Essential role of mean circulatory filling pressure in salt-induced hypertension

1979 ◽  
Vol 236 (1) ◽  
pp. R40-R47 ◽  
Author(s):  
R. D. Manning ◽  
T. G. Coleman ◽  
A. C. Guyton ◽  
R. A. Norman ◽  
R. E. McCaa
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
Isotonic Saline ◽  
Filling Pressure ◽  
Initial Increase ◽  
Experimental Hypertension ◽  
Base Line ◽  
Plasma Aldosterone Concentration ◽  
Salt Loading ◽  
Mean Circulatory Filling Pressure

Experimental hypertension was produced in nine dogs by continuously infusing isotonic saline after renal mass had been surgically reduced to approximately 30% normal. Data were collected during 8 days of base-line measurements and 13 days of saline infusion to determine the cause of the initial increase in cardiac output observed in this type of hypertension and to measure other variables possibly important in the pathogenesis of hypertension. During the infusion period, these dogs demonstrated an increase in arterial pressure to hypertensive levels, transient increases in blood volume, sodium space, and cardiac output, initially depressed then subsequently elevated total peripheral resistance, and decreases in plasma renin activity and plasma aldosterone concentration. The mean circulatory filling pressure increased 4.7 Torr by day 3 and was still elevated 2 Torr at the end of the 2nd wk of infusion. We conclude that the initial increase in cardiac output in salt-loading hypertension is due to elevated fluid volumes and the associated increase in mean circulatory filling pressure.

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

1990 ◽  
Vol 68 (3) ◽  
pp. 384-391 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial Pao2 = 38 mmHg), hypercapnia (Paco2 = 72 mmHg), or hypoxic hypercapnia (Pao2 = 41; Paco2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.Key words: cardiovascular reflex, vascular capacitance, hypoxia, hypercapnia, mean circulatory filling pressure, venoconstriction.

Role of β-adrenergic agonists in the control of vascular capacitance

1990 ◽  
Vol 68 (5) ◽  
pp. 575-585 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Filling Pressure ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Central Venous ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance

The role of β-adrenergic agonists, such as isoproterenol, on vascular capacitance is unclear. Some investigators have suggested that isoproterenol causes a net transfer of blood to the chest from the splanchnic bed. We tested this hypothesis in dogs by measuring liver thickness, cardiac output, cardiopulmonary blood volume, mean circulatory filling pressure, portal venous, central venous, pulmonary arterial, and systemic arterial pressures while infusing norepinephrine (2.6 μg∙min−1∙kg−1), or isoproterenol (2.0 μg∙min−1∙kg−1), or histamine (4 μg∙min−1∙kg−1), or a combination of histamine and isoproterenol. Norepinephrine (an α- and β1-adrenergic agonist) decreased hepatic thickness and increased mean circulatory filling pressure, cardiac output, cardiopulmonary blood volume, total peripheral resistance, and systemic arterial and portal pressures. Isoproterenol increased cardiac output and decreased total peripheral resistance, but it had little effect on liver thickness or mean circulatory filling pressure and did not increase the cardiopulmonary blood volume or central venous pressure. Histamine caused a marked increase in portal pressure and liver thickness and decreased cardiac output, but it had little effect on the estimated mean circulatory filling pressure. Isoproterenol during histamine infusions reduced histamine-induced portal hypertension, reduced liver size, and increased cardiac output. We conclude that the β-adrenergic agonist, isoproterenol, has little influence on vascular capacitance or liver volume of dogs, unless the hepatic outflow resistance is elevated by agents such as histamine.Key words: β-adrenergic agonists, vascular capacitance, mean circulatory filling pressure, isoproterenol, histamine, liver sphincters.

Measurement of mean circulatory filling pressure and vascular compliance in domestic pigs

1990 ◽  
Vol 258 (6) ◽  
pp. H1925-H1932 ◽  
Author(s):  
R. I. Ogilvie ◽  
D. Zborowska-Sluis ◽  
B. Tenaschuk
Keyword(s):  
Cardiac Arrest ◽  
Circulatory Arrest ◽  
Filling Pressure ◽  
Right Atrial ◽  
Base Line ◽  
Pentobarbital Sodium ◽  
Closed Chest ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance ◽  
Venous Circulation

To measure mean circulatory filling pressure (Pmcf), a balloon was placed in the right atrium of seven pentobarbital sodium-anesthetized open-chest pigs for transient occlusion of flow combined with mechanical transfer of blood from the arterial to the venous circulation. Equilibration occurred within 6-8 s at a pressure at 12.3 +/- 0.3 (SE) mmHg after a 2.9 +/- 0.2 ml/kg transfer of blood. In another group of pentobarbital sodium-anesthetized closed-chest pigs, acetylcholine (ACh) was used to induce cardiac arrest. The Pmcf was 11.6 +/- 1.0 mmHg in the 7:17 pigs that arrested for 6-8 s. In four isoflurane-anesthetized closed-chest pigs, the Pmcf was 12.0 +/- 1.0 mmHg after terminal cardiac arrest induced by KCl. The pressure gradient for venous return [Pmcf--right atrial pressure (Pra)] averaged 5.9 +/- 0.2 mmHg. Total vascular compliance estimated from plots of Pmcf at base line, 5, and 10 ml/kg increases in circulating volume was 2.1 +/- 0.3 and 3.5 +/- 0.9 ml.kg-1.mmHg-1 in the balloon and ACh groups, respectively compared with 2.8 +/- 0.4 ml.kg-1.mmHg-1 using a volume infusion-withdrawal method without circulatory arrest. The use of ACh for the estimate of Pmcf in the pig is not recommended because of failure to consistently induce circulatory arrest and probable failure to achieve sufficient equilibrium of vascular pressures 6-8 s postarrest when it occurs.

