Grotle Ann-Katrin, Garcia Elizabeth A, Huo Yu, Stone Audrey J
Department of Kinesiology and Health Education, The University of Texas at Austin, Austin Texas.
Department of Kinesiology and Health Education, The University of Texas at Austin, Austin Texas
Am J Physiol Heart Circ Physiol. 2017 Oct 1;313(4):H708-H714. doi: 10.1152/ajpheart.00399.2017. Epub 2017 Aug 4.
Previous studies have shown that diabetic peripheral neuropathy affects both unmyelinated and myelinated afferents, similar to those evoking the exercise pressor reflex. However, the effect of type 1 diabetes (T1DM) on this reflex is not known. We examined, in decerebrate male and female T1DM [streptozotocin (STZ)] and healthy control (CTL) rats, pressor and cardioaccelerator responses to isometric contraction of the hindlimb muscles during the early and late stages of the disease. STZ (50 mg/kg) was injected to induce diabetes, and experiments were conducted at 1, 3, and 6 wk after injection. On the day of the experiment, we statically contracted the hindlimb muscles by stimulating the sciatic nerve and measured changes in mean arterial pressure and heart rate. We found that the pressor but not cardioaccelerator response was exaggerated in STZ rats at 1 wk (STZ: 21 ± 3 mmHg, = 10, and CTL: 14 ± 2 mmHg, = 10, < 0.05) and at 3 wk (STZ: 26 ± 5 mmHg, = 10, and CTL: 17 ± 3 mmHg, = 11, < 0.05) after injection. However, at 6 wk, and only in male rats, both the pressor (STZ: 13 ± 3 mmHg, = 12, and CTL: 17 ± 3 mmHg, = 13, < 0.05) and cardioaccelerator responses (STZ: 7 ± 3 beats/min, = 12, and CTL: 10 ± 3 beats/min, = 13, < 0.05) to contraction were significantly attenuated in STZ rats compared with CTL rats. These data indicate that T1DM exaggerates the exercise pressor reflex during the early stages of the disease in both male and female rats. Conversely, T1DM attenuates this reflex in the late stage of the disease in male but not female rats. This is the first study to provide evidence that the pressor and cardioaccelerator responses to skeletal muscle contraction vary depending on the duration of type 1 diabetes.
先前的研究表明，糖尿病性周围神经病变会影响无髓鞘和有髓鞘传入神经，这与引发运动升压反射的神经相似。然而，1型糖尿病（T1DM）对该反射的影响尚不清楚。我们在去大脑的雄性和雌性T1DM[链脲佐菌素（STZ）]大鼠及健康对照（CTL）大鼠中，研究了疾病早期和晚期后肢肌肉等长收缩时的升压和心脏加速反应。注射STZ（50mg/kg）诱导糖尿病，并在注射后1、3和6周进行实验。在实验当天，我们通过刺激坐骨神经使后肢肌肉静态收缩，并测量平均动脉压和心率的变化。我们发现，在注射后1周（STZ组：21±3mmHg，n = 10，CTL组：14±2mmHg，n = 10，P<0.05）和3周（STZ组：26±5mmHg，n = 10，CTL组：17±3mmHg，n = 11，P<0.05）时，STZ大鼠的升压反应而非心脏加速反应增强。然而，在6周时，仅在雄性大鼠中，与CTL大鼠相比，STZ大鼠对收缩的升压反应（STZ组：13±3mmHg，n = 12，CTL组：17±3mmHg，n = 13，P<0.05）和心脏加速反应（STZ组：7±3次/分钟，n = 12，CTL组：10±3次/分钟，n = 13，P<0.05）均显著减弱。这些数据表明，T1DM在疾病早期会增强雄性和雌性大鼠的运动升压反射。相反，T1DM在疾病晚期会减弱雄性大鼠而非雌性大鼠对该反射的反应。这是第一项提供证据表明对骨骼肌收缩的升压和心脏加速反应会因1型糖尿病病程而异的研究。
