Cardiovascular responses of the red-blooded antarctic fishes Pagothenia bernacchii and P. borchgrevinki

1992 ◽  
Vol 167 (1) ◽  
pp. 179-201 ◽  
Author(s):  
M. Axelsson ◽  
W. Davison ◽  
M. E. Forster ◽  
A. P. Farrell

The aim of this study was to investigate cardiac performance and cardiovascular control in two red-blooded nototheniid species of antarctic fishes, Pagothenia bernacchii (a benthic fish) and P. borchgrevinki (a cryopelagic fish), and to make comparisons with existing information on haemoglobin-free antarctic teleosts. In quiescent P. bernacchii at 0 degrees C ventral aortic pressure (PVA) was 3.09 kPa and cardiac output (Q) was 17.6 ml min-1 kg-1, with a heart rate (fH) of 10.5 beats min-1 and stroke volume of 1.56 ml kg-1. Following atropine treatment, Q was maintained but heart rate increased and stroke volume decreased. Resting heart rate resulted from an inhibitory cholinergic tone of 80.4% and an excitatory adrenergic tone of 27.5%. The intrinsic heart rate was 21.7 beats min-1 at 0 degrees C. In quiescent P. borchgrevinki at 0 degrees C, PVA was 3.6 kPa, Q was 29.6 ml min-1 kg-1 and stroke volume was 2.16 ml kg-1. The resting heart rate in P. borchgrevinki of 11.3 beats min-1 resulted from an inhibitory cholinergic tone of 54.5% and an excitatory adrenergic tone of 3.2%. The intrinsic heart rate was 23.3 beats min-1. P. bernacchii maintained Q during a progressive decrease in water oxygen tension from 20 to 6.7 kPa, but fH was increased significantly. Thus, although there is cholinergic control of the heart, no hypoxic bradycardia was observed. Recovery from hypoxia was associated with increases in Q and fH; stroke volume returned to control values. PVA declined in recovery as total vascular resistance decreased. Hypoxic exposure following atropine treatment resulted in progressive increases in PVA, Q and stroke volume; fH decreased during the recovery period. Hypoxic exposure in P. borchgrevinki produced similar cardiovascular responses to those observed in P. bernacchii. During an acute increase in water temperature from 0 to 5 degrees C, P. bernacchii regulated Q and total vascular resistance. Stroke volume decreased as fH increased. The intrinsic heart rate had a Q10 of 1.96 over this temperature range. P. bernacchii maintained chronotropic inhibition up to a temperature of 2.5-3.0 degrees C. However, by 5 degrees C this chronotropic inhibition of the heart rate was lost. Infusion of adrenaline into the ventral aorta of P. bernacchii resulted in significant increases in Q, fH, PVA and total vascular resistance. Infusion of adrenaline after atropine treatment caused similar cardiovascular changes without the change in fH. P. borchgrevinki could sustain swimming in a water tunnel at approximately 1 body length per second for 6–10 min.(ABSTRACT TRUNCATED AT 400 WORDS)

2019 ◽  
Vol 20 (13) ◽  
pp. 3149 ◽  
Author(s):  
Lackner ◽  
Papousek ◽  
Schmid-Zalaudek ◽  
Cervar-Zivkovic ◽  
Kolovetsiou-Kreiner ◽  
...  

Women with pregnancies complicated by preeclampsia appear to be at increased risk of metabolic and vascular diseases in later life. Previous research has also indicated disturbed cardiorespiratory adaptation during pregnancy. The aim of this study was to follow up on the physiological stress response in preeclampsia several weeks postpartum. A standardized laboratory test was used to illustrate potential deviations in the physiological stress responding to mildly stressful events of the kind and intensity in which they regularly occur in further everyday life after pregnancy. Fifteen to seventeen weeks postpartum, 35 women previously affected by preeclampsia (19 mild, 16 severe preeclampsia), 38 women after uncomplicated pregnancies, and 51 age-matched healthy controls were exposed to a self-relevant stressor in a standardized stress-reactivity protocol. Reactivity of blood pressure, heart rate, stroke index, and systemic vascular resistance index as well as baroreceptor sensitivity were analyzed. In addition, the mutual adjustment of blood pressure, heart rate, and respiration, partitioned for influences of the sympathetic and the parasympathetic branches of the autonomic nervous system, were quantified by determining their phase synchronization. Findings indicated moderately elevated blood pressure levels in the nonpathological range, reduced stroke volume, and elevated systemic vascular resistance in women previously affected by preeclampsia. Despite these moderate abnormalities, at the time of testing, women with previous preeclampsia did not differ from the other groups in their physiological response patterns to acute stress. Furthermore, no differences between early, preterm, and term preeclampsia or mild and severe preeclampsia were observed at the time of testing. The findings suggest that the overall cardiovascular responses to moderate stressors return to normal in women who experience a pregnancy with preeclampsia a few weeks after delivery, while the operating point of the arterial baroreflex is readjusted to a higher pressure. Yet, their regulation mechanisms may remain different.


