Atriopeptin II lowers cardiac output in conscious sheep

1985 ◽  
Vol 249 (6) ◽  
pp. R776-R780 ◽  
Author(s):  
B. A. Breuhaus ◽  
H. H. Saneii ◽  
M. A. Brandt ◽  
J. E. Chimoskey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Smooth Muscle ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure

Atrial natriuretic peptides cause natriuresis, kaliuresis, diuresis, and hypotension. They relax vascular smooth muscle in vitro, and they dilate renal vessels in vivo. Hence, we tested the hypothesis that they produce hypotension by lowering total peripheral resistance. The studies were performed in conscious chronically instrumented sheep standing quietly in their cages. Atriopeptin II (AP II) was infused into the right atrium for 30 min at 0.1 nmol X kg-1 X min-1. Atriopeptin II lowers arterial pressure (9%, P less than 0.05) by lowering cardiac output (18%, P less than 0.05), stroke volume (28%, P less than 0.05), and right atrial pressure (2.3 mmHg, P less than 0.05). Heart rate and total peripheral resistance increase (16 and 13%, respectively, P less than 0.05). Partial ganglionic blockade with trimethaphan camsylate during AP II infusion prevents the increases in heart rate and total peripheral resistance. The changes in right atrial pressure, stroke volume, and cardiac output persist, and arterial pressure falls further (27%, P less than 0.05). These hemodynamic data are consistent with direct AP II-induced relaxation of venous smooth muscle with reduction of venous return, right atrial pressure, stroke volume, cardiac output, and arterial pressure, followed by reflex activation of the sympathetic nervous system to increase heart rate and total peripheral resistance. Because partial ganglionic blockade alone and AP II alone cause similar reductions in right atrial pressure (2.1 and 2.3 mmHg, respectively) but AP II causes a greater fall in stroke volume (28 vs. 13%), it is possible that AP II also causes coronary vasoconstriction.

Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

1963 ◽  
Vol 204 (5) ◽  
pp. 888-894 ◽  
Author(s):  
Eugene Evonuk ◽  
John P. Hannon
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Room Temperature ◽  
Metabolic Response ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Systemic Resistance

The cardiovascular and metabolic actions of norepinephrine (NE) and their inter-relationships were studied at normal room temperature in anesthetized, warm-acclimatized (W-A) (26 ± 1 C) and cold-acclimatized (C-A) (3 ± 1 C) rats. The cardiac output, heart rate, stroke volume, arterial pressure, right atrial pressure, and systemic resistance were measured prior to NE infusion; during NE infusion (2 µg/min) at the 25, 50, 75, and 100% levels of increased metabolism; and after infusion of NE had ceased. Norepinephrine caused a greater increase in the cardiac output, heart rate, stroke volume, and right atrial pressure in the C-A animals than it did in W-A animals. During the early metabolic response to NE (i.e., up to 25% increase in O2 consumption) there was a marked increase in the arterial pressure of both W-A and C-A rats, with the latter showing the greater maximum response. Beyond the 25% level of increased metabolism the arterial pressure and concomitantly the systemic resistance of the C-A animals declined sharply to the preinfusion levels where they remained throughout the course of infusion. In contrast to this, the arterial pressure and systemic resistance of the W-A animals remained high. It was concluded that norepinephrine-calorigenesis in the C-A rat is supported by a greater capacity to increase the cardiac output and an ability to preferentially reduce the systemic resistance to actively metabolizing areas (i.e., the viscera).

Hemodynamic studies in DOCA-salt hypertensive rats after opening of an arteriovenous fistula

1992 ◽  
Vol 262 (6) ◽  
pp. H1802-H1808 ◽  
Author(s):  
M. Huang ◽  
R. L. Hester ◽  
A. C. Guyton ◽  
R. A. Norman
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Hypertensive Rats

We determined the cardiovascular responses in normal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats with reduced total peripheral resistance due to an arteriovenous (a-v) fistula. Animals were divided into four groups: control, fistula, DOCA-salt, and DOCA-salt fistula. The fistula was made by anastomosing the aorta and vena cava below the renal arteries. Four weeks after the creation of the fistula both DOCA-salt and DOCA-salt fistula animals received DOCA and salt for 6–8 wk. At the end of 10–12 wk we measured mean arterial pressure, cardiac output, tissue flows, and right atrial pressure. Flow measurements using radioactive microspheres were made in anesthetized animals. Cardiac index (CI) was 202% higher in the fistula group than in the control animals and 165% higher in the DOCA-salt fistula than in the DOCA-salt animals. There was no difference in cardiac output between the control and DOCA-salt animals. The increase in cardiac output was due to the fistula flow as evidenced by a significant increase in the number of microspheres in the lung. Mean arterial pressure was 115 +/- 4 mmHg (control) and 108 +/- 5 mmHg (fistula) in non-DOCA rats but increased in both DOCA groups, 159 +/- 3 mmHg (DOCA-salt) and 145 +/- 5 mmHg (DOCA-salt fistula). Right atrial pressure was increased above control in both fistula animals but was normal in DOCA-salt animals. Total peripheral resistance (TPR) was higher than control in DOCA-salt animals, but TPR in both the fistula and DOCA-salt fistula animals was lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Haemodynamic Alterations after Reversal of Renal Hypertension in Rats

