Joffe I I, Travers K E, Perreault-Micale C L, Hampton T, Katz S E, Morgan J P, Douglas P S
Charles A. Dana Research Institute, Boston, Massachusetts, USA.
J Am Coll Cardiol. 1999 Dec;34(7):2111-9. doi: 10.1016/s0735-1097(99)00436-2.
We sought to evaluate in vivo and in vitro left ventricular (LV) geometry and function in streptozotocin-induced diabetic rats and the possible role of the nitric oxide (NO) pathway.
Diabetes results in cardiac dysfunction; however, the specific abnormalities are unknown. Because decreased NO contributes to abnormal vascular function in diabetics, we hypothesized that NO pathway abnormalities may contribute to diabetic cardiomyopathy.
Control rats and those with non-insulin-dependent diabetes mellitus (NIDDM) underwent echocardiography, hemodynamic assessment, isolated heart perfusion and measurement of exhaled NO and LV endothelial constitutive nitric oxide synthase (ecNOS).
Diabetic rats had increased LV mass (3.3 +/- 0.6 vs. 2.6 +/- 0.3 g/g body weight [BW], p < 0.001) and cavity dimensions (diastolic 2.0 +/- 0.1 vs. 1.8 +/- 0.2 cm/cm tibial length [TL], p < 0.05). Diabetic rats had prolonged isovolumic relaxation time (IVRT) (40 +/- 8 vs. 26 +/- 6 ms, p < 0.0001), increased atrial contribution to diastolic filling (0.47 +/- 0.09 vs. 0.30 +/- 0.08 m/s, p < 0.0001), and elevated in vivo LV end-diastolic pressure (7 +/- 6 vs. 2 +/- 1 mm Hg, p = 0.04). Diabetic rats had increased chamber stiffness. Shortening was similar in both groups, despite reduced meridional wall stress in diabetics, suggesting impaired systolic contractility. Exhaled NO was lower in diabetic rats (1.8 +/- 0.2 vs. 3.3 +/- 0.3 parts per billion, p < 0.01) and correlated with Doppler LV filling. The ecNOS was similar between the groups.
Diabetic cardiomyopathy is characterized by LV systolic and diastolic dysfunction, the latter correlating with decreased exhaled NO. The NO pathway is intact, suggesting impaired availability of NO as contributor to cardiomyopathy.
我们试图评估链脲佐菌素诱导的糖尿病大鼠的体内和体外左心室（LV）几何结构及功能，以及一氧化氮（NO）途径的可能作用。
糖尿病会导致心脏功能障碍；然而，具体异常情况尚不清楚。由于NO减少会导致糖尿病患者血管功能异常，我们推测NO途径异常可能导致糖尿病性心肌病。
对对照大鼠和非胰岛素依赖型糖尿病（NIDDM）大鼠进行超声心动图检查、血流动力学评估、离体心脏灌注，并测量呼出的NO和左心室内皮型一氧化氮合酶（ecNOS）。
糖尿病大鼠的左心室质量增加（3.3±0.6 vs. 2.6±0.3 g/g体重[BW]，p<0.001），腔径增大（舒张期2.0±0.1 vs. 1.8±0.2 cm/cm胫骨长度[TL]，p<0.05）。糖尿病大鼠的等容舒张时间（IVRT）延长（40±8 vs. 26±6 ms，p<0.0001），心房对舒张期充盈的贡献增加（0.47±0.09 vs. 0.30±0.08 m/s，p<0.0001），体内左心室舒张末期压力升高（7±6 vs. 2±1 mmHg，p = 0.04）。糖尿病大鼠的心室僵硬度增加。尽管糖尿病大鼠的经壁应力降低，但两组的缩短情况相似，提示收缩期收缩力受损。糖尿病大鼠呼出的NO较低（1.8±0.2 vs. 3.3±0.3十亿分之一，p<0.01），且与多普勒左心室充盈相关。两组之间的ecNOS相似。
糖尿病性心肌病的特征是左心室收缩和舒张功能障碍，后者与呼出的NO减少相关。NO途径完整，提示NO可用性受损是导致心肌病的原因。
