Cardiovascular responses to diving and their relation to lung and blood oxygen stores in vertebrates

1988 ◽  
Vol 66 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Warren Burggren
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Lung Perfusion ◽  
Blood Oxygen ◽  
Arterial Blood ◽  
Resistance Reduction ◽  
Lower Vertebrates ◽  
Oxygen Stores ◽  
Cardiovascular Performance

Air-breathing vertebrates generally respond to apnea during diving by adjusting cardiovascular performance (e.g., bradycardia, selective increases in peripheral resistance, reduction and redistribution of cardiac output). In mammals, and to a lesser extent in birds, the major O2 stores at the beginning of a dive reside within blood and tissues rather than in lung gas. Consequently, there is limited respiratory benefit during apnea in either maintaining or transiently restoring extensive lung perfusion to predive levels, and so cardiac output (and thus lung perfusion) remains low during the dive. In contrast, in most amphibians and reptiles the major O2 stores at the beginning of a dive reside within lung gas rather than in blood and tissues. Recent experiments on frogs and turtles reveal that pulmonary blood flow during diving can transiently increase to or above predive levels when it becomes necessary during the dive to transfer O2 from lung gas to arterial blood. In this regard, cardiovascular responses to diving in lower vertebrates are qualitatively different from those of higher vertebrates.

scholarly journals Prior head-down tilt does not impair the cerebrovascular response to head-up tilt

2015 ◽  
Vol 118 (11) ◽  
pp. 1356-1363 ◽  
Author(s):  
Changbin Yang ◽  
Yuan Gao ◽  
Danielle K. Greaves ◽  
Rodrigo Villar ◽  
Thomas Beltrame ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Cardiovascular Responses ◽  
Mean Flow ◽  
Cerebrovascular Autoregulation ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
S Period

The hypothesis that cerebrovascular autoregulation was not impaired during head-up tilt (HUT) that followed brief exposures to varying degrees of prior head-down tilt (HDT) was tested in 10 healthy young men and women. Cerebral mean flow velocity (MFV) and cardiovascular responses were measured in transitions to a 60-s period of 75° HUT that followed supine rest (control) or 15 s HDT at −10°, −25°, and −55°. During HDT, heart rate (HR) was reduced for −25° and −55°, and cardiac output was lower at −55° HDT. MFV increased during −10° HDT, but not in the other conditions even though blood pressure at the middle cerebral artery (BPMCA) increased. On the transition to HUT, HR increased only for −55° condition, but stroke volume and cardiac output transiently increased for −25° and −55°. Total peripheral resistance index decreased in proportion to the magnitude of HDT and recovered over the first 20 s of HUT. MFV was significantly less in all HDT conditions compared with the control in the first 5-s period of HUT, but it recovered quickly. An autoregulation correction index derived from MFV recovery relative to BPMCA decline revealed a delay in the first 5 s for prior HDT compared with control but then a rapid increase to briefly exceed control after −55° HDT. This study showed that cerebrovascular autoregulation is modified by but not impaired by brief HDT prior to HUT and that cerebral MFV recovered quickly and more rapidly than arterial blood pressure to protect against cerebral hypoperfusion and potential syncope.

Cardiovascular responses to blockade of angiotensin and alpha-adrenergic receptors

1978 ◽  
Vol 235 (3) ◽  
pp. F199-F202
Author(s):  
L. J. Borucki ◽  
D. Levenson ◽  
N. K. Hollenberg
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Adrenergic Blockade ◽  
Venous Tone ◽  
Arterial Blood ◽  
Adrenergic Blocking

