Effect of isoflurane and halothane on in vivo ischemia-induced dopamine release in the corpus striatum of the rat: A study using cerebral microdialysis

R. Koorn, R. A. Kahn, T. S. Brannan, J. Martinez-Tica, J. Weinberger, D. L. Reich

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Background: Dopamine is released in large quantities into the corpus striatum during cerebral ischemia and may exacerbate tissue damage. Methods: Using cerebral microdialysis, the effect of isoflurane on in vivo ischemia- induced dopamine release was studied in rat corpus striatum. Reversible cerebral ischemia was induced using carotid ligatures and induced hypovolemia and was monitored with laser-Doppler flowmetry. Following baseline measurements, 28 normothermic, anesthetized rats were subjected to cerebral ischemia followed by reperfusion. The rats were divided into four groups. Group 1 (n = 10) was anesthetized using chloral hydrate. Groups 2 and 3 received 1.5% end-tidal isoflurane. In group 2 (n = 6), hypotension was left untreated during the reperfusion period, and in group 3 (n = 6), mean arterial pressure was maintained using phenylephrine. Group 4 (n = 6) received 1-1.2% end-tidal halothane. Results: Compared with pre-ischemic levels, large quantities of dopamine (350 x baseline levels) were released in group 1 animals during cerebral ischemia. Compared with group 1, ischemia- induced dopamine release was significantly reduced in group 2 (by 58%) and in group 3 (by 56%), but not in group 4. Group 2 animals were uniformly hypotensive during reperfusion and continued to release substantial amounts of dopamine (8 x baseline levels). In groups 1, 3, and 4, dopamine release decreased to near baseline levels during reperfusion. In group 3, dopamine metabolite production was significantly increased during ischemia, suggesting that enzymatic function and neuronal reuptake of dopamine was preserved. Conclusions: Isoflurane, compared with chloral hydrate and halothane, inhibits the release of the neurotransmitter dopamine during cerebral ischemia.

Original languageEnglish (US)
Pages (from-to)827-835
Number of pages9
JournalAnesthesiology
Volume79
Issue number4
StatePublished - 1993
Externally publishedYes

Fingerprint

Corpus Striatum
Isoflurane
Microdialysis
Halothane
Dopamine
Ischemia
Brain Ischemia
Reperfusion
Chloral Hydrate
Laser-Doppler Flowmetry
Hypovolemia
Phenylephrine
Hypotension
Ligation
Neurotransmitter Agents
Arterial Pressure

Keywords

  • Anesthetics, volatile: halothane; isoflurane
  • Blood pressure: hypotension
  • Brain: corpus striatum; metabolism
  • Cerebral microdialysis
  • Sympathetic nervous system, catecholamines: dopamine

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Koorn, R., Kahn, R. A., Brannan, T. S., Martinez-Tica, J., Weinberger, J., & Reich, D. L. (1993). Effect of isoflurane and halothane on in vivo ischemia-induced dopamine release in the corpus striatum of the rat: A study using cerebral microdialysis. Anesthesiology, 79(4), 827-835.

Effect of isoflurane and halothane on in vivo ischemia-induced dopamine release in the corpus striatum of the rat : A study using cerebral microdialysis. / Koorn, R.; Kahn, R. A.; Brannan, T. S.; Martinez-Tica, J.; Weinberger, J.; Reich, D. L.

In: Anesthesiology, Vol. 79, No. 4, 1993, p. 827-835.

Research output: Contribution to journalArticle

Koorn, R, Kahn, RA, Brannan, TS, Martinez-Tica, J, Weinberger, J & Reich, DL 1993, 'Effect of isoflurane and halothane on in vivo ischemia-induced dopamine release in the corpus striatum of the rat: A study using cerebral microdialysis', Anesthesiology, vol. 79, no. 4, pp. 827-835.
Koorn, R. ; Kahn, R. A. ; Brannan, T. S. ; Martinez-Tica, J. ; Weinberger, J. ; Reich, D. L. / Effect of isoflurane and halothane on in vivo ischemia-induced dopamine release in the corpus striatum of the rat : A study using cerebral microdialysis. In: Anesthesiology. 1993 ; Vol. 79, No. 4. pp. 827-835.
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abstract = "Background: Dopamine is released in large quantities into the corpus striatum during cerebral ischemia and may exacerbate tissue damage. Methods: Using cerebral microdialysis, the effect of isoflurane on in vivo ischemia- induced dopamine release was studied in rat corpus striatum. Reversible cerebral ischemia was induced using carotid ligatures and induced hypovolemia and was monitored with laser-Doppler flowmetry. Following baseline measurements, 28 normothermic, anesthetized rats were subjected to cerebral ischemia followed by reperfusion. The rats were divided into four groups. Group 1 (n = 10) was anesthetized using chloral hydrate. Groups 2 and 3 received 1.5{\%} end-tidal isoflurane. In group 2 (n = 6), hypotension was left untreated during the reperfusion period, and in group 3 (n = 6), mean arterial pressure was maintained using phenylephrine. Group 4 (n = 6) received 1-1.2{\%} end-tidal halothane. Results: Compared with pre-ischemic levels, large quantities of dopamine (350 x baseline levels) were released in group 1 animals during cerebral ischemia. Compared with group 1, ischemia- induced dopamine release was significantly reduced in group 2 (by 58{\%}) and in group 3 (by 56{\%}), but not in group 4. Group 2 animals were uniformly hypotensive during reperfusion and continued to release substantial amounts of dopamine (8 x baseline levels). In groups 1, 3, and 4, dopamine release decreased to near baseline levels during reperfusion. In group 3, dopamine metabolite production was significantly increased during ischemia, suggesting that enzymatic function and neuronal reuptake of dopamine was preserved. Conclusions: Isoflurane, compared with chloral hydrate and halothane, inhibits the release of the neurotransmitter dopamine during cerebral ischemia.",
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T1 - Effect of isoflurane and halothane on in vivo ischemia-induced dopamine release in the corpus striatum of the rat

