scholarly journals Collateralizaton of projections of rostral ventrolateral medulla (RVLM) neurons to levels of the thoracic spinal cord that regulate upper‐ and lower‐body blood flow

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Michael F Gowen ◽  
Sarah A Weber ◽  
Takeshi Suzuki ◽  
Yoichiro Sugiyama ◽  
Bill J Yates
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Lower Body ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla

1991 ◽  
Vol 260 (1) ◽  
pp. H267-H275 ◽  
Author(s):  
M. K. Bazil ◽  
F. J. Gordon
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Nmda Receptors ◽  
Excitatory Amino Acid ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Pressor Responses

These studies investigated the role of spinal N-methyl-D-aspartic acid (NMDA) receptors in the mediation of cardiovascular responses evoked by L-glutamate (L-Glu) stimulation of the rostral ventrolateral medulla (RVM). Microinjections of L-Glu into the RVM of urethan-anesthetized rats increased mean arterial pressure (MAP) and heart rate. Intrathecal administration of the NMDA receptor antagonists D-(-)-2-amino-7-phosphonoheptanoic acid (D-AP-7) or 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP) reduced MAP and heart rate. Blockade of NMDA receptors by D-AP-7 or CPP in the caudal thoracic spinal cord markedly reduced RVM pressor responses with little effect on evoked tachycardia. Administration of D-AP-7 to the rostral thoracic spinal cord had no effect on RVM pressor or tachycardic responses. Intrathecal D-AP-7 and CPP abolished the cardiovascular effects of intrathecal NMDA without reducing those produced by intrathecal kainic acid or the quisqualate agonist DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). These results indicate that 1) tonic activation of spinal NMDA receptors participates in the maintenance of sympathetic outflow to the heart and blood vessels, 2) pressor responses evoked from the RVM require synaptic activation of spinal NMDA receptors, and 3) an excitatory amino acid may be the neurotransmitter of pressor pathways descending from the RVM to the spinal cord.

scholarly journals Collateralization of projections from the rostral ventrolateral medulla to the rostral and caudal thoracic spinal cord in felines

2012 ◽  
Vol 220 (2) ◽  
pp. 121-133 ◽  
Author(s):  
Michael F. Gowen ◽  
Sarah W. Ogburn ◽  
Takeshi Suzuki ◽  
Yoichiro Sugiyama ◽  
Lucy A. Cotter ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

57 CLINICAL MEASUREMENT OF BLOOD FLOW TO THE CERVICAL AND THORACIC SPINAL CORD

1986 ◽  
Vol 21 (9) ◽  
pp. S15
Author(s):  
A. Khandji ◽  
S. K. Hilal ◽  
A. J. Silver ◽  
J. A. Bello
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Thoracic Spinal Cord ◽  
Clinical Measurement ◽  
Thoracic Spinal

scholarly journals Exaggerated sympathoexcitatory reflexes develop with changes in the rostral ventrolateral medulla in obese Zucker rats

2016 ◽  
Vol 311 (2) ◽  
pp. R243-R253 ◽  
Author(s):  
Domitila A. Huber ◽  
Ann M. Schreihofer
Keyword(s):  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Zucker Rats ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Obese Zucker Rats ◽  
Sciatic Nerve Stimulation ◽  
Upper Thoracic

Obesity leads to altered autonomic reflexes that reduce stability of mean arterial pressure (MAP). Sympathoinhibitory reflexes such as baroreflexes are impaired, but reflexes that raise MAP appear to be augmented. In obese Zucker rats (OZR) sciatic nerve stimulation evokes larger increases in MAP by unknown mechanisms. We sought to determine the autonomic underpinnings of this enhanced somatic pressor reflex and whether other sympathoexcitatory reflexes are augmented. We also determined whether their final common pathway, glutamatergic activation of the rostral ventrolateral medulla (RVLM), was enhanced in male OZR compared with lean Zucker rats (LZR). Sciatic nerve stimulation or activation of the nasopharyngeal reflex evoked larger rises in splanchnic sympathetic nerve activity (SNA) (79% and 45% larger in OZR, respectively; P < 0.05) and MAP in urethane-anesthetized, ventilated, paralyzed adult OZR compared with LZR. After elimination of baroreflex feedback by pharmacological prevention of changes in MAP and heart rate, these two sympathoexcitatory reflexes were still exaggerated in OZR (167% and 69% larger, respectively, P < 0.05). In adult OZR microinjections of glutamate, AMPA, or NMDA into the RVLM produced larger rises in SNA (∼61% larger in OZR, P < 0.05 for each drug) and MAP, but stimulation of axonal fibers in the upper thoracic spinal cord yielded equivalent responses in OZR and LZR. In juvenile OZR and LZR, sympathoexcitatory reflexes and physiological responses to RVLM activation were comparable. These data suggest that the ability of glutamate to activate the RVLM becomes enhanced in adult OZR and may contribute to the development of exaggerated sympathoexcitatory responses independent of impaired baroreflexes.

Experimental acute balloon compression of the spinal cord

1979 ◽  
Vol 51 (6) ◽  
pp. 841-845 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Delbert E. Evans ◽  
Hugo V. Rizzoli
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Spinal Cord Ischemia ◽  
Evoked Response ◽  
Physical Injury ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Balloon Compression ◽  
Thoracic Spinal ◽  
Flow Changes

✓ Acute balloon compression of the thoracic spinal cord for 15, 7, 5, 3, and 1 minute in monkeys caused immediate disappearance of the spinal evoked response and complete focal ischemia of the compressed segment in all animals. Only the animals in the 1-minute group, however, demonstrated return of the evoked response. These data, coupled with data from previous experiments of slow balloon compression of the spinal cord and spinal cord ischemia, suggest that the major pathological substrate for neural dysfunction after balloon compression of the spinal cord, be it acute or slow, is physical injury of the neural membrane, irrespective of blood flow changes. These findings also suggest that the ability of that membrane to recover is related to rapidity and length of time of compression. Focal changes in blood flow do not appear to be significant in this mechanism.

scholarly journals Delayed detection of motor pathway dysfunction after selective reduction of thoracic spinal cord blood flow in pigs

2002 ◽  
Vol 123 (3) ◽  
pp. 531-538 ◽  
Author(s):  
Jeroen Lips ◽  
Peter de Haan ◽  
Gerrit J. Bouma ◽  
Michael J. Jacobs ◽  
Cor J. Kalkman
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cord Blood ◽  
Selective Reduction ◽  
Spinal Cord Blood Flow ◽  
Thoracic Spinal Cord ◽  
Motor Pathway ◽  
Thoracic Spinal

Alteration of posttraumatic ischemia in experimental spinal cord trauma by a central nervous system depressant

1979 ◽  
Vol 50 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Howard J. Senter ◽  
Joan L. Venes ◽  
John S. Kauer
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Blood Flow ◽  
Nervous System ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Thoracic Spinal ◽  
Gamma Hydroxybutyrate ◽  
Central Nervous System Depressant ◽  
Experimental Injury

✓ Blood flow after severe experimental injury to the thoracic spinal cord was studied in cats, using a modification of the hydrogen clearance technique. Gamma hydroxybutyrate, a central nervous system depressant, was shown to markedly alter the ischemic response to injury if given during the early posttraumatic period. Other vasoactive drugs investigated had no effect on posttraumatic ischemia. Therapeutic intervention during the early posttraumatic period aimed at increasing blood flow while decreasing the metabolic requirements of the injured cord may prove of value in reversing or limiting some elements of long-tract dysfunction due to the secondary ischemic insult.

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