Both angiotensin and alpha-adrenergic blocking agents reduce arterial blood pressure in hypovolemic states. We have compared the effects of an angiotensin antagonist (saralasin) and an alpha-adrenergic blocking agent (phenoxybenzamine) in supramaximal dosage on cardiac output, total peripheral resistance, and venous tone in rabbits rendered hypovolemic by restriction of sodium intake, supplemented by a furosemide-induced diuresis 48 h prior to study. Saralasin (10 microgram/kg per min) reduced arterial blood pressure significantly (-15 +/- 1.2 mmHg) despite an unchanged cardiac output (P less than 0.025) due to a fall in total peripheral resistance. Phenoxybenzamine (5 mg/kg) induced a much larger fall in arterial blood pressure (-28 +/- 3.6 mmHg), despite an identical reduction in total peripheral resistance, because cardiac output also fell (+/- 9 ml/kg per min). The reduction in cardiac output was associated with a significant increase in hindlimb venous distensibility (P less than 0.001) after alpha-adrenergic blockade. Saralasin, conversely, had no influence on venous tone. Adrenergic mechanisms contribute to cardiovascular homeostasis through an influence on both arteriolar and venous tone, whereas the effect of angiotensin is directed entirely to the arteriolar side of the circulation.

Cardiovascular effect of V1 vasopressinergic blockade during acute hypercapnia in conscious rats

1987 ◽  
Vol 252 (1) ◽  
pp. R127-R133 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Hypercapnic Acidosis ◽  
Conscious Rat ◽  
Arterial Pco2 ◽  
Arterial Blood

Experiments were performed to test the possible involvement of arginine vasopressin (AVP) in the systemic cardiovascular responses to acute hypercapnic acidosis in conscious chronically instrumented rats. Exposure to 6% CO2 caused arterial PCO2 to rise from 34 +/- 2 to 53 +/- 1 Torr. This level of hypercapnia was associated with a consistent bradycardia; however, cardiac output, blood pressure, and total peripheral resistance were not significantly affected. Administration of 10 micrograms/kg iv of the specific V1 vasopressinergic antagonist d(CH2)5Tyr(Me)AVP during 6% CO2 had no effect on any of the measured hemodynamic variables. Furthermore, d(CH2)5Tyr(Me)AVP also had no effect in normocapnic control animals. Exposure to a more severe level of hypercapnia (10% CO2, arterial PCO2 = 89 +/- 1 Torr) resulted in marked hemodynamic alterations. Profound bradycardia and decreased cardiac output in addition to increases in mean arterial blood pressure and total peripheral resistance were observed. V1 vasopressinergic antagonism during 10% CO2 had no effect on heart rate but greatly increased cardiac output. In addition, blood pressure fell and resistance was decreased below prehypercapnic levels. These data suggest that a number of the hemodynamic alterations associated with severe hypercapnic acidosis in the conscious rat may be mediated by the peripheral cardiovascular effects of enhanced AVP release.

Comparison of cardiovascular response to passive tilt in young and elderly men

1988 ◽  
Vol 66 (11) ◽  
pp. 1425-1432 ◽  
Author(s):  
D. A. Cunningham ◽  
R. J. Petrella ◽  
D. H. Paterson ◽  
P. M. Nichol
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Age Effects ◽  
Hemodynamic Responses ◽  
Arterial Blood ◽  
Postural Changes

To test the hypothesis that altered hemodynamic responses to postural changes are associated with aging, cardiovascular responses to head-up tilt (HUT) and head-down tilt (HDT) were examined in 12 healthy young (average age, 24.6 ± 1.7 years) and 12 healthy elderly (average age, 68.6 ± 2.2 years) men. Subjects were passively tilted from supine to 30°, 60°, and 90° HUT and HDT. Responses to these perturbations were determined 5 min after tilting with measures of heart rate (HR), blood pressure (SBP, DBP), and echocardiographically determined left ventricular diameter in systole and diastole (LVIDs, LVIDd). In HUT there were no significant age effects. In both young and elderly, SBP decreased significantly (p < 0.05), and DBP and HR increased significantly. Ejection fraction (EF), mean arterial blood pressure (MABP), and rate-pressure product (RPP) were unchanged in both groups. In HDT, the hemodynamic responses of the young and elderly were in opposite directions and significant age effects were found for SBP, DBP, HR, LVIDs, EF, MABP, and RPP. In HDT, the young appear to increase cardiac output primarily due to an increase in EF and end-diastolic volume (LVIDd), while HR is unchanged and SBP is decreased. MABP is unchanged, suggesting a small decrease in total peripheral resistance. The elderly may increase cardiac output slightly, owing to an increase in LVIDd with no change in EF, and a large increase in HR. Afterload increased markedly, therefore attenuating any increase in cardiac output. These results suggest that in healthy men, the cardiovascular response to HUT is not age related, while conversely there appear to be significant differences between young and elderly in response to HDT.

