Cardiovascular responses to global cerebral ischemia: role of excitatory amino acids in the ventrolateral medullary pressor area

1993 ◽  
Vol 78 (6) ◽  
pp. 922-928 ◽  
Author(s):  
Robert F. Heary ◽  
Allen H. Maniker ◽  
Abbott J. Krieger ◽  
Hreday N. Sapru

✓ The object of this study was to investigate the role of the ventrolateral medullary pressor area in mediating the cardiovascular responses to experimentally induced global cerebral ischemia, and to test if excitatory amino acids or acetylcholine are the transmitters released in this brain region during these responses. The cerebral ischemic response was elicited in pentobarbital-anesthetized, artificially ventilated male Wistar rats by bilateral ligation of vertebral arteries followed by temporary clamping of the common carotid arteries. The pressor area was identified by microinjections of L-glutamate. Inhibition of neurons in this area by microinjections of muscimol, a γ-aminobutyric acid receptor agonist, abolished the ischemic response, which demonstrated that this area is important in mediating these responses. Microinjections of a broad-spectrum excitatory amino acid receptor blocker (kynurenate), of specific antagonists for N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors (injected alone or in combination), and of atropine failed to block the ischemic responses. These results indicate that: 1) the ventrolateral medullary pressor area mediates pressor responses to cerebral ischemia, and 2) excitatory amino acids or acetylcholine in this area do not mediate the cardiovascular responses to cerebral ischemia.

1996 ◽  
Vol 85 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Ken Nakashima ◽  
Michael M. Todd

Background Hypothermia and anesthetics may protect the brain during ischemia by blocking the release of excitatory amino acids. The effects of hypothermia (28 degrees C), pentobarbital, and isoflurane on postischemic excitatory amino acid concentrations were compared. Methods Rats were anesthetized with 0.8% halothane/50% N2O, vascular catheters were placed, and a glass microelectrode and microdialysis cannula were inserted into the cerebral cortex. Experimental groups were: (1) control, pericranial, t = 38 degrees C; (2) hypothermia, t = 28 degrees C; (3) pentobarbital, t = 38 degrees C; and (4) isoflurane, t = 38 degrees C. Halothane/N2O was continued in groups 1 and 2, whereas a deep burst-suppression or isoelectric electroencephalogram was achieved with the test drugs in groups 3 and 4. Cerebral metabolic rates were similar in groups 2, 3, and 4. After a baseline dialysis sample was collected, animals were killed with potassium chloride. The time to terminal depolarization was recorded, after which three consecutive 10-min dialysate samples were collected. Glutamate, aspartate, gamma-aminobutyric acid, and glycine concentrations were measured using high-performance liquid chromatography. Results Times to terminal depolarization were shorter in both pentobarbital and isoflurane groups than with hypothermia (103 +/- 15 and 127 +/- 10 vs. 195 +/- 20 s respectively, mean +/- SD). However, times to terminal depolarization in all three groups were longer than in control subjects (control = 70 +/- 9s). Postdepolarization concentrations of all compounds were lower in hypothermic animals (vs. normothermic control animals), but no reductions in glutamate, aspartate, or glycine concentrations were noted in pentobarbital or isoflurane groups. gamma-Aminobutyric acid concentrations were reduced by both anesthetics, but not to the same degree as with hypothermia. Conclusions Pentobarbital and isoflurane prolonged the time to terminal depolarization, but did not influence the rate at which the extracellular concentrations of glutamate, aspartate, or glycine increased. By contrast, hypothermia reduced the release of all excitatory amino acids. These differences may explain the greater protective efficacy of hypothermia in the face of cerebral ischemia.


1982 ◽  
Vol 56 (4) ◽  
pp. 482-497 ◽  
Author(s):  
Jens Astrup

✓ The energy-requiring cell functions in the brain are described. The role of specific inhibition of these functions, and their critical low-supply levels of blood flow and oxygen are reviewed in relation to clinical management of focal and complete global cerebral ischemia.


Endocrine ◽  
2005 ◽  
Vol 28 (3) ◽  
pp. 295-302 ◽  
Author(s):  
Enrique Aguilar ◽  
Manuel Tena-Sempere ◽  
Leonor Pinilla

1989 ◽  
Vol 93 (1) ◽  
pp. 195-201 ◽  
Author(s):  
J.D.C Lambert ◽  
R.S.G Jones ◽  
M Andreasen ◽  
M.S Jensen ◽  
U Heinemann

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