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KMID : 0356920080550020210
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Korean Journal of Anesthesiology
2008 Volume.55 No. 2 p.210 ~ p.216
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The influence of propofol administration time on oxygen-glucose deprivation-reperfusion injury in rat mixed cortical cultures focused on N-Methyl-D-Aspartate (NMDA) receptors
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Kim Eun-Jin
Park Sung-Yong
Park Kwan-Sik
Joo Eun-Jin
Kim Jin-Soo
Lee Sook-Young
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Abstract
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Background: Propofol has been shown to have neuroprotective properties. However, the effect of propofol administration time on neuroprotection is not well understood. This study was conducted to determine if propofol administration time would influence its neuroprotective effects on an in vitro ischemia-reperfusion model, with special attention directed toward NMDA-induced calcium influx.
Methods: Primary mixed cortical cultures of thirteen-day-old rats were exposed to 5 min of oxygen-glucose deprivation (OGD), followed by 2 hr of reperfusion. Propofol (1?100?M) was administered before OGD or administered from the time of OGD to the end of the reperfusion period. In the blank and full kill groups, no drug or NMDA 500?M treatment was given. The surviving cells were counted using trypan-blue staining, and cell death rate (CDR) was determined. To measure the maximum Ca2+ influx, 50?M propofol was pre-treated or co-treated with 100?M NMDA. In the control and NMDA 100?M groups, no drug or NMDA 100?M was given. A P ＜ 0.05 was considered statistically significant.
Results: Cells pre-treated with propofol (10?100?M) or co-treated (50?100?M) at the time of OGD injury had a decreased CDR compared to the blank group. Cells pre-treated (2,713 nA) or co-treated (3,626 nA) with propofol had a decreased maximum Ca2+ influx compared to the 100?M NMDA group (4,075 nA). Cells pre-treated with propofol had a decreased maximum Ca2+ influx compared to co-treated rats.
Conclusions: Propofol demonstrated neuroprotective effects at lower concentrations when administered prior to OGD injury. This may be partially attributable to the reduction of Ca2+ influx against NMDA receptor activation. (Korean J Anesthesiol 2008; 55: 210∼6)
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KEYWORD
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ischemia-reperfusion injury, N-Methyl-D-Aspartate receptor, propofol
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