Department of Dental Anesthesiology Osaka University Graduate School of Dentistry, Suita, Japan.
Cardiovasc Diabetol. 2010 Nov 25;9:78. doi: 10.1186/1475-2840-9-78.
The various autonomic control systems lead to characteristic changes in heart rate (HR) and blood pressure (BP) during acute hemorrhage. However, cardiovascular autonomic neuropathy due to diabetes mellitus may interfere with the normal compensation for hemorrhage.
A controlled graded bleeding (6 - 36% loss of estimated total blood volume: ETBV) was performed in streptozotocin-induced diabetic rats (STZ rats) under a conscious state. Hemodynamic and autonomic responses to acute hemorrhage were examined using analysis of BP-HR variability. The effects of dextran treatment after hemorrhage were also examined.
A significant reduction in mean arterial pressure began at 12% ETBV loss in STZ rats and 18% in the control rats, respectively. When blood loss reached 18% of TEBV, the decrease in HR was prominent in STD rats due to the activation of a parasympathetic drive, as indicated by the increase in high frequency (HF; 0.75~3.0 Hz) power in HR variability, while in the control rats this response was not observed. The administration of dextran prevented the activation of the parasympathetic drive in STZ rats during hemorrhaging. In the control rats, the dextran treatment sustained the initial increase in HR with reduced HF power in HR variability.
STZ rats showed different hemodynamic and autonomic responses to acute hemorrhage from the control rats. STZ rats were prone to develop bradycardiac hypotension characterized by marked parasympathetic activation during hemorrhaging. This finding suggests enhancement of the Bezold-Jarisch reflex in STZ rats. Dextran treatment to maintain a normovolemic hemorrhage state inhibits this reflex.
各种自主控制系统导致急性出血期间心率（HR）和血压（BP）出现特征性变化。然而，糖尿病引起的心血管自主神经病变可能会干扰对出血的正常代偿。
在清醒状态下，用链脲佐菌素诱导的糖尿病大鼠（STZ 大鼠）进行控制性分级出血（6-36%估计总血容量损失：ETBV）。使用血压-心率变异性分析检查急性出血时的血流动力学和自主神经反应。还检查了出血后右旋糖酐治疗的效果。
STZ 大鼠在 ETBV 损失 12%时，平均动脉压开始显著下降，而对照组大鼠在 ETBV 损失 18%时开始下降。当血液损失达到 TEBV 的 18%时，由于副交感神经驱动的激活，STZ 大鼠的 HR 明显下降，如 HR 变异性中高频（HF；0.75-3.0 Hz）功率增加所示，而在对照组大鼠中未观察到这种反应。右旋糖酐的给药可防止 STZ 大鼠在出血期间副交感神经驱动的激活。在对照组大鼠中，右旋糖酐治疗维持 HR 的初始增加，并减少 HR 变异性中的 HF 功率。
STZ 大鼠对急性出血的血流动力学和自主神经反应与对照组大鼠不同。STZ 大鼠在出血期间容易发生以明显副交感神经激活为特征的心动过缓和低血压。这一发现表明 STZ 大鼠中的 Bezold-Jarisch 反射增强。右旋糖酐治疗以维持正常血容量出血状态可抑制这种反射。
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