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.

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.

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.

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.

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.

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.

Cardiovascular responses to hypoxia and hypercapnia in barodenervated rats

1990 ◽  
Vol 68 (2) ◽  
pp. 678-686 ◽  
Author(s):  
B. R. Walker ◽  
B. L. Brizzee
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Conscious Rat ◽  
Hypercapnic Hypoxia ◽  
Intact Rats

Experiments were performed to examine the role of the arterial baroreceptors in the cardiovascular responses to acute hypoxia and hypercapnia in conscious rats chronically instrumented to monitor systemic hemodynamics. One group of rats remained intact, whereas a second group was barodenervated. Both groups of rats retained arterial chemoreceptive function as demonstrated by augmented ventilation in response to hypoxia. The cardiovascular effects to varying inspired levels of O2 and CO2 were examined and compared between intact and barodenervated rats. No differences between groups were noted in response to mild hypercapnia (5% CO2); however, the bradycardia and reduction in cardiac output observed in intact rats breathing 10% CO2 were eliminated by barodenervation. In addition, hypocapnic hypoxia caused a marked fall in blood pressure and total peripheral resistance (TPR) in barodenervated rats compared with controls. Similar differences in TPR were observed between the groups in response to isocapnic and hypercapnic hypoxia as well. It is concluded that the arterial baroreflex is an important component of the overall cardiovascular responses to both hypercapnic and hypoxic stimuli in the conscious rat.

Regional distribution of blood flow during diving in the duck (Anas platyrhynchos)

1979 ◽  
Vol 57 (5) ◽  
pp. 995-1002 ◽  
Author(s):  
David R. Jones ◽  
Robert M. Bryan Jr. ◽  
Nigel H. West ◽  
Raymond H. Lord ◽  
Brenda Clark
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Regional Distribution ◽  
Peripheral Resistance ◽  
Tissue Blood Flow ◽  
Arterial Blood ◽  
The Brain

The regional distribution of blood flow, both before and during forced diving, was studied in the duck using radioactively labelled microspheres. Cardiac output fell from 227 ± 30 to 95 ± 16 mL kg−1 min−1 after 20–72 s of submergence and to 59 ± 18 mL kg−1 min−1 after 144–250 s of submergence. Mean arterial blood pressure did not change significantly as total peripheral resistance increased by four times during prolonged diving. Before diving the highest proportion of cardiac output went to the heart (2.6 ± 0.5%, n = 9) and kidneys (2.7 ± 0.5%, n = 9), with the brain receiving less than 1%. The share of cardiac output going to the brain and heart increased spectacularly during prolonged dives to 10.5 ± 3% (n = 5) and 15.9 ± 3.8% (n = 5), respectively, while that to the kidney fell to 0.4 ± 0.26% (n = 3). Since cardiac output declined during diving, tissue blood flow (millilitres per gram per minute) to the heart was unchanged although in the case of the brain it increased 2.35 times after 20–75 s of submergence and 8.5 times after 140–250 s of submergence. Spleen blood flow, the highest of any tissue predive (5.6 ± 1.3 mL g−1 min−1, n = 4), was insignificant during diving while adrenal flow increased markedly, in one animal reaching 7.09 mL g−1 min−1. The present results amplify general conclusions from previous research on regional distribution of blood flow in diving homeotherms, showing that, although both heart and brain receive a significant increase in the proportionate share of cardiac output during diving only the brain receives a significant increase in tissue blood flow, which increases as submergence is prolonged.

Total peripheral resistance during cardiac tamponade: adrenergic and angiotensin roles

1986 ◽  
Vol 251 (5) ◽  
pp. R916-R922
Author(s):  
T. L. Cogswell ◽  
G. A. Bernath ◽  
H. Raff ◽  
R. G. Hoffmann ◽  
H. S. Klopfenstein
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Tamponade ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Ang Ii ◽  
Beta Adrenergic ◽  
Renin Angiotensin ◽  
Arterial Blood

During progressive cardiac tamponade in conscious dogs, cardiac output falls continuously while arterial blood pressure is maintained until cardiovascular decompensation by increases in total peripheral resistance (TPR). Plasma renin activity (PRA) is known to increase at decompensation. We hypothesized that the increase in TPR during cardiac tamponade was mediated by alpha-adrenergic and renin-angiotensin mechanisms. Twelve adult dogs were instrumented to measure cardiac output (electromagnetic flow probe), aortic and right atrial blood pressures, and intrapericardial pressure (IPP). TPR was calculated as the conscious euvolemic animals underwent cardiac tamponade induced by intrapericardial saline infusion at 20 ml/min. Six dogs underwent cardiac tamponade in the control condition (no medications) and during independent alpha- and beta-adrenergic and angiotensin-converting enzyme (ACE) inhibition. PRA and angiotensin II (ANG II) were measured during control tamponade. We found that TPR increased continuously to levels of greater than 200% of base line as IPP rose during cardiac tamponade (P less than 0.01). This increase in TPR was unaffected by beta-adrenergic or ACE blockade but was blunted by alpha-adrenergic blockade. PRA and ANG II increased only at decompensated tamponade (P less than 0.05) when arterial blood pressure had fallen by 30%. These changes in PRA and ANG II during tamponade were not altered by beta-blockade in six separate animals. We conclude that cardiac tamponade stimulates renin release and ANG II generation by a non-beta-receptor-mediated mechanism. The increase in TPR during cardiac tamponade is primarily dependent on alpha-adrenergic mechanisms, with a limited late contribution from the renin-angiotensin system.

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