Relationship Between Time Course of Ruffier Index and Stress-Dependent Heart Rate During Eight Days of Skiing/Snowboarding

2009 ◽  
pp. 311-311-9 ◽  
Author(s):  
P Hofmann ◽  
B Stockinger
Keyword(s):  
Heart Rate ◽  
Time Course ◽  
Stress Dependent

scholarly journals Heart rate reduction with ivabradine promotes shear stress-dependent anti-inflammatory mechanisms in arteries

2016 ◽  
Vol 116 (07) ◽  
pp. 181-190 ◽  
Author(s):  
Luong Le ◽  
Hayley Duckles ◽  
Torsten Schenkel ◽  
Marwa Mahmoud ◽  
Jordi Tremoleda ◽  
...  
Keyword(s):  
Heart Rate ◽  
Shear Stress ◽  
Carotid Arteries ◽  
Vascular Inflammation ◽  
Protective Effects ◽  
En Face ◽  
Inflammatory Activation ◽  
Anti Inflammatory ◽  
Stress Dependent

SummaryBlood flow generates wall shear stress (WSS) which alters endothelial cell (EC) function. Low WSS promotes vascular inflammation and atherosclerosis whereas high uniform WSS is protective. Ivabradine decreases heart rate leading to altered haemodynamics. Besides its cardio-protective effects, ivabradine protects arteries from inflammation and atherosclerosis via unknown mechanisms. We hypothesised that ivabradine protects arteries by increasing WSS to reduce vascular inflammation. Hypercholesterolaemic mice were treated with ivabradine for seven weeks in drinking water or remained untreated as a control. En face immunostaining demonstrated that treatment with ivabradine reduced the expression of pro-inflammatory VCAM-1 (p<0.01) and enhanced the expression of anti-inflammatory eNOS (p<0.01) at the inner curvature of the aorta. We concluded that ivabradine alters EC physiology indirectly via modulation of flow because treatment with ivabradine had no effect in ligated carotid arteries in vivo, and did not influence the basal or TNFα-induced expression of inflammatory (VCAM-1, MCP-1) or protective (eNOS, HMOX1, KLF2, KLF4) genes in cultured EC. We therefore considered whether ivabradine can alter WSS which is a regulator of EC inflammatory activation. Computational fluid dynamics demonstrated that ivabradine treatment reduced heart rate by 20 % and enhanced WSS in the aorta. In conclusion, ivabradine treatment altered haemodynamics in the murine aorta by increasing the magnitude of shear stress. This was accompanied by induction of eNOS and suppression of VCAM-1, whereas ivabradine did not alter EC that could not respond to flow. Thus ivabradine protects arteries by altering local mechanical conditions to trigger an anti-inflammatory response.

A mathematical model of cardiovascular dynamics for the diagnosis and prognosis of hemorrhagic shock

2021 ◽  
Author(s):  
Laura D’Orsi ◽  
Luciano Curcio ◽  
Fabio Cibella ◽  
Alessandro Borri ◽  
Lilach Gavish ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Time Course ◽  
Differential Algebraic Equations ◽  
Model Parameters ◽  
Algebraic Equations ◽  
Cardiovascular Dynamics ◽  
Compensation Mechanisms

Abstract A variety of mathematical models of the cardiovascular system have been suggested over several years in order to describe the time-course of a series of physiological variables (i.e. heart rate, cardiac output, arterial pressure) relevant for the compensation mechanisms to perturbations, such as severe haemorrhage. The current study provides a simple but realistic mathematical description of cardiovascular dynamics that may be useful in the assessment and prognosis of hemorrhagic shock. The present work proposes a first version of a differential-algebraic equations model, the model dynamical ODE model for haemorrhage (dODEg). The model consists of 10 differential and 14 algebraic equations, incorporating 61 model parameters. This model is capable of replicating the changes in heart rate, mean arterial pressure and cardiac output after the onset of bleeding observed in four experimental animal preparations and fits well to the experimental data. By predicting the time-course of the physiological response after haemorrhage, the dODEg model presented here may be of significant value for the quantitative assessment of conventional or novel therapeutic regimens. The model may be applied to the prediction of survivability and to the determination of the urgency of evacuation towards definitive surgical treatment in the operational setting.