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.

Hemodynamic effects of posterior hypothalamic injection of neuropeptide Y in awake rats

1991 ◽  
Vol 261 (3) ◽  
pp. H814-H824 ◽  
Author(s):  
J. R. Martin ◽  
M. M. Knuepfer ◽  
T. C. Westfall
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Neuropeptide Y ◽  
Cardiovascular System ◽  
Peripheral Resistance ◽  
Hypothalamic Nucleus ◽  
Initial Increase ◽  
System Control ◽  
Posterior Hypothalamic Nucleus ◽  
Freely Moving

Unilateral microinjection of neuropeptide Y (NPY) into the posterior hypothalamic nucleus was previously found to evoke a sympathoexcitatory-mediated increase in mean arterial pressure (MAP) in urethan-anesthetized rats. In this study, the effect of unilateral injection of NPY into the posterior hypothalamic nucleus on the cardiovascular system of conscious, freely moving rats was determined. Microinjection of NPY (0.2-2.4 nmol) or the cholinergic agonist carbachol (0.5-5.5 nmol) resulted in concentration-dependent increases in MAP. Pretreatment of animals with 7.5 mg/kg iv of the ganglionic blocker pentolinium resulted in a blockade of the increase in MAP evoked by microinjection of NPY (2.4 nmol) or carbachol (3.3 nmol). Despite their similarity of effects on MAP, NPY and carbachol evoked different changes in heart rate. NPY increased heart rate, whereas carbachol evoked a biphasic change in heart rate that consisted of an initial increase followed by a decrease. In addition, carbachol caused increases in both hindquarter and mesenteric vascular resistances, whereas NPY caused a short-lasting increase in mesenteric resistance and a tendency toward an increase in hindquarter resistance. Both NPY and carbachol increased total peripheral resistance while NPY decreased stroke volume. Cardiac output was not significantly affected by either NPY or carbachol, although NPY had a tendency to decrease cardiac output. These results suggest that microinjection of NPY or carbachol into the posterior hypothalamic nucleus of conscious rats evokes an increase in MAP primarily as a result of sympathoexcitation and that NPY and carbachol selectively affect autonomic nervous system control of the cardiovascular system.

Hemodynamic consequences of renin tachyphylaxis and norepinephrine failure of response

1960 ◽  
Vol 198 (3) ◽  
pp. 561-564 ◽  
Author(s):  
H. G. Langford
Keyword(s):  
Blood Pressure ◽  
Peripheral Resistance ◽  
Initial Increase ◽  
Base Line ◽  
Cardiovascular Failure ◽  
Noradrenaline Infusion ◽  
Sustained Hypertension

Renin infusion produced initial increase in blood pressure and peripheral resistance. As infusion continued, blood pressure returned to base-line levels, but peripheral resistance remained slightly elevated. Noradrenaline infusion in the dog did not produce sustained hypertension, but the peripheral resistance remained elevated. Repeated renin injections finally produced no change of blood pressure or peripheral resistance. At this time the animal was nonresponsive to angiotensin. Return of blood pressure to base-line levels despite continued infusion of renin was felt to represent both a ‘cardiovascular failure of response’ and a more specific blockade of angiotensin response.

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.

Regional Blood Flows in High-Cardiac-Output Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 355s-356s ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Initial Increase ◽  
Water Load ◽  
Blood Flows ◽  
Vascular Bed ◽  
Regional Blood Flows ◽  
Electromagnetic Flow Meter ◽  
Secondary Rise

1. Mean arterial pressure, cardiac output (electromagnetic flow-meter) and regional blood flows (15 μm radioactive microspheres) were measured repeatedly in eight dogs receiving a salt and water load after renal mass reduction as well as in six control animals. 2. As previously observed, hypertension developed in the salt-loaded dogs with an initial increase in cardiac output followed by a secondary rise in total peripheral resistance. 3. Much of the early increase in cardiac output was distributed to the skeletal muscle vascular bed. 4. Total peripheral resistance changes did not reflect the resistance of individual vascular beds in the early stages of salt and water load hypertension; indeed, resistance in the muscle vascular bed was decreased and that in the splanchnic area and the bone increased on the first day of salt and water load when total peripheral resistance was unchanged.

Regional blood flows in salt loading hypertension in the dog

1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Salt Loading ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
Regional Blood Flows

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

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