scholarly journals Fructose ingestion acutely elevates blood pressure in healthy young humans

2008 ◽  
Vol 294 (3) ◽  
pp. R730-R737 ◽  
Author(s):  
Clive M. Brown ◽  
Abdul G. Dulloo ◽  
Gayathri Yepuri ◽  
Jean-Pierre Montani
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Energy Expenditure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Health Concern ◽  
Arterial Blood ◽  
Glucose Ingestion

Overconsumption of fructose, particularly in the form of soft drinks, is increasingly recognized as a public health concern. The acute cardiovascular responses to ingesting fructose have not, however, been well-studied in humans. In this randomized crossover study, we compared cardiovascular autonomic regulation after ingesting water and drinks containing either glucose or fructose in 15 healthy volunteers (aged 21–33 yr). The total volume of each drink was 500 ml, and the sugar content 60 g. For 30 min before and 2 h after each drink, we recorded beat-to-beat heart rate, arterial blood pressure, and cardiac output. Energy expenditure was determined on a minute-by-minute basis. Ingesting the fructose drink significantly increased blood pressure, heart rate, and cardiac output but not total peripheral resistance. Glucose ingestion resulted in a significantly greater increase in cardiac output than fructose but no change in blood pressure and a concomitant decrease in total peripheral resistance. Ingesting glucose and fructose, but not water, significantly increased blood pressure variability and decreased cardiovagal baroreflex sensitivity. Energy expenditure increased by a similar amount after glucose and fructose ingestion, but fructose elicited a significantly greater increase in respiratory quotient. These results show that ingestion of glucose and fructose drinks is characterized by specific hemodynamic responses. In particular, fructose ingestion elicits an increase in blood pressure that is probably mediated by an increase in cardiac output without compensatory peripheral vasodilatation.

Differential contribution of central command to the cardiovascular responses during static exercise of ankle dorsal and plantar flexion in humans

2011 ◽  
Vol 110 (3) ◽  
pp. 670-680 ◽  
Author(s):  
Nan Liang ◽  
Tomoko Nakamoto ◽  
Seina Mochizuki ◽  
Kanji Matsukawa
Keyword(s):  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Plantar Flexion ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Central Command ◽  
Static Exercise ◽  
Maximum Increase ◽  
Arterial Blood ◽  
Differential Contribution

To examine whether central command contributes differently to the cardiovascular responses during voluntary static exercise engaged by different muscle groups, we encouraged healthy subjects to perform voluntary and electrically evoked involuntary static exercise of ankle dorsal and plantar flexion. Each exercise was conducted with 25% of the maximum voluntary force of the right ankle dorsal and plantar flexion, respectively, for 2 min. Heart rate (HR) and mean arterial blood pressure (MAP) were recorded, and stroke volume, cardiac output (CO), and total peripheral resistance were calculated. With voluntary exercise, HR, MAP, and CO significantly increased during dorsal flexion (the maximum increase, HR: 12 ± 2.3 beats/min; MAP: 14 ± 2.0 mmHg; CO: 1 ± 0.2 l/min), whereas only MAP increased during plantar flexion (the maximum increase, 6 ± 2.0 mmHg). Stroke volume and total peripheral resistance were unchanged throughout the two kinds of voluntary static exercise. With involuntary exercise, there were no significant changes in all cardiovascular variables, irrespective of dorsal or plantar flexion. Furthermore, before the force onset of voluntary static exercise, HR and MAP started to increase without muscle contraction, whereas they had no significant changes with involuntary exercise at the moment. The present findings indicate that differential contribution of central command is responsible for the different cardiovascular responses to static exercise, depending on the strength of central control of the contracting muscle.

