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.

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.

Sympathetic and Parasympathetic Components of Reflex Cardiostimulation during Vasodilator Treatment of Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 329s-332s ◽  
Author(s):  
A. J. Man in 't Veld ◽  
G. J. Wenting ◽  
R. P. Verhoeven ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hypertensive Patients ◽  
Treatment Of Hypertension ◽  
Before And After ◽  
Vasodilator Treatment

1. Haemodynamic responses to diazoxide (300 mg intravenously) were studied in 15 hypertensive patients before and after chronic β-adrenoreceptor blockade by 320 mg of propranolol daily. After diazoxide alone, mean arterial pressure and total peripheral resistance were lowered by 24 ± 3 and 35 ± 5% (mean ± sem) respectively. Cardiac output and heart rate rose by 25 ± 9 and 21 ± 3%. During β-adrenoreceptor blockade, the percentage changes of mean arterial pressure, heart rate, cardiac output and total peripheral resistance after vasodilatation were not significantly different from those after diazoxide alone. 2. Atropine, 0·04 mg/kg body weight, was given to 12 hypertensive patients chronically treated with β-adrenoreceptor blockade, before acute vasodilatation by diazoxide. Diazoxide caused no increase in heart rate after combined β-adrenoreceptor and parasympathetic blockade. However, cardiac output rose by 14 ± 5%. 3. We conclude that withdrawal of parasympathetic tone is an important determinant of circulatory homeostasis after acute vasodilatation during β-adrenoreceptor blockade.

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)

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.

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.

Vasopressin-Induced Increase in Total Peripheral Resistance in Deoxycorticosterone Acetate Hypertensive Rats is Buffered by the Baroreceptor Reflex

1981 ◽  
Vol 61 (s7) ◽  
pp. 153s-156s ◽  
Author(s):  
W. Rascher ◽  
R. E. Lang ◽  
M. Taubitz ◽  
H. Meffle ◽  
TH. Unger ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Control Groups ◽  
Deoxycorticosterone Acetate ◽  
Normotensive Control

1. The role of arginine-vasopressin (AVP) in the maintenance of high blood pressure in rats with deoxycorticosterone acetate (DOCA) hypertension was investigated. 2. Plasma concentrations of AVP were significantly elevated in DOCA hypertensive rats compared with normotensive control rats, whether or not they received 1% sodium chloride solution or demineralized water to drink. 3. The specific antagonist of the vasopressor response to AVP, d(CH2)5VDAVP (100 μg/kg intravenously), significantly increased cardiac output and decreased total peripheral resistance, but had no effect on mean arterial pressure in DOCA hypertensive rats. No changes of mean arterial pressure, cardiac output and total peripheral resistance were observed in the normotensive control groups after d(CH2)5VDAVP. 4. After sino-aortic baroreceptor deafferentation, d(CH2)5VDAVP decreased mean arterial pressure in DOCA—salt hypertensive rats, but not in the control groups. 5. It is concluded that elevated circulating AVP causes vasoconstriction in DOCA hypertensive rats. The AVP-induced increase in total peripheral resistance is counter-regulated by an activation of the baroreceptor reflex and subsequent reduction in cardiac output.

Effects of a specific antidiuretic agonist on cardiac output and its distribution in intact and anephric dogs

1988 ◽  
Vol 74 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Jean-Francois Liard
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Regional Blood Flow ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Before And After

1. The specific antidiuretic agonist [4-valine, 8-d-arginine]vasopressin (VDAVP) was administered intravenously to seven conscious dogs at a rate of 10 ng min−1 kg−1. Cardiac output (aortic electromagnetic flowmeter), mean arterial pressure and regional blood flows (radioactive microspheres) were measured before and after 30 min of infusion. 2. Mean arterial pressure fell from 89.9 ± 4.5 (mean ± sem) to 82.3 ± 5.9 mmHg and cardiac output increased from 115.4 ± 8.7 to 163.0 ± 14.4 ml min−1 kg−1. Total peripheral resistance decreased from 41.6 ± 3.7 to 27.8 ± 3.6 units and heart rate increased from 79.2 ± 5.9 to 123.2 ± 5.9 beats/min. Blood flow increased significantly in the myocardium, fat and skeletal muscle vascular bed. 3. In another group of six dogs subjected to a similar protocol 24 h after bilateral nephrectomy, mean arterial pressure fell from 102.2 ± 5.3 to 82.7 ± 3.4 mmHg and cardiac output increased from 125.6 ± 3.0 to 171.2 ± 4.0 ml min−1 kg−1. Total peripheral resistance decreased from 39.3 ± 3.4 to 23.4 ± 1.3 units and heart rate increased from 84 ± 4.9 to 113.3 ± 4.3 beats/min. The increase in cardiac output and the fall in total peripheral resistance did not differ significantly between intact and anephric dogs. Regional blood flow responses differed in some respects in the two groups studied, but there was no evidence that the vasodilatory action of VDAVP depended on the presence of the kidneys. 4. These results indicate that the vasodilatation elicited by the antidiuretic agonist VDAVP in intact dogs is limited to a few vascular beds. Furthermore, this vasodilatation appears to be independent from the renal V2-vasopressin receptors.

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.

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.

Sign in / Sign up

Export Citation Format

Share Document