Effect of a left atrium-pulmonary vein baroreflex on peripheral vascular beds

1977 ◽  
Vol 233 (5) ◽  
pp. H587-H591 ◽  
Author(s):  
T. C. Lloyd ◽  
J. J. Fried
Keyword(s):  
Left Atrial ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Radioactive Microspheres ◽  
Peripheral Vascular ◽  
Blood Flows ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Response Peak ◽  
Vascular Beds

A step increase of left atrial and pulmonary venous pressure from 0 to 25 mmHg was used in anesthetized dogs with controlled arterial blood pressure to generate reflex systemic vasodilation. The resultant response of total peripheral resistance was an initial transient fall of about 40% which spontaneously regressed while the stimulus was maintained. Injections of differently tagged radioactive microspheres were used to measure selected organ blood flows prior to raising atrial pressure, at the response peak, during the steady state, and after recovery. Resistances of skin, skeletal muscle, kidney, and large intestine significantly fell upon atriovenous distention. The response in muscle, which greatly exceeded that of the other organs, was not sustained, whereas resistances of other responding beds remained depressed until the stimulus was removed. No significant responses occurred in small intestine, liver (hepatic artery), or adrenal gland.

Prostacyclin release following endoperoxide analogue infusion in the intact dog

1984 ◽  
Vol 246 (2) ◽  
pp. R205-R210 ◽  
Author(s):  
J. Mehta ◽  
W. W. Nichols ◽  
R. Goldman
Keyword(s):  
Thromboxane A2 ◽  
Left Ventricular ◽  
Cyclooxygenase Inhibitors ◽  
Blood Samples ◽  
Blood Flows ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Anesthetized Dogs ◽  
Vascular Beds ◽  
Autoregulatory Mechanism

We examined the systemic and coronary hemodynamic responses after infusion of an endoperoxide analogue U 46,619 in anesthetized dogs and related the hemodynamic effects to the release of thromboxane A2 (TXA2) and prostacyclin (PGI2). Immediately after U 46,619 infusion, increases in mean arterial and left ventricular end-diastolic pressures (LVEDP) occurred, whereas coronary and aortic blood flows were unchanged. Calculated vascular resistances in the systemic and coronary vascular beds increased significantly. At 3-5 min after infusion, mean arterial pressure and LVEDP spontaneously decreased and vascular resistances also declined, whereas coronary and aortic blood flows were unchanged. Simultaneously measured plasma TXB2 and 6-keto-PGF1 alpha (stable hydrolysis metabolites of TXA2 and PGI2, respectively) increased in the femoral and coronary arterial blood samples in conjunction with the vasoconstrictor effects. At 3-5 min, plasma 6-keto-PGF1 alpha concentrations showed a further increase, whereas TXB2 concentrations slightly decreased, suggesting release of PGI2 as a possible mechanism of vasodilation. To examine this possibility, nine dogs were treated with cyclooxygenase inhibitors (aspirin or indomethacin) and given U 46,619. In these animals neither vasoconstrictor nor vasodilator effects were observed. Plasma TXB2 and 6-keto-PGF1 alpha concentrations also did not increase after U 46,619. These data show that the vasoconstrictor and platelet aggregatory agent U 46,619 results in PGI2 release in the dog. Release of PGI2 may be a protective and autoregulatory mechanism in the canine systemic and coronary vascular beds.

In vivo characterization of vasocontractile activities in erythrocytes

1983 ◽  
Vol 58 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Michael P. McIlhany ◽  
Lydia M. Johns ◽  
Thomas Leipzig ◽  
Nicholas J. Patronas ◽  
Frederick D. Brown ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Content Type ◽  
Control Value ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Chronic Cerebral Vasospasm ◽  
In Vivo Characterization

