Modulation of carotid sinus baroreceptor reflex by sciatic nerve stimulation

1975 ◽  
Vol 228 (5) ◽  
pp. 1535-1541 ◽  
Author(s):  
M Kumada ◽  
K Nogami ◽  
K Sagawa
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Baroreceptor Reflex ◽  
Equilibrium Pressure ◽  
Sciatic Nerve Stimulation

In anethetized, immobilized, and vagotomized cats we analyzed the effect of sciatic nerve stimulation (SNS) on the relationships between intrasinus pressure (ISP) and arterial pressure (AP) and between ISP and heart rate (HR). At each of seven ISP levels between 60 and 240 mmHg, AP and HR before and 20 s after the onset of SNS were plotted against ISP to obtain the ISP-AP and ISP-HR relationships before and during SNA. SNA caused increases in AP, HR, and total peripheral resistance (TPR) and a decrease in cardiac output (CO). SNS raised the equilibrium pressure (the value of AP at which AP equaled ISP), but it significantly (P smaller than 0.005) decreased the slope (or gain) of the ISP-AP relationship at ISP's between 90 and 150 mmHg. SNS also significantly (P smaller than 0.05) diminished the gain of ISP-HR relationship at ISP's between 120 and 210 mmHg. Modulation of the gain of ISP-AP relationship was ascribable to that of CO but not of TPR. We conclude that in vagotomized cats 1) SNS attenuates the sensitivity of AP and HR responses in the carotid sinus baroreceptor reflex, and 2) the inhibition of the reflex AP response was caused by modulation of the reflex CO response.

Chronic isolation of carotid sinus baroreceptor region in conscious normotensive and hypertensive rats

1998 ◽  
Vol 275 (1) ◽  
pp. H322-H329 ◽  
Author(s):  
Kelly P. McKeown ◽  
Artin A. Shoukas
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Conscious Rat ◽  
Sd Rats ◽  
The Right ◽  
Reflex System

We have developed a chronic technique to isolate the carotid sinus baroreceptor region in the conscious rat model. Our technique, when used in conjunction with other methods, allows for the study of the control of arterial pressure, heart rate, and cardiac output by the carotid sinus baroreceptor reflex in conscious, unrestrained rats. The performance of our technique was evaluated in two strains: normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Each rat was instrumented with an aortic flow probe and a catheter placed in the right femoral artery to monitor cardiac output and arterial pressure, respectively. The cervical sympathetic trunk and aortic depressor nerve were ligated and cut bilaterally, leaving vagus nerves intact. The right and left carotid sinuses were isolated using our new technique. We tested the open-loop function of the carotid sinus baroreceptor reflex system in the conscious rat after recovery from the isolation surgery. We found that changes in nonpulsatile carotid sinus pressure caused significant changes in arterial pressure, heart rate, and total peripheral resistance in both rat strains. However, the cardiac output responses differed dramatically between strains. Significant changes were seen in the cardiac output response of SHR, whereas no significant changes were observed in normotensive SD rats. We have found this technique to be a highly reliable tool for the study of the carotid sinus baroreceptor reflex system in the conscious rat.

Hemodynamic effects of vasopressin compared with angiotensin II in conscious rats

1987 ◽  
Vol 252 (3) ◽  
pp. H628-H637 ◽  
Author(s):  
J. W. Osborn ◽  
M. M. Skelton ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Fold Increase ◽  
Adrenergic Blockade ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Potent Vasoconstrictor

The mechanisms whereby arginine vasopressin influences hemodynamic and autonomic function were investigated in conscious rats. In normal rats, 60-min intravenous infusions produced dose-related increases of arterial pressure and total peripheral resistance with marked decreases of both heart rate and cardiac output. Cholinergic blockade with methscopolamine attenuated the bradycardia at higher doses of vasopressin, whereby the fall of cardiac output was not affected. beta-Adrenergic blockade with atenolol attenuated the fall of heart rate seen with lower doses of vasopressin but did not prevent the fall of cardiac output. Ganglionic blockade with methscopolamine and hexamethonium resulted in nearly a 60-fold enhancement of vasopressin pressor sensitivity. This was related to a greater rise of peripheral resistance, since the fall of cardiac output was not altered compared with normal rats. Hemodynamic responses to angiotensin II were determined in other groups of conscious, normal rats and rats with ganglionic blockade. Peripheral resistance increased in the normal rats, whereas the related decreases in cardiac output and heart rate were only 30% of the responses seen with equipressor doses of vasopressin. Ganglionic blockade increased pressor activity only two- to eightfold compared with the 60-fold increase observed with vasopressin. We conclude that vasopressin is a more potent vasoconstrictor than angiotensin II, decreases cardiac output independent of neural mechanisms, and results in withdrawal of sympathetic vascular tone to buffer rises of arterial pressure.

