TY - JOUR
T1 - An in vitro rabbit retina model to study electrophysiologic and metabolic function during and following ischemia
AU - Quiñones-Hinojosa, Alfredo
AU - Ames, Adelbert
AU - Malek, Junaid Y.
AU - Maynard, Kenneth I.
PY - 1999/8/15
Y1 - 1999/8/15
N2 - Most in vitro studies involving neuronal ischemia use biochemical measures and/or cell counting to assess cellular death. We describe an in vitro rabbit retina model in which we measured glucose utilization, lactate production, and light-evoked compound action potentials (CAPs) to assess metabolic and functional recovery following ischemia. Under control conditions, retinal glucose utilization and lactate production (n=7), as well as CAPs (n=8) remained quite constant for 6-8 h. During ischemia (glucose reduced from 6 to 1 mM and oxygen from 95 to 15%), glucose utilization and lactate production fell to 50%. CAPs fell to 50% in 3-4 min, and to 0% in 8-10 min. Recovery during 3-4 h of 'return-to-control' was dependent upon the length of ischemia. Glucose utilization recovered to 63% after 1 h (n=4) and to 18% after 2 h of ischemia (n=6, P<0.001). Lactate production recovered to 77% after 1 h (n=4) and to 54% after 2 h of ischemia (n=6, P<0.001). CAPs returned to 51, 15, and 0.13% of the control responses after 0.5 h (n=7), 1 h (n=8), and 2 h (n=5) of ischemia, respectively (P<0.001). This avascular, blood-brain barrier-free preparation provides an opportunity to use both metabolic and functional criteria to test protection against neuronal ischemia. Copyright (C) 1999 Elsevier Science B.V.
AB - Most in vitro studies involving neuronal ischemia use biochemical measures and/or cell counting to assess cellular death. We describe an in vitro rabbit retina model in which we measured glucose utilization, lactate production, and light-evoked compound action potentials (CAPs) to assess metabolic and functional recovery following ischemia. Under control conditions, retinal glucose utilization and lactate production (n=7), as well as CAPs (n=8) remained quite constant for 6-8 h. During ischemia (glucose reduced from 6 to 1 mM and oxygen from 95 to 15%), glucose utilization and lactate production fell to 50%. CAPs fell to 50% in 3-4 min, and to 0% in 8-10 min. Recovery during 3-4 h of 'return-to-control' was dependent upon the length of ischemia. Glucose utilization recovered to 63% after 1 h (n=4) and to 18% after 2 h of ischemia (n=6, P<0.001). Lactate production recovered to 77% after 1 h (n=4) and to 54% after 2 h of ischemia (n=6, P<0.001). CAPs returned to 51, 15, and 0.13% of the control responses after 0.5 h (n=7), 1 h (n=8), and 2 h (n=5) of ischemia, respectively (P<0.001). This avascular, blood-brain barrier-free preparation provides an opportunity to use both metabolic and functional criteria to test protection against neuronal ischemia. Copyright (C) 1999 Elsevier Science B.V.
KW - Compound action potentials
KW - Electrophysiology
KW - Energy metabolism
KW - Glucose deprivation
KW - Neuroprotection
KW - Oxygen deprivation
KW - Stroke
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U2 - 10.1016/S0165-0270(99)00068-0
DO - 10.1016/S0165-0270(99)00068-0
M3 - Article
C2 - 10513594
AN - SCOPUS:0345035481
SN - 0165-0270
VL - 90
SP - 107
EP - 115
JO - Journal of Neuroscience Methods
JF - Journal of Neuroscience Methods
IS - 2
ER -