. 14.2 ml·min−1·kg−1) when compared with trout in freshwater. Furthermore, these hemodynamic modifications coincided with a significant increase in the proportion of compact myocardium, which may be necessary to compensate for the increased wall tension associated with a larger stroke volume. Following a temperature increase from 10 to 16.5°C, both acclimation groups exhibited similar increases in heart rate (Q10 of ~2), but SV tended to decrease in seawater-acclimated trout despite the fact that CVP was maintained in both groups. This resulted in CO of seawater- and freshwater-acclimated trout stabilizing at a similar level after warming (~26 ml·min−1·kg−1). The consistently higher CVP of seawater-acclimated trout suggests that factors other than compromised cardiac filling constrained the SV and CO of these individuals at high temperatures. The present study highlights, for the first time, the complex interacting effects of temperature and water salinity on cardiovascular responses in a euryhaline fish species.


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