scholarly journals Heart rate and blood pressure dependence of aortic distensibility in rats: comparison of measured and calculated pulse wave velocity

2020 ◽  
Vol 39 (1) ◽  
pp. 117-126
Author(s):  
Bart Spronck ◽  
Isabella Tan ◽  
Koen D. Reesink ◽  
Dana Georgevsky ◽  
Tammo Delhaas ◽  
...  
1975 ◽  
Vol 228 (1) ◽  
pp. 238-243 ◽  
Author(s):  
PG Katona ◽  
KS Tan

Changes in pulse-wave velocity were simulated by changing the relative timing between aortic and carotid sinus barorecptor activity in anesthetized rabbits and dogs. In the rabbit, electrical stimulation was used to vary the timing; in the dog, it was also varied by perfusing the carotid sinuses with externally generated pressure pulses that could be triggered in any portion of the cardiac cycle. Changing the relative delay between aortic and carotid sinsus nerve stimulation did not result in variations of blood pressure or heart rate in the rabbit. Varing the time of electrical stimulation of the carotid sinus nerve caused at most 5 mmHg change of blood pressure in the dog. Delay-related heart-rate changes could be usually observed only when the stimulus consisted of short, high-intensity bursts. When the carotid sinus was externally perfused with pulses of pressure, only one out of five dogs showed delay-related variations in blood pressure (3mmHg) and heart rate (6 beats/min). It is concluded that variations in pulse-wave velocity are unlikely to play a significant role in acute cardiovascular control.


PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107852 ◽  
Author(s):  
Anxin Wang ◽  
Jie Tao ◽  
Xiuhua Guo ◽  
Xuemei Liu ◽  
Yanxia Luo ◽  
...  

Author(s):  
Pierre Lantelme ◽  
Christine Mestre ◽  
Alain Gressard ◽  
Hugues Milon ◽  
Michel Lievre

1995 ◽  
Vol 89 (3) ◽  
pp. 247-253 ◽  
Author(s):  
E. D. Lehmann ◽  
K. D. Hopkins ◽  
R. L. Jones ◽  
A. G. Rudd ◽  
R. G. Gosling

1. Non-invasive aortic compliance measurements have been used previously to assess the distensibility of the aorta in several pathological conditions associated with increased cardiovascular risk. We set out to establish whether aortic compliance is abnormal in patients with stroke. 2. Pulse wave velocity measurements of thoracoabdominal aortic compliance were made in 20 stroke patients and 25 age- and sex-matched hospitalized, non-stroke control subjects putatively free of cardiovascular disease. Since compliance varies with non-chronic changes in blood pressure, a blood pressure corrected index of aortic distensibility, Cp, was calculated. 3. Aortic compliance was significantly reduced in patients with stroke compared with non-stroke control subjects (0.46 ± 0.27 versus 0.86 ± 0.34%/10 mmHg, P < 0.0002), corresponding with higher values for pulse wave velocity. Stroke patients also had significantly higher systolic and diastolic blood pressures (P < 0.02 and P < 0.002 respectively) and total cholesterol levels (P < 0.004) than the control subjects. Calculation of Cp did not alter the observation of stiffer aortas in the stroke cohort (P < 0.0007). 4. In both stroke patient and control cohorts, as expected, inverse trends were observed between aortic compliance and blood pressure. Also as expected, in the control group Cp values did not show a relationship with blood pressure (r = 0.02, P = 0.092, not significant). However, in the stroke cohort a marked dependence of Cp on blood pressure was observed (r = −0.48, P = 0.03). 5. Transoesophageal echocardiographic studies have recently identified advanced atherosclerosis in the ascending aorta as a possible source of cerebral emboli and an independent risk factor for ischaemic stroke. Our observations of significantly stiffer thoracoabdominal aortas in patients with stroke lead us to hypothesize that a totally non-invasive assessment of aortic compliance may potentially prove a useful surrogate marker of such atherosclerotic risk. 6. Blood pressure-corrected indices of arterial elastic properties based on normotensive models are widely applied in the literature. Our observation that these indices exhibit a considerable blood pressure dependence leads us to urge caution in the use of such corrections, especially in hypertensive patients.


2021 ◽  
Vol 12 ◽  
Author(s):  
Kenneth S. Noguchi ◽  
Kevin Moncion ◽  
Elise Wiley ◽  
Maureen J. MacDonald ◽  
Julie Richardson ◽  
...  

BackgroundStroke is a highly disabling condition and is the second leading cause of death globally. Engaging in aerobic exercise is important for the prevention of a recurrent stroke through improving markers of cardiovascular health such as blood pressure and arterial stiffness. While higher intensities of aerobic exercise generally elicit greater cardioprotective effects, little is known about the acute cardiovascular effects of a single session of high intensity aerobic exercise in people with stroke. The objective of this study was to model the recovery of arterial stiffness (carotid-femoral pulse wave velocity, cfPWV), heart rate and blood pressure following peak intensity aerobic exercise in individuals with chronic stroke.MethodsTen participants with chronic stroke (mean ± SD age = 56.9 ± 11.8 years, median [IQR] years post-stroke = 2.9 [1.9]) performed a symptom-limited cardiopulmonary exercise test (CPET) on a recumbent stepper. Before the CPET, resting cfPWV, heart rate and blood pressure were measured. Immediately following the CPET, all outcomes were measured again continuously for 20 min to use all available observations (n = 245 observations) and capture any potential non-linear changes. Mixed model analyses were then applied to model post-exercise changes of cfPWV, heart rate and blood pressure.ResultsCarotid-femoral pulse wave velocity was increased from rest following the CPET (9.0 ± 0.53 to 9.9 ± 0.52 m/s, p &lt; 0.001) and remained elevated for 20 min into post-exercise recovery, independent of heart rate (p = 0.001). Heart rate also increased from baseline (71.2 ± 3.2 to 77.4 ± 3.1 bpm, p &lt; 0.001) and remained elevated for 10 min post-exercise (p &lt; 0.001). Finger systolic blood pressure was reduced from rest (117.3 ± 4.7 to 111.8 ± 4.6 mmHg, p &lt; 0.001) and remained reduced for 15 min after exercise (p &lt; 0.001). There were no significant differences in finger diastolic or mean arterial pressures from rest.ConclusionThis was the first study to capture continuous changes in cfPWV following peak aerobic exercise in any clinical population. The present study revealed that cfPWV is elevated for 20 min after peak aerobic exercise in individuals with stroke, which was independent of heart rate. These findings suggest there may be autonomic imbalances in large arteries following peak intensity aerobic exercise in individuals with stroke.


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