✓ Partially purified protein from washed and artificially hemolyzed erythrocytes, known to cause significant contractions of isolated canine cerebral vessels in vitro, was injected into the cisterna magna of intact anesthetized dogs. Cerebral blood flow, measured by the xenon-133 washout technique, decreased from a control value of 49.5 ± 1.17 ml/100 gm/min to an experimental value of 34.1 ± 1.65 ml/100 gm/min at 2 hours. Cerebral vascular resistance rose from a control value of 2.05 ± 0.17 PRU (peripheral resistance units) to an experimental value of 2.91 ± 0.25 PRU at 2 hours. Mean arterial blood pressure, heart rate, intracranial pressure, and cerebral perfusion pressure remained stable. Cardiac output also fell significantly (in 2-hour control animals it was 2.89 ± 0.37 liter/min, and in 2-hour experimental animals 1.43 ± 0.13 liter/min) and peripheral vascular resistance rose. These changes were evident by 10 minutes after the cisternal injection of the hemolysate protein, and remained for the duration of the 2-hour monitoring period. Serial vertebrobasilar angiograms demonstrated marked narrowing of the intracranial basilar artery when compared to control values. The narrowing persisted for several days in most animals, and tended to increase with time. Relaxation occurred by the 10th through the 14th day. The authors conclude that this experimental preparation may be a useful model for both in vitro and in vivo investigation of chronic cerebral vasospasm.

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.

CARDIORENAL EFFECTS OF LARGE INFUSIONS OF DEXTRAN IN DOGS

1954 ◽  
Vol 32 (1) ◽  
pp. 559-566 ◽  
Author(s):  
C. W. Gowdey ◽  
I. E. Young
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
The Body ◽  
Arterial Blood ◽  
High Output Heart Failure ◽  
Mean Pressure ◽  
Anesthetized Dogs ◽  
The Right ◽  
Dextran Solution ◽  
High Output

The production of hypervolemic dilution anemia in intact, anesthetized dogs by the continuous intravenous infusion of 6% dextran solution caused large increases in the cardiac output and urine flow. No consistent changes were observed in pulse rate or arterial blood pressure. The right auricular mean pressure usually increased early in the infusion, but later there was no consistent relation between right auricular pressure and cardiac output. The total peripheral resistance, glomerular filtration rate, and renal blood flow decreased. With infusion volumes exceeding 10% of the body weight, acute high-output heart failure occurred. The observed hemodilution was consistently greater than that expected from the volume of the infusion, because the dextran solution was, presumably, hypertonic.

scholarly journals Decreased prefrontal oxygenation elicited by stimulation of limb mechanosensitive afferents during cycling exercise

2018 ◽  
Vol 315 (2) ◽  
pp. R230-R240 ◽  
Author(s):  
Ryota Asahara ◽  
Kanji Matsukawa
Keyword(s):  
Blood Flow ◽  
Prefrontal Cortex ◽  
Minute Ventilation ◽  
Peripheral Resistance ◽  
Oxygenation Index ◽  
Tissue Blood Flow ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cutaneous Tissue

Our laboratory reported using near-infrared spectroscopy that feedback from limb mechanoafferents may decrease prefrontal oxygenated-hemoglobin concentration (Oxy-Hb) during the late period of voluntary and passive cycling. To test the hypothesis that the decreased Oxy-Hb of the prefrontal cortex would be augmented depending on the extent of limb mechanoafferent input, the prefrontal Oxy-Hb response was measured during motor-driven one- and two-legged passive cycling for 1 min at various revolutions of pedal movement in 19 subjects. Furthermore, we examined whether calculated tissue oxygenation index (TOI) decreased during passive cycling as the Oxy-Hb did, simultaneously assessing blood flows of extracranial cutaneous tissue and the common and internal carotid arteries (CCA and ICA) with laser and ultrasound Doppler flowmetry. Minute ventilation and cardiac output increased and peripheral resistance decreased during passive cycling, depending on both revolutions of pedal movement and number of limbs, whereas mean arterial blood pressure did not change. Passive cycling did not change end-tidal CO2, suggesting absence of a hypocapnic change. Prefrontal Oxy-Hb decreased during passive cycling, being in proportion to revolution of pedal movement but not number of cycling limbs. In addition, prefrontal TOI decreased during passive cycling as Oxy-Hb did, whereas blood flows of forehead cutaneous tissue, CCA, and ICA did not change significantly. Thus, a decrease in Oxy-Hb reflected a decrease in tissue blood flow of the intracerebral vasculature but not the extracerebral compartment. It is likely that feedback from mechanoafferents decreased regional cerebral blood flow of the prefrontal cortex in relation to the revolutions of pedal movement.