Control of arterial pressure in conscious, sinoaortic-denervated sheep in normoxia and hypoxia

1987 ◽  
Vol 253 (6) ◽  
pp. H1409-H1417 ◽  
Author(s):  
M. Miki ◽  
K. Miki ◽  
G. Hajduczok ◽  
D. Curran-Everett ◽  
J. A. Krasney
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sham Group ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Mean Values ◽  
Coefficients Of Variation ◽  
The Mean ◽  
Arterial Po2 ◽  
Lying Down

The contribution of the sinoaortic reflexes to the control of both the mean level and variability of arterial pressure (Pa) and heart rate (HR) was studied in five adult ewes after chronic section of the carotid sinus and aortic depressor nerves (SAD). SAD group responses were compared with a sham-operated group (n = 6). Pa was 15% lower in the SAD group due to a reduction of total peripheral resistance. The standard deviations and coefficients of variation for both Pa and HR obtained by continuous 16-h monitoring (10-s intervals) in the SAD sheep were not significantly different from those of the sham group. Arterial hypoxia (arterial PO2 = 40 mmHg for 96 h) had no significant influence on the mean values or variability for Pa and HR for either group, although both groups spent more time lying down. Ventilation was unchanged in the SAD group. Thus mean Pa is lower after removal of baroreceptor and chemoreceptor inputs, but the variabilities of both HR and Pa are unaltered during both normoxia and hypoxia in this sedentary species.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Cardiovascular Effects of Moxibustion at Jen Chung (Go-26) during Halothane Anesthesia in Dogs

1975 ◽  
Vol 03 (03) ◽  
pp. 245-261 ◽  
Author(s):  
Do Chil Lee ◽  
Myung O. Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Halothane Anesthesia

The cardiovascular effects of moxibustion at Jen Chung (Go-26) in 10 dogs under halothane anesthesia were compared to 5 dogs under halothane anesthesia without moxibustion and 5 dogs under halothane anesthesia in which moxibustion was effected at a neutral or non-acupuncture site. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two-hour period. A significant increase in cardiac output and stroke volume and a significant decrease in the total peripheral resistance were observed in the group which was stimulated by moxibustion at Jen Chun (Go-26). Heart rate, mean arterial pressure and pulse pressure were significantly increase during the early part of the two-hour period in the same group. The cardiovascular effects of moxibustion at Jen Chung (Go-26) which were observed at the end of the two hours were also present in two dogs in which measurements were continued for two additional hours.

Cardiac output of the hypothermic rat

1959 ◽  
Vol 196 (2) ◽  
pp. 415-419 ◽  
Author(s):  
Robert W. Bullard
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Total Resistance ◽  
Vascular Geometry ◽  
Per Se ◽  
Colonic Temperature

As the colonic temperature of the rat was lowered the heart rate and cardiac output fell linearly with the temperature. The arterial pressure did not fall linearly indicating an increase of total peripheral resistance. The increase of hematocrit ratio and the effect of cold on blood per se combined to increase the in vitro viscosity threefold as the colonic temperature approached 15°C. It appears from these data that the increase in viscosity of the blood is the important factor in the increase in total resistance to flow and that little change in total or average vascular geometry took place. However, comparison of the local clearances of 1131 from specific extravascular areas shows that individual vascular geometries may be changing but in such a fashion as to balance out each other.

