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.

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.

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 EFFECTS OF PENTOLINIUM BITARTRATE IN DOGS

1956 ◽  
Vol 34 (4) ◽  
pp. 747-755 ◽  
Author(s):  
W. E. G. A. Spoerel ◽  
C. W. Gowdey
Keyword(s):  
Pulse Rate ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Minute Volume ◽  
Initial Pulse ◽  
Pressor Responses ◽  
Pulmonary Arterial ◽  
Sinus Pressure

Pentolinium (5 mgm./kgm.) injected intravenously into dogs anesthetized with pentobarbital caused the pulse rate to approach that of dogs with surgical cardiac denervation. The higher the initial pulse rate, the greater the decrease after the drug; rates under 100/min. were increased. Changes in arterial pressure followed a similar pattern, and the changes in both systemic and pulmonary arterial pressures were correlated with the changes in pulse rate. The cardiac output was decreased. Pressor responses to injected adrenaline and noradrenaline were greater after pentolinium. Total peripheral resistance, respiratory rate, respiratory minute volume, and oxygen consumption were not changed significantly, but local (hind-leg) resistance was decreased in two of three experiments. Pentolinium abolished or reduced markedly the cardiovascular responses to reduced carotid sinus pressure, tilting, acute hypoxia, large doses of acetylcholine, and hemorrhage. The cardiac vagus and the cardiovascular part of the sympathetic nervous system are blocked, but the experiments suggest that the adrenal medulla may not be completely blocked by 5 mgm./kgm. pentolinium.

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)

CARDIOVASCULAR EFFECTS OF PENTOLINIUM BITARTRATE IN DOGS

1956 ◽  
Vol 34 (1) ◽  
pp. 747-755
Author(s):  
W. E. G. A. Spoerel ◽  
C. W. Gowdey
Keyword(s):  
Pulse Rate ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Minute Volume ◽  
Initial Pulse ◽  
Pressor Responses ◽  
Pulmonary Arterial ◽  
Sinus Pressure

Pentolinium (5 mgm./kgm.) injected intravenously into dogs anesthetized with pentobarbital caused the pulse rate to approach that of dogs with surgical cardiac denervation. The higher the initial pulse rate, the greater the decrease after the drug; rates under 100/min. were increased. Changes in arterial pressure followed a similar pattern, and the changes in both systemic and pulmonary arterial pressures were correlated with the changes in pulse rate. The cardiac output was decreased. Pressor responses to injected adrenaline and noradrenaline were greater after pentolinium. Total peripheral resistance, respiratory rate, respiratory minute volume, and oxygen consumption were not changed significantly, but local (hind-leg) resistance was decreased in two of three experiments. Pentolinium abolished or reduced markedly the cardiovascular responses to reduced carotid sinus pressure, tilting, acute hypoxia, large doses of acetylcholine, and hemorrhage. The cardiac vagus and the cardiovascular part of the sympathetic nervous system are blocked, but the experiments suggest that the adrenal medulla may not be completely blocked by 5 mgm./kgm. pentolinium.

Glibenclamide does not reverse attenuated vasoreactivity to acute or chronic hypoxia

1995 ◽  
Vol 79 (4) ◽  
pp. 1173-1180 ◽  
Author(s):  
M. R. Eichinger ◽  
T. C. Resta ◽  
D. S. Balderrama ◽  
G. M. Herrera ◽  
L. A. Richardson ◽  
...  
Keyword(s):  
Chronic Hypoxia ◽  
Channel Blocker ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Katp Channels ◽  
Hypoxic Exposure ◽  
Conscious Rat ◽  
Hypoxic Conditions ◽  
Before And After

Recent studies from our laboratory have shown that acute and chronic hypoxic exposures are associated with attenuated systemic vasoreactivity in conscious rats. The present studies examined the role of adenosine triphosphate-sensitive potassium channels (KATP channels) in modulating the pressor and vasoconstrictor responses to phenylephrine (PE) in conscious instrumented rats 1) during acute hypoxia or 2) after chronic hypoxic exposure. Mean arterial pressure, mean cardiac output, and total peripheral resistance were assessed before and after graded infusions of PE in both groups of rats under normoxic or hypoxic conditions. Additionally, the role of KATP channels in attenuating vasoreactivity was determined by administration of glibenclamide (KATP channel blocker) before PE infusions. Acute hypoxia (12% O2) was associated with reduced pressor and constrictor responses to PE in control animals. Furthermore, acute return to room air did not restore the pressor and constrictor responses in the chronically hypoxic rats. Glibenclamide infusion did not influence the pressor or vasoconstrictor responses to PE in either group of animals during normoxia or acute hypoxia. Therefore, our data suggest that opening of KATP channels is not involved in the attenuated vasoreactivity associated with acute and chronic hypoxia in the conscious rat.