scholarly journals Cardiovascular Responses During Downhill Treadmill Walking at Self-Selected Intensity in Older Adults

2013 ◽  
Vol 21 (3) ◽  
pp. 335-347 ◽  
Author(s):  
Mandy L. Gault ◽  
Richard E. Clements ◽  
Mark E.T. Willems
Keyword(s):  
Blood Pressure ◽  
Older Adults ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Treadmill Walking ◽  
Metabolic Demand ◽  
Arterial Blood ◽  
Cardiac Strain ◽  
Downhill Walking ◽  
Future Work

Cardiovascular responses of older adults to downhill (DTW, –10% incline) and level treadmill walking (0%) at self-selected walking speed (SSWS) were examined. Fifteen participants (age 68 ± 4 yr, height 1.69 ± 0.08 m, body mass 74.7 ± 8.1 kg) completed two 15-min walks at their SSWS (4.6 ± 0.6 km/hr). Cardiovascular responses were estimated using an arterial-volume finger clamp and infrared plethysmography. Oxygen consumption was 25% lower during DTW and associated with lower values for stroke volume (9.9 ml/beat), cardiac output (1.0 L/min), arteriovenous oxygen difference (a-v O2 diff, 2.4 ml/L), and systolic blood pressure (10 mmHg), with no differences in heart rate or diastolic and mean arterial blood pressure. Total peripheral resistance (TPR) was higher (2.11 mmHg) during DTW. During downhill walking, an exercise performed with reduced cardiac strain, endothelial changes, and reduced metabolic demand may be responsible for the different responses in TPR and a-v O2 diff. Future work is warranted on whether downhill walking is suitable for higher risk populations.

Role of vasopressin in acutely altered baroreflex sensitivity during hemorrhage in rats

1991 ◽  
Vol 261 (3) ◽  
pp. R677-R685 ◽  
Author(s):  
B. L. Brizzee ◽  
R. D. Russ ◽  
B. R. Walker
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Blood Loss ◽  
Baroreflex Sensitivity ◽  
Peripheral Resistance ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Arterial Hemorrhage ◽  
Moderate Elevation

Experiments were performed to examine the potential role of circulating arginine vasopressin (AVP) on baroreflex sensitivity during hypotensive and nonhypotensive hemorrhage in the conscious rat. Animals were chronically instrumented for measurement of cardiac output, blood pressure, and heart rate (HR). Three potential stimuli for release of AVP were utilized: 1) rapid 20% arterial hemorrhage that resulted in hypotension, 2) nonhypovolemic hypotension induced by intravenous infusion of nitroprusside, and 3) nonhypotensive hemorrhage (rapid 10% arterial blood withdrawal). Hypotensive hemorrhage was associated with significant reductions in blood pressure, cardiac output, HR, and calculated total peripheral resistance, an increase in baroreflex (BRR) bradycardia in response to pressor infusions of phenylephrine, and a moderate elevation in circulating AVP. Prior intravenous administration of a specific V1-vasopressinergic antagonist augmented the hypotensive response to hemorrhage; however, neither V1- nor V2-blockade affected hemorrhage-induced augmentation of the BRR. Inducement of hypotension by infusion of nitroprusside did not alter subsequent BRR sensitivity. Finally, nonhypotensive hemorrhage was associated with an increase in resting HR and augmented BRR sensitivity. However, in contrast to hypotensive hemorrhage, either V1- or V2-antagonism attenuated the increase in BRR sensitivity seen with 10% hemorrhage. These data suggest that, although AVP may play a role in blood pressure maintenance via its direct vasoconstrictor actions during hypotensive hemorrhage, the observed augmentation of BRR sensitivity associated with severe blood loss is not attributable to a vasopressinergic mechanism activated by circulating AVP. However, blood-borne AVP may contribute to BRR sensitivity alterations in response to mild blood loss.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Normal Brain ◽  
Spleen Volume ◽  
Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

Sign in / Sign up

Export Citation Format

Share Document