Stimulation of area postrema decreases blood flow to choroid plexus

1991 ◽  
Vol 260 (3) ◽  
pp. H902-H908 ◽  
Author(s):  
J. L. Williams ◽  
M. M. Thebert ◽  
K. A. Schalk ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Choroid Plexus ◽  
Area Postrema ◽  
Blood Gases ◽  
Autonomic Ganglia ◽  
Lateral Ventricles ◽  
Anesthetized Dogs ◽  
The Central Nervous System ◽  
Stimulation Of

The goal of this study was to examine effects of stimulation of the area postrema on blood flow to choroid plexus and brain. In chloralose-anesthetized dogs, the area postrema was stimulated electrically, and arterial pressure and blood gases were maintained at control levels. We measured blood flow to brain and choroid plexus of the fourth and lateral ventricles with microspheres. Stimulation of the area postrema at 10 +/- 2 microA (means +/- SE), which was the threshold for changes in arterial pressure and heart rate, decreased blood flow to choroid plexus of the fourth and lateral ventricles by 41 +/- 11 and 51 +/- 6%, respectively (from 349 +/- 38 and 503 +/- 46 ml.min-1.100 g-1, respectively). Stimulation at high amplitudes (67 +/- 5 microA) produced only slightly greater decreases in blood flow to choroid plexus. In contrast, cerebral blood flow did not change during stimulation of the area postrema. After blockade of autonomic ganglia with intravenous chlorisondamine, stimulation of the area postrema had minimal effects on blood flow to choroid plexus. The results indicate that stimulation of the area postrema decreases blood flow to choroid plexus, probably by an autonomic mechanism. We speculate that the area postrema may play a role in regulation of volume in the central nervous system by modulating production of cerebrospinal fluid.

Effects of stimulation of fastigial nucleus on cerebral blood flow in cats

1989 ◽  
Vol 257 (1) ◽  
pp. H297-H304 ◽  
Author(s):  
J. L. Williams ◽  
D. D. Heistad ◽  
J. L. Siems ◽  
W. T. Talman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Blood Gases ◽  
Vessel Diameter ◽  
Fastigial Nucleus ◽  
Cross Sectional ◽  
Doppler Probe ◽  
Stimulation Of

The goal of this study was to examine effects of electrical stimulation of the rostral fastigial nucleus on cerebral blood flow. Anesthetized cats were studied, and arterial pressure and blood gases were maintained at control levels during fastigial stimulation. In one group, we measured vessel diameter and velocity of blood flow through a pial artery with a Doppler probe and calculated blood flow as the product of cross-sectional area and velocity. Electrical stimulation of the fastigial nucleus produced a small increase in pial arterial flow of 16 +/- 6% (means +/- SE, P less than 0.05). Pial vascular resistance increased during moderate hypertension and decreased during decreases in arterial pressure, which indicates that cerebral vascular responses were not impaired. In a second group, cerebral blood flow was measured with microspheres. Blood flow to the pons and medulla increased 25 +/- 11 and 21 +/- 11%, respectively, during stimulation of the fastigial nucleus, but blood flow to the cerebral cortex did not increase significantly. Stimulation produced decreases in flow to the renal cortex and duodenum of 39 +/- 10 and 39 +/- 15%, respectively, and flow to the heart increased 48 +/- 22%, which indicates that the stimulus was efficacious. Thus electrical stimulation of the rostral fastigial nucleus in cats elicits only a small increase in cerebral blood flow.

