Intensity of halothane- and hypercapnia-induced cerebral hyperemia is strain-dependent in rats

Hiroshi Takahashi, Jeffrey Kirsch, Toshiki Okada, Richard J. Traystman

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Cerebrovascular responses to physiologic and pharmacologic stimuli vary between laboratories using different strains of the same species. We tested whether the cerebral blood flow (CBF) response to 1% halothane or hypercapnia is strain-dependent in rats. Age-matched adult male (n = 14 of each strain) Wistar, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were anesthetized with pentobarbital and mechanically ventilated. Under baseline conditions blood flow to cerebrum (microspheres) in WKY (66 ± 5 mL · min- 1 · 100 g-1) was less than (P <0.05) in Wistar (88 ± 5mL · min-1 · 100 g-1) and SHR (83 ± 5 mL · min-1 · 100 g-1). Blood flow to brainstem was greater (P <0.05) in Wistar (106 ± 8 mL · min-1 · 100 g- 1) than in WKY (71 ± 5mL · min-1 · 100 g-1) and SHR (84 ± 4mL · min-1 · 100 g-1). in the halothane protocol (n = 8 each strain), administration of 1% halothane, during normocapnia, increased blood flow to the cerebrum in WKY (64 ± 6 to 120 ± 12 mL · min-1 · 100 g-1, P <0.05) and SHR (78 ± 6 to 115 ± 8 mL · min-1 · 100 g-1, P <0.05) but not Wistar rats (88 ± 8 to 102 ± 5 mL · min-1 · 100 g-1, not significant). Discontinuing halothane caused blood flow to return to baseline values. In the hypercapnia protocol (n = 6 each strain), exposure to 3% CO2 (to achieve a PaCO2 of 50-55 mm Hg) and 6% CO2 (to achieve a PaCO2 of 60 70 mm Hg) caused blood flow to the cerebrum to increase in Wistar (87 ± 11 to 112 ± 15 to 162 ± 23) to a similar amount as observed in WKY (69 ± 7 to 115 ± 13 to 162 ± 23 mL · min-1 · 100 g-1) but less than that observed in SHR (89 ± 7 to 174 ± 24 to 237 ± 28 mL · min-1 · 100 g- 1). These data demonstrate that the cerebral hyperemic response to vasodilator stimuli is strain-dependent in rats.

Original languageEnglish (US)
Pages (from-to)359-365
Number of pages7
JournalAnesthesia and Analgesia
Volume83
Issue number2
DOIs
StatePublished - 1996
Externally publishedYes

Fingerprint

Hypercapnia
Hyperemia
Halothane
Inbred SHR Rats
Cerebrum
Cerebrovascular Circulation
Pentobarbital
Vasodilator Agents
Microspheres
Brain Stem
Wistar Rats

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Intensity of halothane- and hypercapnia-induced cerebral hyperemia is strain-dependent in rats. / Takahashi, Hiroshi; Kirsch, Jeffrey; Okada, Toshiki; Traystman, Richard J.

In: Anesthesia and Analgesia, Vol. 83, No. 2, 1996, p. 359-365.

Research output: Contribution to journalArticle

Takahashi, Hiroshi ; Kirsch, Jeffrey ; Okada, Toshiki ; Traystman, Richard J. / Intensity of halothane- and hypercapnia-induced cerebral hyperemia is strain-dependent in rats. In: Anesthesia and Analgesia. 1996 ; Vol. 83, No. 2. pp. 359-365.
@article{8c4f2d4d0c424793be7a43f2a4dd5d45,
title = "Intensity of halothane- and hypercapnia-induced cerebral hyperemia is strain-dependent in rats",
abstract = "Cerebrovascular responses to physiologic and pharmacologic stimuli vary between laboratories using different strains of the same species. We tested whether the cerebral blood flow (CBF) response to 1{\%} halothane or hypercapnia is strain-dependent in rats. Age-matched adult male (n = 14 of each strain) Wistar, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were anesthetized with pentobarbital and mechanically ventilated. Under baseline conditions blood flow to cerebrum (microspheres) in WKY (66 ± 5 mL · min- 1 · 100 g-1) was less than (P <0.05) in Wistar (88 ± 5mL · min-1 · 100 g-1) and SHR (83 ± 5 mL · min-1 · 100 g-1). Blood flow to brainstem was greater (P <0.05) in Wistar (106 ± 8 mL · min-1 · 100 g- 1) than in WKY (71 ± 5mL · min-1 · 100 g-1) and SHR (84 ± 4mL · min-1 · 100 g-1). in the halothane protocol (n = 8 each strain), administration of 1{\%} halothane, during normocapnia, increased blood flow to the cerebrum in WKY (64 ± 6 to 120 ± 12 mL · min-1 · 100 g-1, P <0.05) and SHR (78 ± 6 to 115 ± 8 mL · min-1 · 100 g-1, P <0.05) but not Wistar rats (88 ± 8 to 102 ± 5 mL · min-1 · 100 g-1, not significant). Discontinuing halothane caused blood flow to return to baseline values. In the hypercapnia protocol (n = 6 each strain), exposure to 3{\%} CO2 (to achieve a PaCO2 of 50-55 mm Hg) and 6{\%} CO2 (to achieve a PaCO2 of 60 70 mm Hg) caused blood flow to the cerebrum to increase in Wistar (87 ± 11 to 112 ± 15 to 162 ± 23) to a similar amount as observed in WKY (69 ± 7 to 115 ± 13 to 162 ± 23 mL · min-1 · 100 g-1) but less than that observed in SHR (89 ± 7 to 174 ± 24 to 237 ± 28 mL · min-1 · 100 g- 1). These data demonstrate that the cerebral hyperemic response to vasodilator stimuli is strain-dependent in rats.",
author = "Hiroshi Takahashi and Jeffrey Kirsch and Toshiki Okada and Traystman, {Richard J.}",
year = "1996",
doi = "10.1097/00000539-199608000-00027",
language = "English (US)",
volume = "83",
pages = "359--365",
journal = "Anesthesia and Analgesia",
issn = "0003-2999",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Intensity of halothane- and hypercapnia-induced cerebral hyperemia is strain-dependent in rats

