|1.||Xue, Jin: 1 article (02/2008)|
|2.||Zhou, Dan: 1 article (02/2008)|
|3.||Yao, Hang: 1 article (02/2008)|
|4.||Haddad, Gabriel G: 1 article (02/2008)|
|5.||Ikeda, Shota: 1 article (04/2002)|
|6.||Tsuboi, Ayako: 1 article (04/2002)|
|7.||Kusumoto, Keiji: 1 article (04/2002)|
|8.||Shiraishi, Mitsuru: 1 article (04/2002)|
|9.||Abe, Akemi: 1 article (04/2002)|
|10.||Fukumoto, Shoji: 1 article (04/2002)|
02/01/2008 - "Pharmacological studies revealed 1) no significant difference in neuronal injury between controls (no inhibitor) and inhibition of Na(+)-K(+)-ATP pump, voltage-gated Na(+) channel, ATP-sensitive K(+) channel, or reverse mode of Na(+)/Ca(2+) exchanger under hypoxia; however, 2) inhibition of NBCs with 500 microM DIDS did not cause hypoxic death in either cultured cortical neurons or hippocampal slices; 3) in contrast, inhibition of Na(+)/H(+) exchanger isoform 1 (NHE1) with either 10 microM HOE-642 or 2 microM T-162559 resulted in dramatic hypoxic injury (+95% for HOE-642 and +100% for T-162559 relative to normoxic control, P < 0.001) on treatment day 3, when no death occurred for hypoxic controls (no inhibitor). "
04/01/2002 - "4. Intravenous administration of T-162559 (0.03 and 0.1 mg kg(-1)) significantly inhibited the progression of myocardial infarction induced by left coronary artery occlusion and reperfusion in rabbits; the infarct size normalized by area at risk was 74+/-6% in the vehicle group, and 47+/-5% and 51+/-7% in the T-162559-0.03 mg kg(-1) and T-162559-0.1 mg kg(-1) groups (both P<0.05), respectively. "
|4.||4,4'- Diisothiocyanostilbene- 2,2'- Disulfonic Acid (DIDS)
|5.||Adenosine Triphosphate (ATP)
|6.||L-Lactate Dehydrogenase (Lactate Dehydrogenase)