Synaptic transmission in the chronically decentralized middle cervical and stellate ganglia of the dog

1983 ◽  
Vol 61 (10) ◽  
pp. 1149-1155 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Central Nervous System ◽  
Action Potentials ◽  
Autonomic Nerves ◽  
Autonomic Ganglia ◽  
Afferent Nerves ◽  
Stellate Ganglia ◽  
Compound Action Potentials ◽  
The Central Nervous System ◽  
Compound Action ◽  
Stimulation Of

Afferent stimulation of one thoracic cardiopulmonary nerve generated compound action potentials in the efferent axons of other ipsilateral cardiopulmonary nerves in dogs, 14 days after their thoracic autonomic ganglia had been decentralized. The compound action potentials were influenced by the frequency of activation and (in 5 of 12 dogs) by pharmacological autonomic blocking agents (hexamethonium, atropine, phentolamine, and propranolol). Moreover, they were abolished transiently when chymotrypsin was injected locally into the ganglia, and extendedly when manganese was injected. Thus, synapses that can be activated by stimulation of afferent nerves exist in chronically decentralized thoracic autonomic nerves and ganglia. It is proposed that regulation of the heart and lungs occurs in part via thoracic autonomic neural elements independent of the central nervous system.

Effect of PEEP on discharge of pulmonary C-fibers in dogs

1985 ◽  
Vol 59 (4) ◽  
pp. 1085-1089 ◽  
Author(s):  
M. P. Kaufman ◽  
G. A. Ordway ◽  
T. G. Waldrop
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Impulse Activity ◽  
Vena Cava ◽  
Laboratory Animals ◽  
Positive End Expiratory Pressure ◽  
Firing Rates ◽  
C Fibers ◽  
Anesthetized Dogs ◽  
Stimulation Of

Although positive end-expiratory pressure (PEEP) is believed to depress cardiac output and arterial pressure by compressing the vena cava and the heart, it is unclear whether PEEP also depresses these variables by a reflex arising from an inflation-induced stimulation of pulmonary C-fibers. We therefore recorded the impulse activity of 17 pulmonary C-fibers in barbiturate-anesthetized dogs with closed chests, while we placed the expiratory outlet of a ventilator under 5–30 cmH2O. Increasing PEEP in a ramp-like manner stimulated 12 of the 17 pulmonary C-fibers, with activity increasing from 0.0 +/- 0.1 to 0.9 +/- 0.2 imp/s when end-expiratory pressure equaled 15 cmH2O. When PEEP was increased in a stepwise manner to 15–20 cmH2O and maintained at this pressure for 15 min, pulmonary C-fibers increased their firing rates, but the effect was small averaging 0.2–0.3 imp/s after the 1st min of this maneuver. We conclude that pulmonary C-fibers are unlikely to be responsible for causing much of the decreases in cardiac output and arterial pressure evoked by sustained periods of PEEP in both patients and laboratory animals. These C-fibers, however, are likely to be responsible for causing the reflex decreases in these variables evoked by sudden application of PEEP.

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation

1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Ventilatory Response ◽  
Carotid Bifurcation ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation ◽  
Stimulation Of

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

Medullary blood flow responses to changes in arterial pressure in canine kidney

1996 ◽  
Vol 270 (5) ◽  
pp. F833-F838 ◽  
Author(s):  
D. S. Majid ◽  
L. G. Navar
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Medulla ◽  
Doppler Flowmetry ◽  
Cortical Blood Flow ◽  
Surface Probe ◽  
Medullary Blood Flow ◽  
Needle Probe ◽  
Anesthetized Dogs ◽  
Electromagnetic Flow Probe

Although it is well recognized that whole kidney and cortical blood flow exhibit efficient autoregulation in response to alterations in renal arterial pressure (RAP), the autoregulatory behavior of medullary blood flow (MBF) has remained uncertain. We have evaluated MBF responses to stepwise reductions in RAP for both short-term (2 min, n = 6) and longer periods (15 min, n = 7) using single-fiber laser-Doppler flowmetry with needle probes inserted into the mid-medullary region in denervated kidneys of 13 anesthetized dogs. The changes in cortical blood flow (CBF) were assessed with either a surface probe or a needle probe inserted into the cortex. Control total renal blood flow (RBF), assessed by electromagnetic flow probe in these dogs, was 5.2 +/- 0.3 ml.min-1.g-1, and glomerular filtration rate was 0.97 +/- 0.05 ml.min-1.g-1 (n = 7). RBF, MBF, and CBF all exhibited efficient autoregulatory behavior during changes in RAP from 150 to 75 mmHg. The slopes of RAP vs. RBF, CBF, as well as MBF, were not significantly different from zero within this range of RAP. Below RAP of 75 mmHg, all indexes of blood flow showed linear decreases with reductions in pressure. The data indicate that blood flow in the renal medulla of dogs exhibits efficient autoregulatory behavior, similar to that in the cortex.

