SESSION 6：学生研究発表
法医学教室での活動と自分の研究
～"新生仔ラット心筋細胞に対する熱負荷の影響"について～ |
私はMD 研究者育成プログラム履修生として2 年次より大阪大学法医学教
室にお世話になっています。法医学教室において私たちMD 生は自らの研究
はもちろん、研究室での活動にも参加しています。研究室では週に1 度論文
抄読会が行われ、そこで先生方に法医学領域の最新の研究を紹介してもらう
他、自分の研究に関わる論文を読み、研究を進めるアドバイスをいただいて
います。また、教授や6 回生の先輩方とともに教科書の読み合わせも行って
おり、"Forensic Pathology -Principle and Practice-"という事例報告の豊富
な教科書を用いて死因診断について学んでいます。さらに、司法解剖の見学
もさせていただいており、直に解剖の様子を見て様々な死の様相とその診断
について学んでいます。
今回はこうした研究室での活動に加え、自らの研究である熱中症の心筋細
胞への影響についてもご報告させていただきます。
以下に法医学会総会での抄録を掲載いたします。
Recently, heat stroke has been increased as the cause of death in Japan.
However, the pathogenesis of cardiac arrhythmia by heat stroke remains
still unclear. We hypothesized that heat stress affects the electrical
conductance of cardiomyocyte and this causes cardiac arrhythmia. In
the present study, we evaluated the direct effects of heat stress on
cultured neonatal rat cardiomyocytes. Cardiomyocytes were obtained
from the ventricles of 1 to 2 day-old Wistar rats. The experiments were
performed at 4‒5 days in vitro. After that, we used the cardiomyocyte
which moved rhythmically overall. The cells were incubated at 37℃ or
42℃ for 1-6 hours. After incubated, the expression of various mRNAs,
proteins in the cells was revealed. mRNAs encoding connexin 43 (Cx43),
sodium-calcium exchanger and b-catenin were affected by heat stress
for 6 hours. The treatment at 42℃ significantly increased the expression
of Cx43 mRNA compared with that at 37℃. The Cx43 protein was
significantly increased in the 42℃-treated cells for 3 hours. Heat stress
of 42℃ induced the alteration of Cx43 distribution in cardiomyocytes.
Cx43 forms gap junction and has a crucial role in the synchronized
contraction of the heart. Altered gap junctional conductance can change
conduction velocity thereby contributing to initiation and/or
perpetuation of arrhythmias. Therefore, our findings about Cx43 may
lead to not only diagnostic improvement but also therapeutic
development of heat stroke. |
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