AU - Takahashi, Hiroshi

AU - Kirsch, Jeffrey

AU - Okada, Toshiki

AU - Traystman, Richard J.

PY - 1996

Y1 - 1996

N2 - Cerebrovascular responses to physiologic and pharmacologic stimuli vary between laboratories using different strains of the same species. We tested whether the cerebral blood flow (CBF) response to 1% halothane or hypercapnia is strain-dependent in rats. Age-matched adult male (n = 14 of each strain) Wistar, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were anesthetized with pentobarbital and mechanically ventilated. Under baseline conditions blood flow to cerebrum (microspheres) in WKY (66 ± 5 mL · min- 1 · 100 g-1) was less than (P <0.05) in Wistar (88 ± 5mL · min-1 · 100 g-1) and SHR (83 ± 5 mL · min-1 · 100 g-1). Blood flow to brainstem was greater (P <0.05) in Wistar (106 ± 8 mL · min-1 · 100 g- 1) than in WKY (71 ± 5mL · min-1 · 100 g-1) and SHR (84 ± 4mL · min-1 · 100 g-1). in the halothane protocol (n = 8 each strain), administration of 1% halothane, during normocapnia, increased blood flow to the cerebrum in WKY (64 ± 6 to 120 ± 12 mL · min-1 · 100 g-1, P <0.05) and SHR (78 ± 6 to 115 ± 8 mL · min-1 · 100 g-1, P <0.05) but not Wistar rats (88 ± 8 to 102 ± 5 mL · min-1 · 100 g-1, not significant). Discontinuing halothane caused blood flow to return to baseline values. In the hypercapnia protocol (n = 6 each strain), exposure to 3% CO2 (to achieve a PaCO2 of 50-55 mm Hg) and 6% CO2 (to achieve a PaCO2 of 60 70 mm Hg) caused blood flow to the cerebrum to increase in Wistar (87 ± 11 to 112 ± 15 to 162 ± 23) to a similar amount as observed in WKY (69 ± 7 to 115 ± 13 to 162 ± 23 mL · min-1 · 100 g-1) but less than that observed in SHR (89 ± 7 to 174 ± 24 to 237 ± 28 mL · min-1 · 100 g- 1). These data demonstrate that the cerebral hyperemic response to vasodilator stimuli is strain-dependent in rats.

AB - Cerebrovascular responses to physiologic and pharmacologic stimuli vary between laboratories using different strains of the same species. We tested whether the cerebral blood flow (CBF) response to 1% halothane or hypercapnia is strain-dependent in rats. Age-matched adult male (n = 14 of each strain) Wistar, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR) were anesthetized with pentobarbital and mechanically ventilated. Under baseline conditions blood flow to cerebrum (microspheres) in WKY (66 ± 5 mL · min- 1 · 100 g-1) was less than (P <0.05) in Wistar (88 ± 5mL · min-1 · 100 g-1) and SHR (83 ± 5 mL · min-1 · 100 g-1). Blood flow to brainstem was greater (P <0.05) in Wistar (106 ± 8 mL · min-1 · 100 g- 1) than in WKY (71 ± 5mL · min-1 · 100 g-1) and SHR (84 ± 4mL · min-1 · 100 g-1). in the halothane protocol (n = 8 each strain), administration of 1% halothane, during normocapnia, increased blood flow to the cerebrum in WKY (64 ± 6 to 120 ± 12 mL · min-1 · 100 g-1, P <0.05) and SHR (78 ± 6 to 115 ± 8 mL · min-1 · 100 g-1, P <0.05) but not Wistar rats (88 ± 8 to 102 ± 5 mL · min-1 · 100 g-1, not significant). Discontinuing halothane caused blood flow to return to baseline values. In the hypercapnia protocol (n = 6 each strain), exposure to 3% CO2 (to achieve a PaCO2 of 50-55 mm Hg) and 6% CO2 (to achieve a PaCO2 of 60 70 mm Hg) caused blood flow to the cerebrum to increase in Wistar (87 ± 11 to 112 ± 15 to 162 ± 23) to a similar amount as observed in WKY (69 ± 7 to 115 ± 13 to 162 ± 23 mL · min-1 · 100 g-1) but less than that observed in SHR (89 ± 7 to 174 ± 24 to 237 ± 28 mL · min-1 · 100 g- 1). These data demonstrate that the cerebral hyperemic response to vasodilator stimuli is strain-dependent in rats.

UR - http://www.scopus.com/inward/record.url?scp=0030055887&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030055887&partnerID=8YFLogxK

U2 - 10.1097/00000539-199608000-00027

DO - 10.1097/00000539-199608000-00027

M3 - Article

VL - 83

SP - 359

EP - 365

JO - Anesthesia and Analgesia

JF - Anesthesia and Analgesia

SN - 0003-2999

IS - 2

ER -