Inhibition of renal sympathetic nervous activity by area postrema stimulation in rabbits

1987 ◽  
Vol 253 (1) ◽  
pp. H91-H99 ◽  
Author(s):  
E. M. Hasser ◽  
D. O. Nelson ◽  
J. R. Haywood ◽  
V. S. Bishop
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Consistent Change ◽  
Renal Sympathetic ◽  
Stimulation Of

This study investigated the effect of chemical and electrical stimulation of the area postrema on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in urethan-anesthetized rabbits. Electrical stimulation of the area postrema at 2, 5, 10, 20, 40, and 80 Hz using constant currents of 7.5, 15, and 30 microA (pulse duration = 0.3 ms, train duration = 5 s) produced progressive decreases in RSNA and heart rate, with no consistent change in arterial pressure. To control for electrical activation of fibers of passage in or near the area postrema, L-glutamate was injected into the area postrema using glass micropipettes. Micropressure injection of L-glutamate (10 mM) in volumes of 5-10 nl produced rapid decreases in RSNA averaging 27 +/- 5% (P less than 0.05) accompanied by a small bradycardia. The effects of electrical stimulation of the area postrema, but not the adjacent nucleus tractus solitarius, were totally eliminated by micropressure injection of kainic acid (40 ng in 40 nl) into the area postrema. During continuous electrical stimulation of the area postrema using parameters that produced small decrements in RSNA and heart rate, the slope of the line relating baroreflex inhibition of RSNA to increases in arterial pressure during graded infusions of phenylephrine was significantly enhanced (-6.77 +/- 1.30 vs. -3.81 +/- 0.66% RSNA/mmHg). These data are consistent with the hypothesis that activation of neurons in the area postrema results in an inhibition of RSNA. Furthermore, stimulation of the area postrema augments baroreflex inhibition of RSNA during increases in arterial pressure with phenylephrine.

Hemodynamic effects of electrical stimulation of forebrain angiotensin and osmosensitive sites

1978 ◽  
Vol 235 (4) ◽  
pp. H445-H451 ◽  
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Median Eminence ◽  
Regional Blood Flow ◽  
Renal Hypertension ◽  
Brain Structures ◽  
Ventromedial Hypothalamus ◽  
Pressure Changes ◽  
Stimulation Of

Previous studies from this laboratory have indicated an important role for angiotensin-sensitive anteroventral third ventricular (AV3V) brain structures in normal regulation of arterial pressure and development of renal hypertension. The present experiments examined the effects of electrical stimulation of these periventricular areas on arterial pressure and regional blood flow in the anesthetized rat. Electrodes were placed in the AV3V region 3–10 days prior to acute studies. Blood flow was measured in extracorporeal blood flow circuits. Electrical stimulation produced only small changes in arterial pressure. Despite the small pressure changes, stimulation caused marked frequency-dependent alterations in regional blood flow. Renal and splanchnic flows were reduced while hindlimb flow was increased. Resistance changes were abolished by surgical denervation or ganglionic blockade but were unaffected by adrenalectomy. Hemodynamic responses to AV3V stimulation were abolished by a lesion in the area of the median eminence. It may be concluded that AV3V stimulation, through activation of pathways descending through the ventromedial hypothalamus-median eminence region, produces profound regional blood flow shifts without greatly altering arterial pressure.

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