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.

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 reactions to cold exposures differ with age and gender

1985 ◽  
Vol 58 (1) ◽  
pp. 187-192 ◽  
Author(s):  
J. A. Wagner ◽  
S. M. Horvath
Keyword(s):  
Cardiac Output ◽  
Cold Exposure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Similar Response ◽  
Age And Gender ◽  
Ambient Temperatures ◽  
Blood Flows ◽  
Older Subjects ◽  
And Gender

This study was conducted since virtually no information was available concerning age- and gender-related differences in cardiovascular adjustments to cold exposure. Men and women between the ages of 20 and 30 and 51 and 72 yr, wearing swim suits, rested for 2 h in 28, 20, 15, and 10 degrees C ambient temperatures (Ta), with 40% relative humidity. Cardiac output (Qc) and stroke volumes (Qs) were higher in younger than older subjects regardless of Ta. Cardiac output was not influenced by gender, but all cold exposures resulted in increased Qs and decreased heart rate in men but not women. Regardless of age or gender, Qc increased about 10% only during exposure to 10 degrees C. Cold exposure resulted in minimal increases in the mean systolic and diastolic pressures (Pa) of the younger subjects. The Pa of older subjects were higher than in the young during 28 degrees C exposures and increased during all cold exposures. Total peripheral resistance and forearm blood flows were higher in older than young subjects exposed to cold. Total peripheral resistance, systolic and diastolic Pa, and finger and forearm blood flows were not affected by gender, but hand plus forearm blood flows were higher in men than women exposed to 28 degrees C. Although Qc appeared adequate to meet increased oxygen demands of shivering in the older subjects, rising Pa may become limiting in extended exposures. A similar response in hypertensive or angina-prone individuals may result in some untoward responses.

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.

Peripheral vascular resistance and regional blood flows in hypertensive Dahl rats

1991 ◽  
Vol 261 (4) ◽  
pp. R934-R938 ◽  
Author(s):  
M. A. Boegehold ◽  
L. J. Huffman ◽  
G. A. Hedge
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
High Salt ◽  
Renal Vasculature ◽  
Blood Flows ◽  
High Salt Intake ◽  
Regional Blood Flows

The aim of this study was to determine whether different organs undergo similar increases in vascular resistance with hypertension in the Dahl salt-sensitive rat. Cardiac output and organ blood flows were measured with microspheres in anesthetized salt-sensitive and salt-resistant rats fed a high- (7%) or normal- (0.45%) salt diet for 4 wk. High salt intake produced hypertension only in salt-sensitive rats. Cardiac index for the hypertensive group was not different from that for any other group, whereas peripheral resistance index was elevated in proportion to arterial pressure. There were no differences among groups in the fraction of cardiac output supplying the myocardium, intestine, diaphragm, spinotrapezius muscle, or gracilis muscle. The fraction of cardiac output supplying the kidneys was lower in salt-sensitive rats (13%) than in salt-resistant rats (17%) and, among salt-sensitive rats, lowest in the high-salt group. Therefore all the organs studied contribute to increased total peripheral resistance in the hypertensive Dahl rat, with the renal vasculature undergoing the largest resistance increase. Different muscles undergo similar increases in vascular resistance, despite differences in the microvascular abnormalities accompanying salt-induced hypertension.

Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats

1982 ◽  
Vol 243 (4) ◽  
pp. H560-H565
Author(s):  
F. Charocopos ◽  
P. Hatzinikolaou ◽  
W. G. North ◽  
H. Gavras
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Blood Flows ◽  
Fluid Load ◽  
Regional Blood Flows ◽  
Blood Pressures ◽  
Specific Antagonist

We investigated the systemic and regional hemodynamic alterations induced in normotensive anephric rats by stimulation of endogenous vasopressin with an acute sodium and fluid load and following vasopressin inhibition with a specific antagonist of its vasoconstricting action. Blood pressure and total peripheral resistance were significantly higher and cardiac output was lower in rats with stimulated vasopressin, and all were reversed to near control levels in rats receiving the vasopressin inhibitor. Regional blood flows were diminished in most organs and local vascular resistance was elevated compared with control animals, but the magnitude of change varied widely. In fact, heart blood flow did not decrease significantly and brain blood flow actually increased indicating small or no change in vascular resistance of these organs. Moreover, fractional distribution of the diminished cardiac output to these organs was significantly higher, so that blood flow to vital organs was maintained at the expense of blood flow to other tissues. In rats that received the vasopressin antagonist after the saline infusion, regional blood flows were similar to those of control animals. Blood pressures at the base line and after hypertonic NaCl infusion correlated closely with the corresponding plasma levels of control and stimulated vasopressin.

Does vasopressin-induced vasoconstriction persist during prolonged infusion in dogs?

