scholarly journals Estimation of changes in instantaneous aortic blood flow by the analysis of arterial blood pressure

2012 ◽  
Vol 112 (11) ◽  
pp. 1832-1838 ◽  
Author(s):  
Tatsuya Arai ◽  
Kichang Lee ◽  
Robert P. Marini ◽  
Richard J. Cohen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Arterial Blood Pressure ◽  
Aortic Blood Flow ◽  
Windkessel Model ◽  
Arx Model ◽  
Arterial Blood ◽  
Aortic Blood

The purpose of this study was to introduce and validate a new algorithm to estimate instantaneous aortic blood flow (ABF) by mathematical analysis of arterial blood pressure (ABP) waveforms. The algorithm is based on an autoregressive with exogenous input (ARX) model. We applied this algorithm to diastolic ABP waveforms to estimate the autoregressive model coefficients by requiring the estimated diastolic flow to be zero. The algorithm incorporating the coefficients was then applied to the entire ABP signal to estimate ABF. The algorithm was applied to six Yorkshire swine data sets over a wide range of physiological conditions for validation. Quantitative measures of waveform shape (standard deviation, skewness, and kurtosis), as well as stroke volume and cardiac output from the estimated ABF, were computed. Values of these measures were compared with those obtained from ABF waveforms recorded using a Transonic aortic flow probe placed around the aortic root. The estimation errors were compared with those obtained using a windkessel model. The ARX model algorithm achieved significantly lower errors in the waveform measures, stroke volume, and cardiac output than those obtained using the windkessel model ( P < 0.05).

Failure of acute saralasin to reverse chronic hypertension in fetal lambs

1991 ◽  
Vol 260 (4) ◽  
pp. R811-R816
Author(s):  
D. F. Anderson ◽  
N. D. Binder
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Upper Body ◽  
Chronic Hypertension ◽  
Aortic Blood Flow ◽  
Flow Reduction ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Blood Flow Reduction

Upper body arterial hypertension developed in 12 fetal lambs after chronic suprarenal aortic blood flow reduction. Sixty minutes after blood flow reduction, intravenous saralasin infusion was able to reduce upper body mean arterial blood pressure to control levels. Although saralasin infusion was able to decrease upper body arterial blood pressure after 1 day of hypertension, it was not able to return blood pressure to control levels. Three or more days later, saralasin was unable to cause a significant reduction in upper body arterial blood pressure. We conclude that, although the renin-angiotensin system has a role in maintaining the elevated blood pressure after greater than or equal to 1 day of suprarenal aortic blood flow reduction, some other mechanism also participates. We have ruled out a role for changing blood volume, and our results suggest that an elevation of plasma catecholamines is not responsible. Some other pathway for fluid regulation available to the fetus may be responsible.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

A simple module for on-line computation of stroke volume and cardiac output

1975 ◽  
Vol 38 (5) ◽  
pp. 927-929 ◽  
Author(s):  
G. Pinardi ◽  
A. Sainz ◽  
E. Santiago
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Data Analysis ◽  
Stroke Volume ◽  
Simple Module ◽  
Cardiovascular Responses ◽  
Aortic Blood Flow ◽  
Aortic Blood ◽  
On Line ◽  
Aortic Blood Flow Velocity

An easily constructed, low-priced, simple, and reliable module to obtain stroke volume and cardiac output by analog integration of aortic blood flow velocity signals is described. Rapid data analysis of physiologic and pharmacologic cardiovascular responses in dogs is greatly facilitated by on line computation of these parameters.

Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1802-1808 ◽  
Author(s):  
S. N. Hussain ◽  
C. Roussos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Endotoxic Shock ◽  
Organ Blood Flow ◽  
Similar Reduction ◽  
Arterial Blood

Respiratory muscle blood flow and organ blood flow during endotoxic shock were studied in spontaneously breathing dogs (SB, n = 6) and mechanically ventilated dogs (MV, n = 5) with radiolabeled microspheres. Shock was produced by a 5-min intravenous injection of Escherichia coli endotoxin (0.55:B5, Difco, 10 mg/kg) suspended in saline. Mean arterial blood pressure and cardiac output in the SB group dropped to 59 and 45% of control values, respectively. There was a similar reduction in arterial blood pressure and cardiac output in the MV group. Total respiratory muscle blood flow in the SB group increased significantly from the control value of 51 +/- 4 ml/min (mean +/- SE) to 101 +/- 22 ml/min at 60 min of shock. In the MV group, respiratory muscle perfusion fell from control values of 43 +/- 12 ml/min to 25 +/- 3 ml/min at 60 min of shock. In the SB group, 8.8% of the cardiac output was received by the respiratory muscle during shock in comparison with 1.9% in the MV group. In both groups of dogs, blood flow to most organs was compromised during shock; however, blood flow to the brain, gut, and skeletal muscles was higher in the MV group than in the SB group. Thus by mechanical ventilation a fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during endotoxic shock.