1986 ◽  
Vol 251 (6) ◽  
pp. H1316-H1323 ◽  
Author(s):  
B. R. Walker

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)


1994 ◽  
Vol 77 (3) ◽  
pp. 1500-1506 ◽  
Author(s):  
J. L. Fleg ◽  
S. P. Schulman ◽  
F. C. O'Connor ◽  
G. Gerstenblith ◽  
L. C. Becker ◽  
...  

It is unclear whether the markedly enhanced aerobic exercise capacity of older endurance-trained men relative to their sedentary age peers is mediated primarily by central or peripheral cardiovascular mechanisms. To address this question, we performed radionuclide ventriculography with respiratory gas exchange measurements during exhaustive upright cycle ergometry in 16 endurance-trained men aged 63 +/- 7 yr and in 35 untrained men of similar age. As expected, maximal O2 consumption during treadmill exercise was much higher in athletes than in controls. At rest and during fixed submaximal cycle work rates through 100 W, athletes demonstrated lower heart rates and greater stroke volume indexes than controls while maintaining similar cardiac indexes and O2 uptake (VO2). At exhaustion, athletes achieved 53% higher work rates and peak VO2 per kilogram body weight than the sedentary men. The higher peak VO2 in athletes was achieved by a 22.5% larger cardiac index and a 15.6% greater arteriovenous O2 difference. The larger peak cardiac index in the athletes than in sedentary controls was mediated entirely by a greater stroke volume index; peak heart rates were virtually identical. The athletes' greater stroke volume index was achieved through an 11% larger end-diastolic volume index and a 7% higher ejection fraction, both of borderline significance. At exhaustion, athletes demonstrated a lower systemic vascular resistance than controls, despite a higher value at rest. Athletes also showed greater exercise-induced increments in heart rate, stroke volume index, and cardiac index and a greater reduction in systemic vascular resistance from rest to maximal workload.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 68 (2) ◽  
pp. 561-567 ◽  
Author(s):  
K. C. Kregel ◽  
J. M. Overton ◽  
D. R. Seals ◽  
C. M. Tipton ◽  
L. A. Fisher

The effects of intracerebroventricular (icv) administration of a corticotropin-releasing factor (CRF) receptor antagonist, alpha-helical CRF, on systemic and regional hemodynamic adjustments to exercise were studied in conscious rats. On consecutive days, rats received saline icv, alpha-helical CRF icv, and no treatment 30 min before treadmill exercise (TMX). Increases in heart rate (HR) and mean arterial pressure (MAP) in response to TMX (16.1-28.6 m/min) were similar after icv administration of saline or no treatment. In rats receiving saline icv or no treatment, estimated vascular resistance increased in the mesenteric and renal regions and declined in the iliac (hindlimb) region. After icv administration of alpha-helical CRF9-41, HR and MAP responses during TMX were significantly attenuated. In addition, TMX-induced elevations of estimated mesenteric vascular resistance and iliac blood flow velocity were blunted after CRF receptor blockade. These altered cardiovascular and hemodynamic responses were ultimately reflected in the animals' compromised ability to run. The results suggest that the central nervous system actions of endogenous CRF are necessary for the full expression of the cardiovascular adjustments to TMX in the conscious rat.


