Oshiro Y, Shimabukuro M, Takasu N, Asahi T, Komiya I, Yoshida H
Second Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan.
Life Sci. 2001 Sep 7;69(16):1907-18. doi: 10.1016/s0024-3205(01)01274-7.
Acute effects of triiodothyronine (T3) on postischemic myocardial stunning and intracellular Ca2+ contents were studied in the isolated working hearts of streptozotocin-induced diabetic rats and age-matched controls. After two weeks of diabetes, serum T3 and T4 levels were decreased to 62.5% and 33.9% of control values. Basal preischemic cardiac performance did not differ between diabetic and control rats. In contrast, during reperfusion after 20-min ischemia, diabetic rats exhibited an impaired recovery of heart rate (at 30-min reperfusion 57.5% of baseline vs. control 88.5%), left ventricular (LV) systolic pressure (44.1% vs. 89.5%), and cardiac work (23.1% vs. 66.0%). When 1 and 100 nM T3 was added before ischemia, heart rate was recovered to 77.2% and 81.8% of baseline, LV systolic pressure to 68.3% and 81.9%, and cardiac work to 50.8% and 59.0%, respectively. Diabetic rat hearts showed a higher Ca2+ content in the basal state and a further increase after reperfusion (4.96+/-1.17 vs. control 3.78+/-0.48 micromol/g, p<0.01). In diabetic hearts, H+ release was decreased after reperfusion (5.24+/-2.21 vs. 8.70+/-1.41 mmol/min/g, p<0.05). T3 administration caused a decrease in the postischemic Ca2+ accumulation (lnM T3 4.66+/-0.41 and 100 nM T3 3.58+/-0.36) and recovered the H+ release (lnM T3 16.2+/-3.9 and 100 nM T3 11.6+/-0.9). T3 did not alter myocardial O2 consumption. Results suggest that diabetic rat hearts are vulnerable to postischemic stunning, and T3 protects the myocardial stunning possibly via inhibiting Ca2+ overload.
研究了三碘甲状腺原氨酸（T3）对链脲佐菌素诱导的糖尿病大鼠和年龄匹配对照大鼠离体工作心脏缺血后心肌顿抑和细胞内Ca2+含量的急性影响。糖尿病两周后，血清T3和T4水平分别降至对照值的62.5%和33.9%。糖尿病大鼠和对照大鼠缺血前的基础心脏功能无差异。相反，在20分钟缺血后的再灌注期间，糖尿病大鼠的心率恢复受损（再灌注30分钟时为基线的57.5%，而对照为88.5%），左心室（LV）收缩压（44.1%对89.5%）和心脏作功（23.1%对66.0%）。在缺血前加入1和100 nM T3时，心率分别恢复到基线的77.2%和81.8%，LV收缩压恢复到68.3%和81.9%，心脏作功恢复到50.8%和59.0%。糖尿病大鼠心脏在基础状态下Ca2+含量较高，再灌注后进一步增加（4.96±1.17对对照3.78±0.48微摩尔/克，p<0.01）。在糖尿病心脏中，再灌注后H+释放减少（5.24±2.21对8.70±1.41毫摩尔/分钟/克，p<0.05）。给予T3可使缺血后Ca2+蓄积减少（1 nM T3时为4.66±0.41，100 nM T3时为3.58±0.36），并使H+释放恢复（1 nM T3时为16.2±3.9，100 nM T3时为11.6±0.9）。T3未改变心肌耗氧量。结果表明，糖尿病大鼠心脏易发生缺血后顿抑，T3可能通过抑制Ca2+超载保护心肌顿抑。
