この研究は、ラットの血液脳関門（BBB）の透過性に対する2.45 GHzの電磁界（パルス幅2マイクロ秒、毎秒のパルス繰り返し数500、全身平均SAR値2.0 W/kg±2 dB、脳組織平均SAR値3.0 W/kg±3 dB）ばく露の影響を調べた。本実験に先立ち、ムスカリン拮抗薬スコポラミン臭化水素酸塩を投与したSDラットに誘導された記憶消失が12アーム放射状迷路試験で測定されることを確認した。続いて、この拮抗薬の第4アンモニウム誘導体（臭化メチルスコポラミンMBR：本来はBBBをほとんど透過しない）を系統的に投与して、45分間の電磁界ばく露後のラットの12アーム放射状迷路試験の成績が変化するか否かを調べた。成績の変化は、BBB透過性の変化を示すと考えた。実験の結果、電磁界ばく露による成績の変化は見られなかった､と報告している。
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To study whether a systemically-injected derivate of the muscarinic antagonist scopolamine hydrobromide (scopolamine methylbromide) altered maze performance of rats after a 45 min exposure to 2.45 GHz electromagnetic field.
First, it was verified that the maze test enabled demonstration of memory deficits in rats treated with the muscarinic antagonist scopolamine hydrobromide (0.5 mg/kg), which poorly crosses the blood-brain barrier and which is known to induce memory impairments. The drug was injected before and after irradiation.
Scopolamin methylbromide is another muscarinic antagonist that does not cross the blood-brain barrier easily; if observed such an alteration would reflect changes in blood-brain barrier permeability.
Finally, animals were subjected to injections of Evans blue, a dye binding serum albumin, before or after electromagnetic field exposure.
|ばく露時間||continuous for 45 min|
|Pulse width||2 µs|
|Repetition frequency||500 Hz|
|ばく露装置の詳細||Rats (n=12) were placed individually in a transparent plastic chamber (20 cm long x 17.5 cm in diameter, 13.5 cm high) located in the middle of the waveguide where they were able to move freely. Two waveguides were simultaneously excited hence exposing two rats at a time.|
|Additional information||Naive rats (n=12) were brought into the testing room in their home cages and were left in there for 45 min to serve as cage control.|
Whether scopolamine methylbromide was injected before or after exposure, the exposed animals did not perform differently from the naive (no experience of the exposure device) or sham-exposed rats. Thus, electromagnetic fields most probably failed to disrupt the blood-brain barrier. This conclusion was further supported by the absence of Evans blue extravasation into the brain parenchyma of the exposed animals.