scholarly journals Development of cardiovascular responses to hypoxia in larvae of the frog Xenopus laevis

1996 ◽  
Vol 271 (4) ◽  
pp. R912-R917 ◽  
Author(s):  
R. Fritsche ◽  
W. Burggren
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Xenopus Laevis ◽  
Stroke Volume ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Inhibitory Effect ◽  
Show Evidence

Cardiovascular responses (blood pressure, heart rate, stroke volume, cardiac output, and peripheral vascular resistance) to acute hypoxia (Po2 = 70 mmHg) in developing larvae of Xenopus laevis from Nieuwkoop-Faber (NF) stage 45 and up to newly metamorphosed froglets were investigated. The results revealed two distinct response patterns to acute hypoxia in "early" (NF stages 45-48 and 49-51) and "late" (NF stages 52-53, 54-57, and 58-62) larval Xenopus. The early larvae responded to acute hypoxia with a significantly decreased stroke volume, cardiac output, and blood pressure. Peripheral resistance increased, whereas no change in heart rate occurred. In late larvae, stroke volume and blood pressure increased during acute hypoxia, but an offsetting bradycardia prevented major changes in cardiac output. We conclude that, up to stage 51 of development, hypoxia exerts a direct inhibitory effect on the heart and smooth muscle of the blood vessels, with no Frank-Starling relationship apparent. Older larvae show evidence of both intrinsic and extrinsic regulation of the cardiovascular system in response to acute hypoxia, suggesting that there is a specific point in larval development when cardiovascular regulation during hypoxia is expressed.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

Abstract P222: Venous Dilation Contributes to 5-HT-induced Hypotension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Bridget M Seitz ◽  
Teresa Krieger-Burke ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Imaging System ◽  
Isometric Force ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Mesenteric Arteries ◽  
Conscious Rat ◽  
Cross Sectional ◽  
Induced Hypotension ◽  
Vascular Bed

Serotonin (5-hydroxytryptamine, 5-HT) infusion in a normal conscious rat decreases mean arterial pressure (MAP), in part by reduction in total peripheral resistance. Microsphere experiments have shown 5-HT increases blood flow within the splanchnic vascular bed, with the greatest being in the intestine and spleen. Interestingly, 5-HT does not cause a direct relaxation of resistant (small or large) mesenteric arteries. The present study addresses the possibility of the venous circulation contributing to the 5-HT induced fall in blood pressure. Our working hypothesis is venous dilation, specifically dilation of veins measurable within the splanchnic vascular bed, contributes to 5-HT-induced hypotension. Using an ultrasound imaging system (Vevo 2100 imaging system; 21 MHz probe,Visual Sonics Inc.), telemetry-implanted, anesthetized male Sprague Dawley rats underwent cross-sectional imaging which was controlled for respiration and cardiac cycles. The following vessels were imaged: abdominal aorta (AA); portal vein (PV); abdominal inferior vena cava (IVC); and superior mesenteric vein (SMV). Following the collection of baseline MAP and vessel diameter measurements, Alzet osmotic mini-pumps containing vehicle (saline; n=9) or 5-HT (25 ug/kg/min; n=9) were implanted for 1 week. After, 24 hours of infusion, 5-HT increased the vein diameter (SMV 17.48±2%; PV 17.67±2%; IVC 46.87±8%) and maintained the AA diameter ( AA 0.93±1%) from baseline while reducing MAP (vehicle 101.93±3; 5-HT 84.68±2 mm Hg; p<0.05).One-week post removal of all osmotic mini-pumps, there was no difference in the MAP or diameter of all noted vessels between the two treatment groups. To correlate with in vivo findings, the PV and IVC, when isolated in a tissue bath for measurement of isometric force and contracted with endothelin 1, relaxed in a concentration dependent fashion to 5-HT and 5-carboxamidotryptamine (5-HT 1/7 receptor agonist;1 nM-10 uM). Collectively, these findings highlight the contribution of splanchnic venous dilation in 5-HT-induced hypotension and propose a possible mechanism for 5-HT reduction in blood pressure.

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