scholarly journals Organs Blood Flow during Elevation of Body Temperature in Sevoflurane Anesthetized Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Koichi Shimo ◽  
Ko Takakura ◽  
Kenji Shigemi
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Body Temperature ◽  
Arterial Blood Pressure ◽  
Pulse Rate ◽  
Organ Blood Flow ◽  
Aortic Blood Flow ◽  
Sevoflurane Anesthesia ◽  
Arterial Blood ◽  
Small Intestinal

The aim of this study is to investigate how elevation of body temperature changes organs blood flow during sevoflurane anesthesia. We conducted in vivo research on 14 male Wistar rats to monitor pulse rate and arterial blood pressure and measure hepatic, small intestinal, renal, and descending aortic blood flow using a laser Doppler blood flowmeter. We assessed the changes in organ blood flow, pulse rate, and arterial blood pressure during elevation of the rats’ body temperatures up to 41.5°C under anesthesia with 2.0% or 3.0% sevoflurane. We concluded that elevation of body temperature up to 39.5°C does not change hepatic, small intestinal, and renal blood flow during 2.0 and 3.0% sevoflurane anesthesia.

EFFECT OF AURICULAR FIBRILLATION ON CARDIAC OUTPUT, CORONARY BLOOD FLOW AND MEAN ARTERIAL BLOOD PRESSURE

1950 ◽  
Vol 163 (1) ◽  
pp. 135-140 ◽  
Author(s):  
René Wégria ◽  
Charles W. Frank ◽  
George A. Misrahy ◽  
Robert S. Sioussat ◽  
Leonard S. Sommer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Coronary Blood Flow ◽  
Mean Arterial Blood Pressure ◽  
Arterial Blood

Cardiovascular Hemodynamics Consequence to Crossed Circulation in the Dog

1958 ◽  
Vol 192 (2) ◽  
pp. 345-352 ◽  
Author(s):  
W. J. Roberson ◽  
Steven M. Horvath
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Carotid Artery ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Diastolic Pressure ◽  
Recovery Period ◽  
Arterial Blood ◽  
The Mean

Twelve experiments were conducted on anesthetized and paired dogs of similar weights subjected to unimpeded, unregulated crossed circulation. Shunts were made between the carotid arteries and external jugular veins and free flow allowed for 60 minutes or longer. Statistically significant changes occurred in the mean femoral arterial blood pressures, carotid shunt blood flow, heart rate, cardiac output, cardiac work, percentage of cardiac output flowing through the shunt and pulmonary systolic and diastolic pressures of one or both animals from their control values. The mean arterial blood pressure remained at control levels for several minutes and then dropped precipitously to hypotensive levels. The lowest mean pressures between 42 and 49 mm Hg occurred within the first 16.5 minutes of the open shunt phase with a gradual return toward control levels. The volume of blood flowing through the shunt was increased initially 250% above the control carotid blood flow, followed by a reduction in flow after 15 minutes; the volume flow at this moment was still double precross circulation levels. A secondary increase in the shunt blood flow occurred throughout the remainder of the open shunt phase. In general, the heart rates and peripheral vascular resistance were slightly elevated during the open shunt phase while cardiac output and work decreased below their control values. A marked and similar increase in the percentage of the cardiac output flowing through the carotid artery was observed in both animals. During the 60 minutes of the recovery period mean arterial blood pressure, cardiac output and work tended to return to control levels while the carotid artery blood flow and pulmonary systolic and diastolic pressure remained slightly below their control values.

scholarly journals Cardiovascular actions of python bradykinin and substance P in the anesthetized python, Python regius

2000 ◽  
Vol 279 (2) ◽  
pp. R531-R538 ◽  
Author(s):  
Tobias Wang ◽  
Michael Axelsson ◽  
Jorgen Jensen ◽  
J. Michael Conlon
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Substance P ◽  
Stroke Volume ◽  
Receptor Antagonist ◽  
Arterial Blood Pressure ◽  
Adrenergic Receptor ◽  
Python Regius ◽  
Arterial Blood ◽  
Cardiovascular Actions

The cardiovascular actions of python bradykinin (BK) and substance P (SP) have been investigated in the anesthetized ball python, Python regius. Bolus intra-arterial injections of python BK (0.03–3 nmol/kg) produced concentration-dependent increases in arterial blood pressure, heart rate (HR), and cardiac output concomitant with small decreases in systemic resistance and stroke volume. Intra-arterial injection of 3 nmol/kg python BK produced a tenfold increase in circulating concentration of norepinephrine, but epinephrine levels did not change. BK-induced tachycardia was attenuated (>90%) by the β-adrenergic receptor antagonist sotalol, and the hypertensive response was attenuated (>70%) by the α-adrenergic receptor antagonist prazosin, indicating that effects of python BK are mediated at least in part by activation of the extensive network of adrenergic neurons present in vascular tissues. Bolus intra-arterial injections of python SP in the range 0.01–30 pmol/kg produced concentration-dependent decreases in arterial blood pressure and systemic peripheral resistance concomitant with increases in cardiac output and stroke volume but with only minor effects on HR. The data suggest that kinins play a physiologically important role in cardiovascular regulation in the python.

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