Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (6) ◽  
pp. 1-1
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Liver Volume ◽  
Peripheral Resistance ◽  
Spleen Volume ◽  
Carotid Baroreceptor ◽  
On Line

Pages H254–H259: R. Maass-Moreno and C. F. Rothe. “Carotid baroreceptor control of liver and spleen volume in cats.” Page H254: The sentence beginning on line 11 of the abstract should read: 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 0.21 ± 0.05 mm increase in thickness). The sentence beginning on line 16 of the abstract should read: The liver volume decreased, but only by 1.6% (0.06 ± 0.02 mm decrease in thickness), a change opposite that observed in the spleen. Page H256: The sentence beginning on line 20 of the first paragraph should read: The liver thickness significantly decreased 0.06 ± 0.02 mm when increasing Pcs by 100 mmHg, whereas the spleen increased 0.21 ± 0.05 mm.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. 1-1
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Liver Volume ◽  
Peripheral Resistance ◽  
Spleen Volume ◽  
Carotid Baroreceptor ◽  
On Line

Pages H254–H259: R. Maass-Moreno and C. F. Rothe. “Carotid baroreceptor control of liver and spleen volume in cats.” Page H254: The sentence beginning on line 11 of the abstract should read: 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 0.21 ± 0.05 mm increase in thickness). The sentence beginning on line 16 of the abstract should read: The liver volume decreased, but only by 1.6% (0.06 ± 0.02 mm decrease in thickness), a change opposite that observed in the spleen. Page H256: The sentence beginning on line 20 of the first paragraph should read: The liver thickness significantly decreased 0.06 ± 0.02 mm when increasing Pcs by 100 mmHg, whereas the spleen increased 0.21 ± 0.05 mm.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (5) ◽  
pp. 1-1
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Liver Volume ◽  
Peripheral Resistance ◽  
Spleen Volume ◽  
Carotid Baroreceptor ◽  
On Line

Pages H254–H259: R. Maass-Moreno and C. F. Rothe. “Carotid baroreceptor control of liver and spleen volume in cats.” Page H254: The sentence beginning on line 11 of the abstract should read: 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 0.21 ± 0.05 mm increase in thickness). The sentence beginning on line 16 of the abstract should read: The liver volume decreased, but only by 1.6% (0.06 ± 0.02 mm decrease in thickness), a change opposite that observed in the spleen. Page H256: The sentence beginning on line 20 of the first paragraph should read: The liver thickness significantly decreased 0.06 ± 0.02 mm when increasing Pcs by 100 mmHg, whereas the spleen increased 0.21 ± 0.05 mm.

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.

Diastolic pressure and peripheral resistance during stellate ganglion stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Diastolic Pressure ◽  
Stellate Ganglion ◽  
Peripheral Resistance ◽  
Resistance Vessels ◽  
Left Stellate Ganglion ◽  
Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

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.

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.

Autonomic Cardiovascular Dysregulation at Rest and During Stress in Chronically Low Blood Pressure

2019 ◽  
Vol 33 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Stefan Duschek ◽  
Alexandra Hoffmann ◽  
Casandra I. Montoro ◽  
Gustavo A. Reyes del Paso
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Baroreflex Sensitivity ◽  
Peripheral Resistance ◽  
Control Group ◽  
Low Blood Pressure

Abstract. Chronic low blood pressure (hypotension) is accompanied by symptoms such as fatigue, reduced drive, faintness, dizziness, cold limbs, and concentration difficulties. The study explored the involvement of aberrances in autonomic cardiovascular control in the origin of this condition. In 40 hypotensive and 40 normotensive subjects, impedance cardiography, electrocardiography, and continuous blood pressure recordings were performed at rest and during stress induced by mental calculation. Parameters of cardiac sympathetic control (i.e., stroke volume, cardiac output, pre-ejection period, total peripheral resistance), parasympathetic control (i.e., heart rate variability), and baroreflex function (i.e., baroreflex sensitivity) were obtained. The hypotensive group exhibited markedly lower stroke volume, heart rate, and cardiac output, as well as higher pre-ejection period and baroreflex sensitivity than the control group. Hypotension was furthermore associated with a smaller blood pressure response during stress. No group differences arose in total peripheral resistance and heart rate variability. While reduced beta-adrenergic myocardial drive seems to constitute the principal feature of the autonomic impairment that characterizes chronic hypotension, baroreflex-related mechanisms may also contribute to this state. Insufficient organ perfusion due to reduced cardiac output and deficient cardiovascular adjustment to situational requirements may be involved in the manifestation of bodily and mental symptoms.

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.

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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