Respiratory and cardiovascular responses to static handgrip exercise in humans

1993 ◽  
Vol 75 (6) ◽  
pp. 2789-2796 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
R. Manconi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Time Course ◽  
Minute Ventilation ◽  
Muscle Tension ◽  
Maximum Voluntary Contraction ◽  
Cardiovascular Responses ◽  
Inspiratory Flow ◽  
Electromyographic Activity ◽  
Handgrip Exercise ◽  
Cardiovascular Variables

We studied the time course of respiratory and cardiovascular responses by evaluating changes in the breathing pattern, mean blood pressure (MBP), and heart rate elicited by 3 min of static handgrip at 15, 25, and 30% of the maximum voluntary contraction (MVC) in 15 healthy volunteers. Muscle tension and integrated electromyographic activity remained fairly constant during each trial. During 15% MVC bouts, initially only mean inspiratory flow increased; then, tidal volume and minute ventilation (VI) also rose progressively. No significant changes in MBP and heart rate were observed. During 25 and 30% MVC bouts, not only did mean inspiratory flow, VT, and VI increase but MBP and heart rate increased as well. A slight and delayed rise in respiratory rate was also observed. Unlike 15 and 25% MVC handgrip, 30% MVC handgrip caused a small decrease in end-tidal PCO2. Changes in the pattern of breathing occurred more promptly than those in cardiovascular variables in the majority of subjects. Furthermore, we found a positive correlation between changes in VI and those in cardiovascular variables at the end of 25 and 30% MVC trials. This study indicates that respiratory and cardiovascular responses to static handgrip exercise are controlled independently.

scholarly journals Cardiovascular profile after intravenous injection of Africanized bee venom in awake rats

2004 ◽  
Vol 46 (1) ◽  
pp. 55-58 ◽  
Author(s):  
Janaína Valadares Guimarães ◽  
Roberto Silva Costa ◽  
Benedito Honório Machado ◽  
Marlene Antônia dos Reis
Keyword(s):  
Heart Rate ◽  
Intravenous Injection ◽  
Time Course ◽  
Bee Venom ◽  
Experimental Animals ◽  
Tubular Necrosis ◽  
Vascular Beds ◽  
Level 2 ◽  
Cardiovascular Profile ◽  
Awake Rats

The manifestations caused by Africanized bee stings depend on the sensitivity of the victim and the toxicity of the venom. Previous studies in our laboratory have demonstrated cardiac changes and acute tubular necrosis (ATN) in the kidney of rats inoculated with Africanized bee venom (ABV). The aim of the present study was to evaluate the changes in mean arterial pressure (MAP) and heart rate (HR) over a period of 24 h after intravenous injection of ABV in awake rats. A significant reduction in basal HR as well as in basal MAP occurred immediately after ABV injection in the experimental animals. HR was back to basal level 2 min after ABV injection and remained normal during the time course of the experiment, while MAP returned to basal level 10 min later and remained at this level for the next 5 h. However, MAP presented again a significant reduction by the 7th and 8th h and returned to the basal level by the 24th h. The fall in MAP may contribute to the pathogenesis of ATN observed. The fall in MAP probably is due to several factors, in addition to the cardiac changes already demonstrated, it is possible that the components of the venom themselves or even substances released in the organism play some role in vascular beds.

On Respiration in the Dragonet Callionymus Lyra L

1968 ◽  
Vol 49 (3) ◽  
pp. 565-582
Author(s):  
G. M. HUGHES ◽  
SHUN-ICHI UMEZAWA
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Time Course ◽  
Water Pressure ◽  
Minute Volume ◽  
Individual Variations ◽  
Wide Range ◽  
The Relationship ◽  
Respiratory Rhythms ◽  
Normal Ventilation