1979 ◽  
Vol 57 (s5) ◽  
pp. 15s-17s ◽  
Author(s):  
Margareta Hallbäck-Nordlander ◽  
E. Noresson ◽  
Y. Lundgren
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Smooth Muscle ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Vascular Changes ◽  
Hypertensive Rats ◽  
Renal Hypertensive Rats

1. Cardiac output, heart rate and mean arterial pressure were determined in two-kidney Goldblatt hypertensive rats of 4 weeks' duration, in matched normotensive controls and in declipped renal hypertensive rats 2 h-28 days after renal artery declipping. 2. After declipping mean pressure fell rapidly due to a corresponding reduction in total peripheral resistance, this being normalized after 1 day. Cardiac output and heart rate remained initially unchanged, but 1 day after declipping the former was significantly increased compared with output in renal hypertensive rats. 3. The initial normalization of total peripheral resistance must be ascribed to a subnormal vascular smooth muscle tone. The reason is that the hypertensive structural vascular changes are not yet significantly reduced and their presence implies an elevated flow resistance, even when vascular smooth muscle activity equals that in normotension. 4. This considerable ‘overshoot’ in vascular relaxation and lack of reflexogenic tachycardia, despite resetting of baroreceptors, suggest that peripheral as well as central mechanisms contribute to the rapid normalization of mean arterial pressure in two-kidney Goldblatt hypertension in rats, later stabilized by reversal of structural vascular changes.

Hemodynamic responses to acute volume expansion in Dahl salt-sensitive rats

1991 ◽  
Vol 260 (1) ◽  
pp. R32-R38
Author(s):  
R. S. Reddy ◽  
C. Baylis ◽  
T. A. Kotchen
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Hemodynamic Responses ◽  
Cardiopulmonary Baroreflex

The purpose of this study is to evaluate hemodynamic responses to acute volume expansion in chronically instrumented, conscious Dahl salt-sensitive (Dahl-S) and Dahl salt-resistant (Dahl-R) rats that have been maintained on either 0.45% NaCl, 1% NaCl, or 7% NaCl (5 days) intakes. Total peripheral resistance (TPR), but not arterial pressure, was increased by 5 days of 7% NaCl in Dahl-S (P less than 0.05) but not in Dahl-R. In Dahl-S, but not in Dahl-R, right atrial pressure increased with increasing dietary NaCl (P less than 0.05). On the 0.45% NaCl intake, atrial pressure did not differ in the two strains, whereas on both the 1 and 7% NaCl diets atrial pressure was higher in Dahl-S than in Dahl-R (P less than 0.05). In response to acute extracellular fluid volume expansion, arterial pressure did not change, and cardiac output increased in Dahl-S and in Dahl-R. On the 0.45% NaCl intake, TPR decreased (P less than 0.01) similarly in response to volume expansion in both strains; however, on the 1% NaCl intake TPR decreased in Dahl-R (P less than 0.05) but not in Dahl-S. In contrast, in animals fed 7% NaCl for 5 days, TPR decreased acutely in Dahl-S (P less than 0.01) but not in Dahl-R. These observations suggest that cardiopulmonary baroreflex activity is impaired in Dahl-S on a 1% NaCl intake, possibly as a consequence of elevated right atrial pressure. This alteration of the cardiopulmonary baroreflex may contribute to increased TPR in Dahl-S on a high-NaCl intake.

Inhibition of the Cardiovascular Effects of Acupuncture (Moxibustion) by Phenotolamine in Dogs During Halothane Anesthesia

1976 ◽  
Vol 04 (02) ◽  
pp. 153-161 ◽  
Author(s):  
Myung O. Lee ◽  
Do Chil Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Blocking Agent ◽  
Halothane Anesthesia

The cardiovascular effects of acupuncture, moxibustion by electrocautery, at Jen Chung (Go-26) and phentolamine (0.1 mg/kg-i.v.) alone were compared to phentolamine (0.1 mg/kg-i.v.) prior to moxibustion at Go-26 in groups of ten dogs under 0.75 percent halothane anesthesia. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressue, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two hour period. A significant increase (5% level) in cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure and significant decrease in total peripheral resistance were observed following acupuncture, moxibustion with electrocautery, at Jen Chung (Go-26) in dogs under halothane anesthesia. These effects were inhibited by pretreatment with the alpha blocking agent, phentolamine (0.1mg/kg-i.v.). The cardiovascular effects of phentolamine (0.1mg/kg-i.v.) alone were similar to those of dogs in which phenotolamine was administered prior to moxibustion.

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.

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.

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.

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