T2 - A study using cerebral microdialysis

AU - Koorn, R.

AU - Kahn, R. A.

AU - Brannan, T. S.

AU - Martinez-Tica, J.

AU - Weinberger, J.

AU - Reich, D. L.

PY - 1993

Y1 - 1993

N2 - Background: Dopamine is released in large quantities into the corpus striatum during cerebral ischemia and may exacerbate tissue damage. Methods: Using cerebral microdialysis, the effect of isoflurane on in vivo ischemia- induced dopamine release was studied in rat corpus striatum. Reversible cerebral ischemia was induced using carotid ligatures and induced hypovolemia and was monitored with laser-Doppler flowmetry. Following baseline measurements, 28 normothermic, anesthetized rats were subjected to cerebral ischemia followed by reperfusion. The rats were divided into four groups. Group 1 (n = 10) was anesthetized using chloral hydrate. Groups 2 and 3 received 1.5% end-tidal isoflurane. In group 2 (n = 6), hypotension was left untreated during the reperfusion period, and in group 3 (n = 6), mean arterial pressure was maintained using phenylephrine. Group 4 (n = 6) received 1-1.2% end-tidal halothane. Results: Compared with pre-ischemic levels, large quantities of dopamine (350 x baseline levels) were released in group 1 animals during cerebral ischemia. Compared with group 1, ischemia- induced dopamine release was significantly reduced in group 2 (by 58%) and in group 3 (by 56%), but not in group 4. Group 2 animals were uniformly hypotensive during reperfusion and continued to release substantial amounts of dopamine (8 x baseline levels). In groups 1, 3, and 4, dopamine release decreased to near baseline levels during reperfusion. In group 3, dopamine metabolite production was significantly increased during ischemia, suggesting that enzymatic function and neuronal reuptake of dopamine was preserved. Conclusions: Isoflurane, compared with chloral hydrate and halothane, inhibits the release of the neurotransmitter dopamine during cerebral ischemia.

AB - Background: Dopamine is released in large quantities into the corpus striatum during cerebral ischemia and may exacerbate tissue damage. Methods: Using cerebral microdialysis, the effect of isoflurane on in vivo ischemia- induced dopamine release was studied in rat corpus striatum. Reversible cerebral ischemia was induced using carotid ligatures and induced hypovolemia and was monitored with laser-Doppler flowmetry. Following baseline measurements, 28 normothermic, anesthetized rats were subjected to cerebral ischemia followed by reperfusion. The rats were divided into four groups. Group 1 (n = 10) was anesthetized using chloral hydrate. Groups 2 and 3 received 1.5% end-tidal isoflurane. In group 2 (n = 6), hypotension was left untreated during the reperfusion period, and in group 3 (n = 6), mean arterial pressure was maintained using phenylephrine. Group 4 (n = 6) received 1-1.2% end-tidal halothane. Results: Compared with pre-ischemic levels, large quantities of dopamine (350 x baseline levels) were released in group 1 animals during cerebral ischemia. Compared with group 1, ischemia- induced dopamine release was significantly reduced in group 2 (by 58%) and in group 3 (by 56%), but not in group 4. Group 2 animals were uniformly hypotensive during reperfusion and continued to release substantial amounts of dopamine (8 x baseline levels). In groups 1, 3, and 4, dopamine release decreased to near baseline levels during reperfusion. In group 3, dopamine metabolite production was significantly increased during ischemia, suggesting that enzymatic function and neuronal reuptake of dopamine was preserved. Conclusions: Isoflurane, compared with chloral hydrate and halothane, inhibits the release of the neurotransmitter dopamine during cerebral ischemia.

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KW - Blood pressure: hypotension

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KW - Sympathetic nervous system, catecholamines: dopamine

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