1. The usefulness of a bottom-living fish, the dragonet (Callionymus lyra), in experiments on fish respiration is described. The position and nature of its opercular opening made it possible to determine directly the volume of water pumped over the gills and the PO2 of the mixed expired water. The normal ventilation volume for a 100 g. fish was about 30 c.c./min. 2. The relationship between cardiac and respiratory rhythms was investigated and showed a variety of ratios. The heart usually beats more than once during each respiratory cycle. Individual variations in the coupling between these rhythms was common and close couplings were observed in the absence of anaesthetic and at normal PO2s. 3. Changes in minute volume produced by altering the hydrostatic pressure across the respiratory system did not affect the heart rate. Percentage utilization fell at higher flow rates. Changes in flow per cm. of water pressure gradient was less with negative gradients than when the static pressure on the mouth side exceeded that in the opercular collecting chamber. 4. Oxygen consumption of the fish is directly related to the ambient PO2 over a wide range (30-120 mm. Hg). Sudden lowering of the PO2 in the inspired water leads to compensatory responses in which the minute volume is maintained or increased as a result of a rise in stroke volume and lowered respiratory frequency: there is also a marked bradycardia. During recovery the increased oxygen consumption of the fish resulted from a rise in utilization rather than a change in the respiratory rate or ventilation volume. 5. Analysis of the time course of the changes in heart rate and ventilation volume in experiments in which PO2 was changed supports the view that the receptors mediating bradycardia occur on the gills and respond directly to the change in PO2 rather than to the secondary increase in flow produced by the hypoxia.

Participation of central alpha-receptors on hemodynamic response to E. coli endotoxin

1984 ◽  
Vol 247 (4) ◽  
pp. R655-R662
Author(s):  
S. Koyama
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Heart Rate ◽  
Time Course ◽  
Hypotensive Effect ◽  
Control Group ◽  
E Coli ◽  
Alpha Receptors ◽  
Anesthetized Dogs ◽  
The Central Nervous System

The time course of changes in mean blood pressure (MBP), heart rate (HR), and renal blood flow (RBF) in a control group of anesthetized dogs given only endotoxin (1 mg/kg iv) was compared with groups pretreated with alpha-antagonists either intravenously or intracisternally (ic). The decreases in MBP and RBF in the control group were abolished by intracisternal prazosin (0.1 mg/kg ic). MBP response to endotoxin after intravenous prazosin did not differ from that of the control group; however, the endotoxin-induced decrease in RBF after intravenous prazosin was significantly greater than that in the control group. HR responses to endotoxin were not altered by either intracisternal or intravenous prazosin. MBP and RBF responses to endotoxin after intravenous or intracisternal yohimbine (0.5 mg/kg iv or ic) did not differ from the control responses. However, significant differences occurred in the time course of changes in HR only when yohimbine was administered intracisternally. These observations suggest that the hypotensive effect and reduction of RBF due to endotoxin may be mediated by alpha 1-adrenoceptors at least in the central nervous system and that of HR response may be mediated alpha 2-adrenoceptors.

Response time of cardiac mitochondrial oxygen consumption to heart rate steps

1991 ◽  
Vol 260 (2) ◽  
pp. H613-H625 ◽  
Author(s):  
J. H. Van Beek ◽  
N. Westerhof
Keyword(s):  
Heart Rate ◽  
Response Time ◽  
Time Course ◽  
Mean Transit Time ◽  
Impulse Response Function ◽  
Heart Tissue ◽  
Experimental Information ◽  
O2 Consumption ◽  
Mean Response Time ◽  
The Mean

We investigated the time course of cardiac mitochondrial O2 consumption following steps in heart rate in 16 isolated rabbit hearts perfused with Tyrode solution. The time course was characterized by the mean response time, i.e., the first statistical moment (mean time) of the impulse response function. Like the mean transit time for an indicator, it provides an important characteristic of the response time course. The venous O2 content transients during steps in heart rate were measured and corrected for O2 diffusion and vascular transport using a mathematical model with experimental information derived from O2 washout following steps in arterial O2 concentration or perfusion flow. We deduce from these washout experiments that the effective O2 solubility in heart tissue is 86 +/- 13% (mean +/- SE) of solubility in water. The measured venous mean response time following a step in heart rate at 37 degrees C was 17.6 +/- 1.1 s. The mean response time of cardiac mitochondrial O2 consumption to changes in heart rate after correction for O2 transport was 7.7 +/- 0.7 s.

scholarly journals Time course of the adaptive responses of aerobic power and heart rate to training

1981 ◽  
Vol 13 (1) ◽  
pp. 17???20 ◽  
Author(s):  
R. C. HICKSON ◽  
J. M. HAGBERG ◽  
A. A. EHSANI ◽  
J. O. HOLLOSZY
Keyword(s):  
Heart Rate ◽  
Time Course ◽  
Aerobic Power ◽  
Adaptive Responses
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