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.

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 Haemodynamic Responses to Acute Blood Loss: New Roles for the Heart, Brain and Endogenous Opioids

1989 ◽  
Vol 17 (3) ◽  
pp. 312-319 ◽  
Author(s):  
A. F. Van Leeuwen ◽  
R. G. Evans ◽  
J. Ludbrook
Keyword(s):  
Blood Pressure ◽  
Blood Loss ◽  
Peripheral Resistance ◽  
Endogenous Opioids ◽  
Acute Blood Loss ◽  
Endogenous Opioid ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Blood Pressure Fall ◽  
Human Volunteers

Information has come forward recently from several sources which provides new insights into the mechanisms that underlie the haemodynamic responses to acute blood loss. In unanaesthetised animals and human volunteers there are two distinct phases to these responses. At first, the engagement of baroreflexes results in a progressive rise in sympathetic vasoconstrictor drive and peripheral resistance, and the maintenance of arterial blood pressure at a near-normal level. When about one-third of blood volume has been lost, reflex sympathetic drive is switched off, and peripheral resistance and blood pressure fall abruptly to low levels despite a burst of vasopressin release. Research in conscious animals has now shown that the onset of this decompensatory phase is triggered by a signal from the heart, which activates an endogenous opioid mechanism in the brain. Activation of this mechanism can be prevented by administering a selective δ-receptor antagonist, or selective μ-receptor agonists (including alfentanil). It has not yet been established that this endogenous opioid mechanism is responsible for the decompensatory phase of acute blood loss in man, nor that it can be prevented or reversed by selective opioid agonists or antagonists.

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.

Circulatory effects of acute or chronic endotoxemia in rats

1981 ◽  
Vol 59 (2) ◽  
pp. 204-208 ◽  
Author(s):  
R. Keeler ◽  
Anamaria Barrientos ◽  
K. Lee
Keyword(s):  
Escherichia Coli ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gastrointestinal Tract ◽  
Peripheral Resistance ◽  
Circulatory Effects ◽  
Arterial Blood ◽  
Flow Changes ◽  
Fractional Distribution

A study was made of the effects of acute (4 h) or chronic (4 days) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastrointestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced.Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.

Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat

1986 ◽  
Vol 251 (6) ◽  
pp. H1316-H1323 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Hypoxic Exposure ◽  
Conscious Rat ◽  
Time Control ◽  
Hemodynamic Variables

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of sinoaortic reflexes in hemodynamic patterns of natural defense behaviors in the cat

1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Carotid Sinus ◽  
Emotional Behavior ◽  
Natural Defense ◽  
Arterial Blood ◽  
Hemodynamic Pattern ◽  
Before And After

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.

Cardiac Output by the Dye Dilution Technique Under Thiopental Sodium-Oxygen and Ether Anesthesia

1956 ◽  
Vol 186 (1) ◽  
pp. 101-104 ◽  
Author(s):  
Esther M. Greisheimer ◽  
Dorothy W. Ellis ◽  
George Stewart ◽  
Lydia Makarenko ◽  
Nadia Oleksyshyn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Stroke Index ◽  
Ether Anesthesia ◽  
Dye Dilution ◽  
Arterial Blood ◽  
Thiopental Sodium

One hundred-twenty determinations of cardiac output by the dye dilution technic utilizing the cuvette oximeter were made on 20 dogs. Of these, 60 were done under thiopental sodium-oxygen analgesia and 60 were done after supplementing with ether. Arterial blood pressure was recorded by strain gauge. Electrocardiograms were taken periodically. Concentrations of thiopental and ether in arterial blood were determined. Cardiac output began to increase under thiopental analgesia and continued to increase when ether was administered. Arterial blood pressure and heart rate decreased slightly when ether was administered. Stroke index increased when ether was administered. Total peripheral resistance decreased markedly under thiopental analgesia, and continued to decrease when ether was administered. When compared with an earlier study in which cyclopropane was used as the supplementing agent, it was found that cyclopropane and ether exert opposite effects on cardiac output and peripheral resistance despite the fact that the effect on arterial blood pressure is similar under the two agents. Increase in cardiac output was found to be parallel with decrease in total peripheral resistance in this study. Amount of dye injected did not influence cardiac output. Under the conditions of this study, cardiac output was in no way dependent on the concentration of thiopental in the blood nor on the amount injected. Level of ether in the blood did not show much effect, if any, on cardiac output. It is probable that the changes observed in this study are comparable with those which obtain clinically when thiopental-oxygen analgesia is supplemented with ether. Systolic blood pressure is not an infallible guide to other cardiovascular functions since it may remain fairly steady while cardiac output and peripheral resistance undergo marked changes under anesthesia.