Effect of Exercise on Gain of the Carotid-Sinus Reflex in Rabbits

1982 ◽  
Vol 63 (2) ◽  
pp. 115-119 ◽  
Author(s):  
I. B. Faris ◽  
G. G. Jamieson ◽  
J. Ludbrook
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Carotid Sinus ◽  
Treadmill Exercise ◽  
Baroreceptor Reflex ◽  
Average Blood Pressure ◽  
Reflex Gain ◽  
Dynamic Gain

1. Blood pressure, heart rate and cardiac output were measured in six rabbits before, during and immediately after treadmill exercise. During the same periods the dynamic gain of the carotid-sinus baroreceptor reflex was estimated by creating a sinusoidal oscillation of carotid-distending pressure. 2. The average blood pressure did not change significantly during or after exercise, but heart rate and cardiac output rose markedly and there was a concomitant fall in systemic vascular resistance. 3. The reflex gain for blood pressure decreased by one-fifth during exercise, and the gains for heart rate and vascular resistance by two-fifths. Immediately after exercise the gains for all three variables decreased further, to between one-half and one-third of the resting values. 4. Our results indicate that during and after dynamic exercise the correction of a potential disturbance of blood pressure by the carotid-sinus baroreceptor reflex is decreased in magnitude or in speed.

Hemodynamic effects of angiotensin, norepinephrine, and bradykinin continuously measured in unanesthetized dogs

1961 ◽  
Vol 201 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Irvine H. Page ◽  
Frederick Olmsted
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Partial Recovery ◽  
Slight Rise ◽  
Abrupt Rise

Cardiac output, arterial pressure, heart rate and the derived functions, peripheral resistance and stroke volume, were registered continuously from intact, unanesthetized, unrestrained dogs. Isoleucyl5- or valyl5-angiotensin octapeptide caused output, heart rate and stroke volume to fall sharply when peripheral resistance rose. When infused for an hour, systolic and diastolic pressure remained elevated with unchanged infusion rate. Heart rate decreased in most animals, stroke volume and cardiac output fell, while peripheral resistance rose. Pentobarbital anesthesia increased somewhat the pressor response and decreased the bradycardia. Norepinephrine elicited, first, an abrupt rise in pressure and peripheral resistance, slight rise in heart rate and stroke volume. Arterial pressure then tended to stabilize, followed by a slow decrease associated with continued depression of cardiac output. Bradykinin caused fall in pressure, partial recovery, then further fall. Heart rate slowed, then rose. Cardiac output rose sharply during the initial fall in arterial pressure and remained elevated during the hypotensive response. Stroke volume was reduced during the initial fall but was reduced less during the rest of the response. Peripheral resistance was decreased sharply.

scholarly journals Dissection of carotid sinus hypersensitivity: the timing of vagal and vasodepressor effects and the effect of body position

2011 ◽  
Vol 121 (9) ◽  
pp. 389-396 ◽  
Author(s):  
C. T. Paul Krediet ◽  
David L. Jardine ◽  
Wouter Wieling
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Body Position ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Head Up Tilt

We assessed the timing of vagal and sympathetic factors that mediate hypotension during CSM (carotid sinus massage) in patients with carotid sinus hypersensitivity. We hypothesized that a fall in cardiac output would precede vasodepression, and that vasodepression would be exaggerated by head-up tilt. We performed pulse contour analyses on blood pressure recordings during CSM in syncope patients during supine rest and head-up tilt. In a subset we simultaneously recorded muscle sympathetic nerve activity supine. During supine rest, systolic blood pressure decreased from 150±7 to 107±7 mmHg (P<0.001) and heart rate from 64±2 to 39±3 beats/min (P<0.01). Cardiac output decreased with heart rate to nadir (66±6% of baseline), 3.1±0.4 s after onset of bradycardia. In contrast, total peripheral resistance reached nadir (77±3% of baseline) after 11±1 s. During head-up-tilt, systolic blood pressure fell from 149±10 to 90±11 mmHg and heart rate decreased from 73±4 to 60±7 beats/min. Compared with supine rest, cardiac output nadir was lower (60±8 compared with 83±4%, P<0.05), whereas total peripheral resistance nadir was similar (81±6 compared with 80±3%). The time to nadir from the onset of bradycardia did not differ from supine rest. At the onset of bradycardia there was an immediate withdrawal of muscle-sympathetic nerve activity while total peripheral resistance decay occurred much later (6–8 s). The haemodynamic changes following CSM have a distinct temporal pattern that is characterized by an initial fall in cardiac output (driven by heart rate), followed by a later fall in total peripheral resistance, even though sympathetic withdrawal is immediate. This pattern is independent of body position.

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