2010 ◽  
Vol 32 (3) ◽  
pp. 339-358 ◽  
Author(s):  
Sarah E. Williams ◽  
Jennifer Cumming ◽  
George M. Balanos

The present study investigated whether imagery could manipulate athletes’ appraisal of stress-evoking situations (i.e., challenge or threat) and whether psychological and cardiovascular responses and interpretations varied according to cognitive appraisal of three imagery scripts: challenge, neutral, and threat. Twenty athletes (Mage = 20.85; SD = 1.76; 10 female, 10 male) imaged each script while heart rate, stroke volume, and cardiac output were obtained using Doppler echocardiography. State anxiety and self-confidence were assessed following each script using the Immediate Anxiety Measures Scale. During the imagery, a significant increase in heart rate, stroke volume, and cardiac output occurred for the challenge and threat scripts (p < .05). Although there were no differences in physiological response intensities for both stress-evoking scripts, these responses, along with anxiety symptoms, were interpreted as facilitative during the challenge script and debilitative during the threat script. Results support using imagery to facilitate adaptive stress appraisal.


1991 ◽  
Vol 80 (1) ◽  
pp. 39-45 ◽  
Author(s):  
M. A. Rahman ◽  
I. Farquhar ◽  
T. Bennett

1. Cardiovascular responses to three different interventions, namely the Valsalva manoeuvre, deep breathing and a cold stimulus on the face, were studied in two ethnic groups (European and Bangladeshi) that have been shown to differ in the prevalence of hypertensive-vascular disease. The data obtained consisted of systolic blood pressure, diastolic blood pressure, mean blood pressure, heart rate measured by using a beat-by-beat non-invasive blood pressure monitor (the Finapres), forearm blood flow determined by venous occlusion plethysmography, and calculated forearm vascular resistance. 2. The resting haemodynamic status was similar in European and Bangladeshi subjects. However, Bangladeshi subjects showed a greater increase in heart rate, but only after 20 s into the Valsalva manoeuvre, and greater overshoots in mean blood pressure after the manoeuvre than the European subjects. Furthermore, after cold face stimulation the fall in forearm vascular resistance to baseline levels was delayed in Bangladeshi subjects relative to that in the European subjects. 3. There were no inter-group differences in the reflex bradycardia relative to mean blood pressure or in the cardiac baroreflex sensitivity estimated from systolic blood pressure and pulse interval after the Valsalva manoeuvre. In addition, values for the mean difference between maximum and minimum pulse intervals during deep breathing did not differ in Bangladeshi and European subjects. 4. These findings together suggest that, although cardiac vagal reflex responses appear similar in the two groups, sympatho-adrenal influences on the heart and vasculature may be greater in Bangladeshi subjects than in European subjects.


2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.


2007 ◽  
Vol 103 (6) ◽  
pp. 2018-2025 ◽  
Author(s):  
D. Fischer ◽  
P. Arbeille ◽  
J. K. Shoemaker ◽  
D. D. O'Leary ◽  
R. L. Hughson

This study tested the hypothesis that cardiovascular and hormonal responses to lower body negative pressure (LBNP) would be altered by 4-h head down bed rest (HDBR) in 11 healthy young men. In post-HDBR testing, three subjects failed to finish the protocol due to presyncopal symptoms, heart rate was increased during LBNP compared with pre-HDBR, mean arterial blood pressure was elevated at 0, −10, and −20 mmHg and reduced at −40 mmHg, central venous pressure (CVP) and cardiac stroke volume were reduced at all levels of LBNP. Plasma concentrations of renin, angiotensin II, and aldosterone were significantly lower after HDBR. Renin and angiotensin II increased in response to LBNP only post-HDBR. There was no effect of HDBR or LBNP on norepinephrine while epinephrine tended to increase at −40 mmHg post-HDBR ( P = 0.07). Total blood volume was not significantly reduced. Splanchnic blood flow taken from ultrasound measurement of the portal vein was higher at each level of LBNP post-compared with pre-HDBR. The gain of the cardiopulmonary baroreflex relating changes in total peripheral resistance to CVP was increased after HDBR, but splanchnic vascular resistance was actually reduced. These results are consistent with our hypothesis and suggest that cardiovascular instability following only 4-h HDBR might be related to altered hormonal and/or neural control of regional vascular resistance. Impaired ability to distribute blood away from the splanchnic region was associated with reduced stroke volume, elevated heart rate, and the inability to protect mean arterial pressure.


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