scholarly journals Continuous cardiac output monitoring in humans by invasive and noninvasive peripheral blood pressure waveform analysis

2006 ◽  
Vol 101 (2) ◽  
pp. 598-608 ◽  
Author(s):  
Zhenwei Lu ◽  
Ramakrishna Mukkamala
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Waveform Analysis ◽  
Cardiac Output Monitoring ◽  
Time Interval ◽  
Data Sets ◽  
Data Set ◽  
Arterial Blood ◽  
Output Monitoring

We present an evaluation of a novel technique for continuous (i.e., automatic) monitoring of relative cardiac output (CO) changes by long time interval analysis of a peripheral arterial blood pressure (ABP) waveform in humans. We specifically tested the mathematical analysis technique based on existing invasive and noninvasive hemodynamic data sets. With the former data set, we compared the application of the technique to peripheral ABP waveforms obtained via radial artery catheterization with simultaneous thermodilution CO measurements in 15 intensive care unit patients in which CO was changing because of disease progression and therapy. With the latter data set, we compared the application of the technique to noninvasive peripheral ABP waveforms obtained via a finger-cuff photoplethysmography system with simultaneous Doppler ultrasound CO measurements made by an expert in 10 healthy subjects during pharmacological and postural interventions. We report an overall CO root-mean-squared normalized error of 15.3% with respect to the invasive hemodynamic data set and 15.1% with respect to the noninvasive hemodynamic data set. Moreover, the CO errors from the invasive and noninvasive hemodynamic data sets were only mildly correlated with mean ABP (ρ = 0.41, 0.37) and even less correlated with CO (ρ = −0.14, −0.17), heart rate (ρ = 0.04, 0.19), total peripheral resistance (ρ = 0.38, 0.10), CO changes (ρ = −0.26, −0.20), and absolute CO changes (ρ = 0.03, 0.38). With further development and successful prospective testing, the technique may potentially be employed for continuous hemodynamic monitoring in the acute setting such as critical care and emergency care.

scholarly journals Dynamics of Concatenation between Cardiac Output and Indices of Arterial Blood Presure during Graded Exercise Stress in Endurance Cohort

2018 ◽  
Vol 1 (88) ◽  
Author(s):  
Vilma Papievienė ◽  
Eugenijus Trinkūnas ◽  
Alfonsas Buliuolis ◽  
Albinas Grūnovas ◽  
Jonas Poderys
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Matrix Theory ◽  
Blood Pressure Reduction ◽  
Peripheral Resistance ◽  
Exercise Stress ◽  
Bicycle Ergometry ◽  
Linear Type ◽  
Arterial Blood

Research background and hypothesis. Potential mechanisms through which muscle perfusion is altered during prolonged exercise are not fully understood. The methods applied in the  analysis of human data are very important  because  many crucial variables are not directly measureble or even identifiable.Research aim  was to  find out the peculiarities in concatenation between  central and peripheral cardiovascular changes under conditions of increasing fatigue.Research methods. Well-trained endurance runners underwent a 50 W increase in workload (bicycle ergometry) every 6 minutes and they exercised until inability to continue the task. Dynamics of concatenation between cardiac output and systolic arterial blood pressure (ABP), diastolic ABP and total peripheral resistance were assessed using a method based on matrix theory proposed by Lithuanian scientists.Research results. The increase of cardiac output during exercising has the same tendency of stepwise increase of workload, but changes of systolic and diastolic ABP with accumulation of fatigue could be characterized as linear type dependent with the time of exercising. The concatenation between the changes in cardiac performance and behaviour of peripheral vasculature increased at onset of exercising and the decrease or loss of the concatenation led up to inability to continue exercising.Discussion and conclusions. The importance of peripheral factors, i. e. decrease of diastolic blood pressure, reduction  of  total  peripheral  vascular  resistance  plays  an  increasingly  significant  role  for  cardiac  output  during continuous exercising. The concatenations between the changes of these indices and cardiac output increase and in the case of high-grade fatigue concatenations begin to decline.Keywords: cardiac output, periferal vascular resistance, concatenation.

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