TY - JOUR
T1 - Reversible focal ischemia in the rat
T2 - Effects of halothane, isoflurane, and methohexital anesthesia
AU - Warner, D. S.
AU - Zhou, J.
AU - Ramani, R.
AU - Todd, M. M.
PY - 1991
Y1 - 1991
N2 - Barbiturates and the volatile anesthetic isoflurane reduce CMR to similar values. If the mechanism of barbiturate protection against local ischemic injury is due to a reduction in cellular energy requirements, then isoflurane should similarly reduce ischemic injury. To evaluate this, spontaneously hypertensive rats underwent 2 h of reversible middle cerebral artery occlusion (MCAO) while receiving deep methohexital, isoflurane, or halothane anesthesia. Ninety-six hours postischemia, neurologic deficits were present but without a difference between groups. Mean ± SD infarct volume, as assessed by triphenyl tetrazolium chloride staining and computerized planimetry, was significantly less in the methohexital group (n = 8; 166 ± 74 mm3) than in either the halothane (n = 9; 249 ± 71 mm3; p < 0.04) or the isoflurane (n = 9; 243 ± 62 mm3; p < 0.03) groups. One possible explanation for the lack of protective effect for isoflurane might he related to its vasodilative properties, which could result in a cerebral vascular steal. To examine this possibility, rats anesthetized with methohexital or isoflurane underwent autoradiographic determination of CBF with or without MCAO. In isoflurane-anesthetized sham rats (n = 5; no ischemia), CBF was approximately three times greater than in methohexital-treated (n = 5) sham rats. During ischemia, although a regional reduction in flow was noted in both anesthetic groups, mean flow remained greater in the isoflurane group. When the ischemic hemisphere was analyzed for percentage of cross-sectional area where flow was <25 ml/100 g/min, significantly less tissue appeared to be at risk for infarction in the isoflurane group (n = 7; 32.9 ± 19.4%) versus the methohexital group (n = 8; 49.1 ± 12.6%; p < 0.05). These results are consistent with the following conclusions: (a) CMR reduction is not a sufficient criterion for anesthetic-mediated brain protection: (b) isoflurane does not cause cerebrovascular steal: and (c) ischemic flow thresholds for infarction are different for methohexital and isoflurane.
AB - Barbiturates and the volatile anesthetic isoflurane reduce CMR to similar values. If the mechanism of barbiturate protection against local ischemic injury is due to a reduction in cellular energy requirements, then isoflurane should similarly reduce ischemic injury. To evaluate this, spontaneously hypertensive rats underwent 2 h of reversible middle cerebral artery occlusion (MCAO) while receiving deep methohexital, isoflurane, or halothane anesthesia. Ninety-six hours postischemia, neurologic deficits were present but without a difference between groups. Mean ± SD infarct volume, as assessed by triphenyl tetrazolium chloride staining and computerized planimetry, was significantly less in the methohexital group (n = 8; 166 ± 74 mm3) than in either the halothane (n = 9; 249 ± 71 mm3; p < 0.04) or the isoflurane (n = 9; 243 ± 62 mm3; p < 0.03) groups. One possible explanation for the lack of protective effect for isoflurane might he related to its vasodilative properties, which could result in a cerebral vascular steal. To examine this possibility, rats anesthetized with methohexital or isoflurane underwent autoradiographic determination of CBF with or without MCAO. In isoflurane-anesthetized sham rats (n = 5; no ischemia), CBF was approximately three times greater than in methohexital-treated (n = 5) sham rats. During ischemia, although a regional reduction in flow was noted in both anesthetic groups, mean flow remained greater in the isoflurane group. When the ischemic hemisphere was analyzed for percentage of cross-sectional area where flow was <25 ml/100 g/min, significantly less tissue appeared to be at risk for infarction in the isoflurane group (n = 7; 32.9 ± 19.4%) versus the methohexital group (n = 8; 49.1 ± 12.6%; p < 0.05). These results are consistent with the following conclusions: (a) CMR reduction is not a sufficient criterion for anesthetic-mediated brain protection: (b) isoflurane does not cause cerebrovascular steal: and (c) ischemic flow thresholds for infarction are different for methohexital and isoflurane.
KW - Anesthetics
KW - Brain
KW - Cerebral blood flow
KW - Halothane
KW - Inhalational and intravenous
KW - Isoflurane
KW - Methohexital
UR - http://www.scopus.com/inward/record.url?scp=0025942334&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025942334&partnerID=8YFLogxK
M3 - Article
C2 - 1874810
AN - SCOPUS:0025942334
SN - 0271-678X
VL - 11
SP - 794
EP - 802
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
IS - 5
ER -