稲毛, 一秀, 折田, 純久, 藤本, 和輝, 山内, かづ代, 國府田, 正雄, 赤澤, 努, 江口, 和, 古矢, 丈雄, 中村, 順一, 鈴木, 都, 佐久間, 詳浩, 久保田, 剛, 及川, 泰宏, 西能, 健, 佐藤, 淳, 志賀, 康浩, 阿部, 幸喜, 金元, 洋人, 井上, 雅寛, 木下, 英幸, 乗本, 将輝, 海村, 朋孝, 高橋, 和久, 大鳥, 精司
千葉医学 = CHIBA IGAKU 94(4) 173-173 2018年8月1日
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[要旨] 【目的】ラット筋損傷モデルを用いて圧迫,冷却療法による治療効果を比較した。 【方法】8 週齢雄性SDラットを用いdrop mass 法にてモデル作成し,損傷後3 時間にゴムで損傷部を30分圧迫した圧迫群(n=36),氷で損傷部を30分冷却した冷却群(n=36),未治療群(n=36)の3 群について比較を行った。損傷後3 , 6 ,18,24時間, 3 日, 1 週, 2 週の腓腹筋をHE染色で評価した。損傷後3 ,6 ,18,24時間の腓腹筋をELISA法にてTNF-α の定量評価を行った。損傷部にフルオロゴールド(FG)を留置し,損傷後3 日のL4 後根神経節でCGRP(疼痛関連ペプチド)による免疫組織化学染色を行った。 【結果】組織では未治療群と比し,圧迫群は損傷後6 時間以降で出血や浮腫が少ない傾向にあった。冷却群は,損傷後6 時間で出血や浮腫は減少するも,損傷後18時間以降で増強した。損傷後1週で未治療群は筋組織の壊死が残存するも,圧迫群,冷却群は筋線維修復が認められた。サイトカインは,圧迫群は未治療群と比し損傷後3 , 6 ,18時間共に低値を示した。特に損傷後6 時間で有意に低値であった(P<0.05)。冷却群は未治療群と比し損傷後3 ,6 時間で一過性な上昇を示すも,損傷後18時間では有意に低下した(P<0.05)。L4 後根神経節でのFG 陽性細胞中のFG とCGRP で二重標識される細胞の割合は,圧迫群,冷却群ともに未治療群と比し有意に低かった(P<0.05)。 【考察】圧迫,冷却療法は筋組織修復を促進し,疼痛の遷延化を予防するが,急性期では異なる経時的変化を示し,組織修復過程に差異がある可能性が示唆された。
[SUMMARY] Purpose. To compare compression and ice treatments in a rat model of muscle injury. Methods. A model of muscle injury was made in 108 eight-week-old Sprague Dawley male rats by dropping a weight onto their right gastrocnemius muscle. We compared compression and ice treatments after the contusion injury with no treatment. We evaluated the injuries using histology andan enzyme-linked immunosorbent assay for tumor necrosis factor α. We used Fluoro-Gold to traceneural afferents from the region of the contusion injury. The proportion of calcitonin gene-related peptide-immunoreactive neurons in all Fluoro-Gold-labeled neurons was determined to evaluate pain. Results. In the compression treatment group, the injured muscle tended to have less hemorrhage and edema at ? 6 h after the injury. Tumor necrosis factor α levels were lower, and the local acutephase in flammatory reaction was milder than in untreated rats. We found less necrosis of muscle tissue on the third day after injury and the replacement of granulation tissue and regeneration of muscle fibers 1 week after the injury. The proportion of calcitonin gene-related peptide-immunoreactive Fluoro-Gold-labeled neurons in total Fluoro-Gold-labeled neurons was significantly lower than in untreated rats. In the ice treatment group, although injured muscle had decreased hemorrhage and edema 6 h after the injury, hemorrhage and edema increased ?18 h after injury. Tumor necrosis factor α levels were transiently increased compared with those in untreated rats( 3 h and 6 h after contusion). On the third day after contusion injury, necrosis of muscle was severe. We observed the replacement of granulation tissue and regeneration of muscle fibers 1 week after the injury. The proportion of calcitonin gene-related peptide-immunoreactive Fluoro-Gold-labeled neurons was significantly lower than in untreated rats. Conclusion. In our study, compression may promote muscle tissue repair by preventing hematoma formation during the repair phase and preventing prolonged pain. On the other hand, ice therapy may prevent prolonged pain through pain relief from the stimulation of cold receptors, enabling animals to proceed with an early range of motion exercise, suppressing hypoactivity and promoting muscle tissue repair during the recovery phase. Overall, our current study indicated that there was a difference between compression and ice treatments during the acute and repair phases of muscle injury.