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.

Modulation of cardiovascular response to dynamic exercise by fastigial nucleus

1984 ◽  
Vol 56 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
K. J. Dormer
Keyword(s):  
Blood Pressure ◽  
Repeated Measures ◽  
Cardiovascular Response ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Fastigial Nucleus ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood

Mongrel dogs (n = 34) were used to record the cardiovascular responses during submaximal exercise-tolerance tests (ETT) before and after the placement of lesions in rostral portions of the cerebellar fastigial nucleus (FN). Sterile surgical procedures were used to implant solid-state pressure transducers into the left ventricle or descending aorta (anesthesia 1% halothane in O2) and multipolar stainless steel electrodes into FN (anesthesia alpha-chloralose 115 mg/kg iv). Heart rate (HR), maximal left ventricular systolic pressure ( LVPmax ) and its first derivative ( dLVP /dt), and mean arterial blood pressure (MAP) were recorded during a motorized treadmill ETT. Electrolytic direct-current or radio-frequency lesions were made through the indwelling FN electrodes, and the ETT was repeated following 10–14 days recovery. Two-way analysis of variance (ANOVA), with repeated measures on one, and one-way ANOVA for simple effects indicated a significant reduction in HR and MAP (P less than 0.01) but not LVPmax and dLVP /dt occurred during exercise as a result of rostral FN lesions. Although the trend for reduced LVPmax and dLVP /dt was also evident, a relatively greater decrease in blood pressure occurred in the peripheral vasculature during exercise. It was concluded that FN acts as a modulator of HR and MAP during dynamic exercise because of the observed deficits, and because FN is known to both send efferent projections to medullary vasomotor areas and receive projections from motor cortex and muscle and joint afferents.

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.

Haemodynamks of Recovery after Strenuous Exercise in Physically Trained Hypertensive and Normotensive Subjects

1994 ◽  
Vol 86 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Edoardo Casiglia ◽  
Paolo Palatini ◽  
Stefano Bongiovi ◽  
Luca Mario ◽  
Giovanna Colangeli ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Anaerobic Threshold ◽  
Recovery Period ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Mean Blood Pressure ◽  
Left Ventricular Ejection ◽  
Arterial Blood ◽  
Normotensive Subjects

1. Central and peripheral post-exercise haemo-dynamics were studied in 18 physically trained male subjects (10 hypertensive and eight normotensive) engaging in sports activities for 3–5 h/week. After a preliminary multistage bicycle ergometric test to evaluate their maximal oxygen consumption and anaerobic threshold, they underwent prolonged exercise at anaerobic threshold in the semi-supine position at 30% grade until exhaustion (mean duration 60.0 + 16.7 min in the normotensive subjects and 61.0 + 5.7 min in the hypertensive subjects, not significant). During the recovery time, intra-arterial blood pressure, echocardiographic cardiac output and indium-gallium strain-gauge plethysmographc peripheral flow were measured, and total, forearm and leg peripheral resistances were calculated respectively from mean blood pressure/cardiac output and mean blood pressure/peripheral resistance. 2. Systolic blood pressure was decreased during the entire recovery period in comparison with the baseline values (−8.4 mmHg, −43.8 mmHg and −39.7 mmHg at the 1st, 5th and 10th min in the hypertensive subjects, P = 0.001, P = 0.0001 and P = 0.0001 respectively; −18.8, −25.5 and −24.1 mmHg in the normotensive subjects, not significant, P = 0.01 and P = 0.01, respectively) without any significant difference between the two groups, whereas the reduction in diastolic blood pressure was not statistically significant. Peripheral flow increased and peripheral resistance decreased in parallel in the forearm and the leg and showed similar trends in the hypertensive subjects and the normotensive subjects. The increase in cardiac output and left ventricular ejection fraction and the decrease in total resistance were also similar in the two groups. 3. In conclusion, after long-lasting strenuous leg exercise central and peripheral haemodynamics vary to the same degree in hypertensive and normotensive trained subjects. Peripheral haemodynamics (similar in the leg and the arm in both groups) closely reflect systemic haemodynamics. The blood pressure reduction observed in the recovery period is totally due to the fall in systemic vascular resistance, while cardiac output is increased.

Roles of cardiac output and peripheral resistance in mediating blood pressure response to stress in rats

1998 ◽  
Vol 274 (4) ◽  
pp. R1065-R1069 ◽  
Author(s):  
Sheng-Gang Li ◽  
David C. Randall ◽  
David R. Brown
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Unconditioned Response ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Behavioral Stress

The change in arterial blood pressure (BP) in response to presentation of an acute behavioral stress (i.e., classical conditioning) in rat includes an initial rapid rise (C1) followed by a delayed, but more sustained, pressor response (C2). The purpose of this experiment is to determine the patterns of change in cardiac output (CO) and total peripheral vascular resistance (TPR) that are associated with the behaviorally induced pressor response. A blood flow probe was implanted around the ascending aorta, and a catheter was implanted in a femoral artery in 10 male Sprague-Dawley rats. The rats were trained by a 15-s tone (CS+) followed by a 0.5-s tail shock; another tone (CS−), never followed by shock, served as a behavioral control. BP responded to the stressful stimulus (CS+) by a rapid C1 increase (8 ± 1 mmHg; mean ± SE) followed by the delayed C2 response (2 ± 0.3 mmHg); the unconditioned response to shock was a 9 ± 2 mmHg increase in BP. The C1 BP increase produced a significant increase in TPR (10 ± 1 dyn ⋅ s/cm5); CO was not significantly changed. TPR decreased during C2 (−4 ± 2 dyn ⋅ s/cm5), whereas CO was significantly increased (2 ± 1 ml/min). These data contribute to our understanding of how the autonomic nervous system organizes the cardiovascular response to a suddenly perceived behavioral stress.

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.

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.

scholarly journals INDIVIDUAL DIFFERENCES IN EMOTION REGULATION AND CARDIOVASCULAR RESPONDING TO STRESS

2021 ◽  
Author(s):  
Siobhán M Griffin ◽  
Siobhán Howard
Keyword(s):  
Blood Pressure ◽  
Emotion Regulation ◽  
Individual Differences ◽  
Acute Stress ◽  
Negative Emotion ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Emotional Valence ◽  
Emotion Words

Instructed use of reappraisal to regulate stress in the laboratory is typically associated with a more adaptive cardiovascular response to stress, indexed by either: (i) lower cardiovascular reactivity (CVR; e.g., lower blood pressure); or (ii) a challenge-oriented response profile (i.e., greater cardiac output paired with lower total peripheral resistance). In contrast, instructed use of suppression is associated with exaggerated CVR (e.g., greater heart rate, blood pressure). Despite this, few studies have examined if the habitual use of these strategies are related to cardiovascular responding during stress. The current study examined the relationship between cardiovascular responses to acute stress and individual differences in emotion regulation style: trait reappraisal, suppression, and emotion regulation difficulties. Forty-eight participants (25 women, 23 men) completed a standardised laboratory stress paradigm incorporating a 20-minute acclimatization period, a 10-minute baseline, and two 5-minute speech tasks separated by a 10-minute inter-task rest period. The emotional valence of the speech task was examined as a potential moderating factor; participants spoke about a block of negative-emotion words and a block of neutral-emotion words. Cardiovascular parameters were measured using the Finometer Pro. Greater habitual use of suppression was associated with exaggerated blood pressure responding to both tasks. However, only in response to the negative-emotion task was greater use of reappraisal associated with a challenge-oriented cardiovascular response. The findings suggest that individual differences in emotion regulation translate to differing patterns of CVR to stress, but the emotional valence of the stressor may play a role.

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.

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