| 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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Eun jin Kim, Sung Yong Park, Kwan Sik Park, Un jin Ju, Jin Soo Kim, Sook Young Lee |
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Department of Anesthesiology and Pain Medicine, Ajou University School of Medicine, Suwon, Korea. anesylee@ajou.ac.kr |
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| Abstract |
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 (1-100micrometer) 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 500micrometer 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, 50micrometer propofol was pre-treated or co-treated with 100micrometer NMDA. In the control and NMDA 100micrometer groups, no drug or NMDA 100micrometer was given. A P < 0.05 was considered statistically significant.
RESULTS
Cells pre-treated with propofol (10-100micrometer) or co-treated (50-100micrometer) 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 100micrometer 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. |
| Key Words:
ischemia-reperfusion injury; N-Methyl-D-Aspartate receptor; propofol |
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