Epinephrine-induced hepatic potassium movements before and after adrenergic blockade

1976 ◽  
Vol 54 (3) ◽  
pp. 347-356 ◽  
Author(s):  
Stephen D. Guthrie ◽  
Quillian R. Murphy
Keyword(s):  
Portal Vein ◽  
Superior Mesenteric Artery ◽  
Adrenergic Receptors ◽  
Mesenteric Artery ◽  
Adrenergic Blockade ◽  
Blood Flows ◽  
Arterial Blood ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Artery Flow

The epinephrine-induced loss and subsequent uptake of K+ by the liver was studied by measuring hepatic arterio–venous K+ differences and splanchnic blood flows in anesthetized dogs with chronically implanted portal vein catheters and celiac and superior mesenteric artery flow probes. When epinephrine was administered intraportally, neither α- nor β-adrenergic blockade, singly or in combination, had significant effects upon the hyper-kalemic or the hypokalemic phases in either hepatic venous or systemic arterial blood. It was concluded that the movements of K+ into and out of the liver caused by epinephrine are not mediated by the classical adrenergic receptors as defined by inhibition by specific blocking agents.

CARDIOVASCULAR RESPONSES IN DOGS TO LARGE INTRAVENOUS INFUSIONS

1954 ◽  
Vol 32 (3) ◽  
pp. 282-292 ◽  
Author(s):  
C. W. Gowdey ◽  
J. D. Hatcher ◽  
F. A. Sunahara
Keyword(s):  
Cardiac Output ◽  
Peripheral Blood ◽  
Cardiovascular Responses ◽  
Blood Flows ◽  
Gum Acacia ◽  
Cardiac Decompensation ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
Slow Intravenous Infusion

The effects of a continuous, slow, intravenous infusion of gum acacia solution have been measured in anesthetized dogs. When the volume of the circulation was increased and the hematocrit value reduced, the cardiac output, intracardiac pressures, and peripheral blood flows began to increase. In some experiments these changes continued until sudden cardiac decompensation occurred during which the arterial blood pressure, cardiac output, and peripheral blood flows were reduced while the mean right auricular and ventricular pressures increased markedly. Analysis of the results indicates that up to the time of the highest cardiac output there is a closer correlation between cardiac output and hematocrit value than between cardiac output and mean right auricular pressure.

Regional hemodynamic effects of neuromedin U in conscious rats

1990 ◽  
Vol 258 (1) ◽  
pp. R32-R38 ◽  
Author(s):  
S. M. Gardiner ◽  
A. M. Compton ◽  
T. Bennett ◽  
J. Domin ◽  
S. R. Bloom
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Peripheral Resistance ◽  
Local Blood Flow ◽  
High Concentration ◽  
Rat Intestine ◽  
Mesenteric Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Long Evans

In conscious unrestrained Long-Evans rats, chronically instrumented with miniaturized pulsed Doppler flow probes, intravenous administration of porcine neuromedin U-8 by bolus (0.1 and 1.0 nmol) or infusion (1 and 10 nmol/h) exerted potent constrictor effects on the superior mesenteric vascular bed. With the choice of an appropriate dose, the reduction in superior mesenteric blood flow was not accompanied by any changes in systemic arterial blood pressure, heart rate, and renal or hindquarters blood flows. Porcine neuromedin U-25 had similar effects to neuromedin U-8, but was generally more potent. In Brattleboro rats the pattern of response to neuromedin U-25 was similar to that seen in Long-Evans rats, indicating that mesenteric vasoconstriction was not dependent on release of endogenous vasopressin. In Long-Evans rats the regional hemodynamic actions of rat neuromedin U were comparable with those of porcine neuromedin U-25. The latter peptide at a dose of 1.0 nmol caused a rise in total peripheral resistance and a reduction in cardiac output, with an inconsistent change in heart rate. The results raise the possibility that the high concentration of neuromedin U in the rat intestine is associated with the control of local blood flow.

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