Chemoreceptor and baroreceptor inputs to ventrolateral medullary neurons

1984 ◽  
Vol 247 (5) ◽  
pp. R872-R879 ◽  
Author(s):  
M. M. Caverson ◽  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Arterial Occlusion ◽  
Firing Frequency ◽  
Single Units ◽  
Ventrolateral Medulla ◽  
Afferent Information ◽  
Thoracic Cord ◽  
Upper Thoracic ◽  
Baroreceptor Activation ◽  
Carotid Arterial ◽  
Intermediolateral Nucleus

Recording experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated cats to identify single units in the ventrolateral medulla (VLM) projecting directly to the region of the intermediolateral nucleus of the spinal cord (T2) and responding to selective activation of peripheral chemoreceptors (sodium cyanide, 20-60 micrograms in 0.1-0.3 ml saline into medial thyroid artery) and baroreceptors (phenylephrine, 2 micrograms/kg iv). The firing frequency of 49 of the 81 antidromically identified single units was altered by activation of the peripheral cardiovascular receptors. Of these responsive units, 25 responded only to activation of chemoreceptors (17 excited and 8 inhibited), 20 responded in various combinations to activation of both chemo- and baroreceptors, and 4 responded only to activation of baroreceptors. In addition, units that altered their firing frequency during baroreceptor activation (n = 24) responded in the opposite direction to baroreceptor unloading (carotid arterial occlusion). These results suggest that neurons in the VLM are components of bulbospinal sympathoexcitatory and -inhibitory pathways that receive cardiovascular afferent information and in turn influence vasoconstrictor and cardioacceleratory neurons in the intermediolateral nucleus of the upper thoracic cord.

Loss of intermediolateral nucleus in the upper thoracic cord increase risk of sudden cardiac arrest in ALS

2007 ◽  
Vol 135 (1-2) ◽  
pp. 136
Author(s):  
Hirohide Asai ◽  
Makito Hirano ◽  
Fukashi Udaka ◽  
Yoshiko Furiya ◽  
Keiji Shimada ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Sudden Cardiac Arrest ◽  
Increase Risk ◽  
Thoracic Cord ◽  
Upper Thoracic ◽  
Intermediolateral Nucleus

Inhibition of rostral VLM by baroreceptor activation is relayed through caudal VLM

1990 ◽  
Vol 258 (5) ◽  
pp. R1271-R1278 ◽  
Author(s):  
S. K. Agarwal ◽  
A. J. Gelsema ◽  
F. R. Calaresu
Keyword(s):  
Kynurenic Acid ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Firing Frequency ◽  
Ventrolateral Medulla ◽  
Cardiovascular Neurons ◽  
Baroreceptor Activation ◽  
Acid Administration ◽  
Stimulation Of

Experiments were done to test the hypothesis that inhibition of neurons in the rostral ventrolateral medulla (RVLM) elicited by stimulation of the nucleus tractus solitarii (NTS) is relayed through the caudal ventrolateral medulla (CVLM). We recorded activity from 56 spontaneously firing units in the right RVLM of urethan-anesthetized and artificially ventilated rats. Eleven of these units were classified as cardiovascular neurons, because they were silenced by baroreceptor activation (1-3 micrograms phenylephrine iv) and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Single pulses (0.1 ms, 30-75 microA) delivered 1/s to depressor sites in the ipsilateral NTS inhibited the activity of all these cardiovascular neurons. Microinjection of the glutamate antagonist kynurenic acid (0.15 M, 50 nl) into the ipsilateral CVLM blocked the inhibitory response of RVLM units to the administration of phenylephrine and increased the firing frequency of cardiovascular neurons in the RVLM by 43%. Moreover, kynurenic acid administration attenuated the inhibitory response of cardiovascular neurons in the RVLM to NTS stimulation. Finally, stimulation of the NTS that elicited depressor responses under control conditions produced a pressor response after kynurenic acid administration. The remaining 45 RVLM neurons were barosensitive but lacked cardiac cycle-related rhythmicity. These results provide direct evidence for the existence of a tonic inhibitory pathway from NTS to RVLM that is relayed through the CVLM probably by a glutamatergic projection from NTS to CVLM.