1987 ◽  
Vol 252 (4) ◽  
pp. R668-R673
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arginine Vasopressin ◽  
Total Peripheral Resistance ◽  
Plasma Concentrations ◽  
Peripheral Resistance ◽  
Plasma Osmolality ◽  
Blood Flows ◽  
Specific Antagonist ◽  
Vascular Beds

I have examined the systemic and regional hemodynamic effects of an intravenous arginine vasopressin (AVP) infusion at a rate of 220 pg X kg-1 X min-1 maintained for 48 h in 12 conscious dogs. Plasma AVP concentration increased from 2.8 +/- 1.1 to 8.2 +/- 1.4 pg/ml, and plasma osmolality fell from 294.8 +/- 1.4 to 287.1 +/- 1.5 mosmol/kg. Mean arterial pressure increased slightly but significantly despite a reduction in blood volume. Contrary to what we previously observed with 1-h AVP infusion at the same rate, cardiac output and heart rate did not decrease, and total peripheral resistance did not increase. Most vascular beds sensitive to the acute vasoconstrictor effects of AVP, such as those of the skeletal muscle, fat, colon, and skin, did not show any significant reduction in blood flow after 48 h. Only in the pancreas and in the thyroid gland was there a significant flow decrease, which was similar in magnitude to that measured after 1 h of infusion. It therefore appears that vasoconstriction induced by modest increases in plasma concentrations of AVP is not maintained during prolonged administration in most vascular beds. However, injection of a specific antagonist of the pressor action of AVP [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin, 10 micrograms/kg, induced a significant increase in cardiac output and heart rate, as well as a fall in total peripheral resistance and significant increases in myocardial, fat, and skin blood flows after 48 h of AVP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of a specific and a nonspecific vasodilator on regional blood flows in experimental heart faiiure

1982 ◽  
Vol 60 (2) ◽  
pp. 174-183 ◽  
Author(s):  
K. L. MacCannell ◽  
G. D. Giraud ◽  
K. Lederis ◽  
P. L. Hamilton ◽  
G. Groves
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Sodium Nitroprusside ◽  
Mechanism Of Action ◽  
Diastolic Pressure ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Blood Flows ◽  
Regional Blood Flows

Urotensin I, a vasoactive peptide isolated from fish urophyses, has previously been demonstrated to cause specific mesenteric dilation in the dog. This mechanism of action should limit its maximal cardiovascular actions: no additional cardiovascular effects should ensue once maximal mesenteric vasodilatation is achieved. Provided that the mesenteric vasodilatation does not result in decreased flow to other organs, the agent may, therefore, offer a theoretical advantage as an afterload reducing agent. In pentobarbital anesthetized dogs which were in heart failure as a result of chronic aortico – left atrial shunt, the effects of urotensin I on cardiovascular hemodynamics were compared with the effects of a nonspecific vasodilator, sodium nitroprusside. At equidepressor doses (approximately 15% decrease in mean arterial pressure; sodium nitroprusside, 2 μg∙kg−1∙min−1 i.v.; urotensin I, 10 mU∙kg−1∙min−1 i.v.), both agents produced comparable falls in total peripheral resistance, left ventricular end diastolic pressure, and pulmonary capillary wedge pressure. Forward cardiac output was increased by both substances, although the increases were not statistically significant. Shunt flow, estimated by echocardiography, was reduced by both. In spite of the marked similarity in hemodynamic effects in this model, the two agents affected regional blood flows differently. Sodium nitroprusside did not significantly alter regional flows measured by radioactive microspheres, although calculated splanchnic, skin, and myocardial vascular resistances were reduced. In contrast, urotensin I, as in the normal dog, greatly increased mesenteric blood flow; this redistribution of cardiac output did not, however, result in underperfusion of other vital organs. These data suggest that urotensin I may be a useful agent in the reduction of afterload in heart failure, particularly since the unique mechanism of action appears to minimize the potential for adverse effects due to excessive dosage.

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.

scholarly journals Elevated Blood Pressure in Adolescence Is Attributable to a Combination of Elevated Cardiac Output and Total Peripheral Resistance

Hypertension ◽  
2018 ◽  
Vol 72 (5) ◽  
pp. 1103-1108 ◽  
Author(s):  
Chloe Park ◽  
Abigail Fraser ◽  
Laura D. Howe ◽  
Siana Jones ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Elevated Blood Pressure ◽  
Elevated Blood

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

1996 ◽  
Vol 271 (2) ◽  
pp. H602-H613 ◽  
Author(s):  
M. P. Kunert ◽  
J. F. Liard ◽  
D. J. Abraham
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Experimental Models ◽  
Metabolic Demand ◽  
Flow Probe ◽  
Inositol Hexaphosphate ◽  
Control Value ◽  
Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

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