Internal carotid arterial occlusion following mandibular osteotomy

1984 ◽  
Vol 42 (6) ◽  
pp. 394-399 ◽  
Author(s):  
K. Singh Sanni ◽  
Robert L. Campbell ◽  
Michael J. Rosner ◽  
W. Brant Goyne
Keyword(s):  
Internal Carotid ◽  
Arterial Occlusion ◽  
Mandibular Osteotomy ◽  
Carotid Arterial

L-arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR

1992 ◽  
Vol 263 (5) ◽  
pp. H1632-H1635 ◽  
Author(s):  
E. Morikawa ◽  
Z. Huang ◽  
M. A. Moskowitz
Keyword(s):  
Cerebral Ischemia ◽  
Infarct Size ◽  
Focal Cerebral Ischemia ◽  
Arterial Occlusion ◽  
Cerebral Blood Vessels ◽  
Hypertensive Rats ◽  
Vessel Occlusion ◽  
Spontaneously Hypertensive ◽  
Cerebral Arterial Occlusion ◽  
Carotid Arterial

L-Arginine, but not D-arginine, serves as a precursor for the synthesis of nitric oxide (NO), a potent dilator of cerebral blood vessels. We examined the effects of administering L-arginine (300 mg/kg ip) on the volume of infarction in two models of focal cerebral ischemia in spontaneously hypertensive rats (SHR). L-Arginine was administered before (16 and 3 h) and after (5 min and 2 h) vessel occlusion, and animals were killed 24 h later. L-Arginine treatment decreased infarct size in rats subjected to distal middle cerebral arterial (MCA) plus ipsilateral common carotid arterial (CCA) occlusion by 31% [147 +/- 12 (saline) vs. 101 +/- 9 mm3 (L-arginine), P < 0.05]. D-Arginine, administered according to the same dosage and protocol, was without effect. In the group subjected to proximal MCA occlusion, L-arginine decreased infarction size in the striatum by 28% [47 +/- 5 (saline) vs. 34 +/- 3 mm3 (L-arginine), P < 0.05] and neocortex by 11% [193 +/- 7 (saline) vs. 171 +/- 8 mm3 (L-arginine), P < 0.05]. Changes in blood pressure or other measured physiological parameters did not account for the observed differences. The possible use of L-arginine for the treatment of focal cerebral ischemia merits further investigation.

Ascending pathways mediating somatoautonomic reflexes in exercising dogs

1987 ◽  
Vol 62 (3) ◽  
pp. 1186-1191 ◽  
Author(s):  
J. W. Kozelka ◽  
G. W. Christy ◽  
R. D. Wurster
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Surgical Techniques ◽  
Arterial Occlusion ◽  
Cardiovascular Responses ◽  
Spinal Pathways ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Dorsolateral Funiculus ◽  
Carotid Arterial

The ascending spinal pathways mediating somatocardiovascular reflexes during exercise were studied in unanesthetized dogs by placing lesions in the lumbar spinal cord. After training to run on a treadmill with hindlimbs only, 20 dogs were anesthetized and instrumented using sterile surgical techniques. To chronically record heart rate and arterial blood pressure, the aorta was cannulated via the omocervical artery. To test the intactness of descending spinal sympathetic pathways, reflex pressor responses to baroreceptor hypotension were produced by bilateral carotid arterial occlusion using pneumatic vessel occluders placed around the common carotid arteries. To generate transient ischemic exercise (120 s), a pneumatic occluder was placed around the left iliac artery. Eight to 10 days after instrumentation, blood pressure and heart rate were monitored at rest and during hindlimb running with and without simultaneous iliac arterial occlusion. The modest pressor response and tachycardia elicited by hindlimb exercise were markedly augmented by simultaneous hindlimb ischemia (i.e., iliac arterial occlusion). Lesion placement in the dorsolateral sulcus area and the dorsolateral funiculus at L2 significantly reduced the blood pressure and heart rate responses to simultaneous exercise occlusion. The cardiovascular responses to nonischemic exercise and bilateral carotid arterial occlusion were not altered by such spinal sections. It is concluded that in the dog the ascending spinal pathways mediating cardiovascular responses to ischemic exercise are located in the lateral funiculus, including the dorsolateral sulcus area and dorsolateral funiculus.

Effects of substance P and thyrotropin-releasing hormone on sympathetic preganglionic neurones in the upper thoracic intermediolateral nucleus of the cat

1984 ◽  
Vol 62 (2) ◽  
pp. 248-251 ◽  
Author(s):  
S. B. Backman ◽  
J. L. Henry
Keyword(s):  
Substance P ◽  
Synaptic Transmission ◽  
Thyrotropin Releasing Hormone ◽  
Excitatory Effect ◽  
Releasing Hormone ◽  
Spinal Segments ◽  
Time Courses ◽  
Upper Thoracic ◽  
Intermediolateral Nucleus ◽  
Chemical Mediators

When applied by iontophoresis onto single sympathetic preganglionic neurones in the intermediolateral nucleus of spinal segments T1–T3 in the cat, substance P and thyrotropin-releasing hormone (TRH) each had a weak excitatory effect. Two-thirds of the neurones studied were excited by substance P while one-fifth were excited by TRH. The time courses of the responses to substance P and to TRH were similar, and consisted of an increase in the rate of discharge with a latency of approximately 30 s from the onset of application. They were also prolonged (30–320 s) in afterdischarge following termination of application. These results indicate that substance P and TRH exert excitatory effects on single sympathetic preganglionic neurones, and support the possibility that they may be chemical mediators of synaptic transmission in the intermediolateral nucleus.

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