Benthem L, Taborsky G J
Division of Endocrinology and Metabolism, Veterans Affairs Medical Center, Seattle, WA 98108, USA.
J Auton Nerv Syst. 1998 Nov 10;73(2-3):149-55. doi: 10.1016/s0165-1838(98)00133-7.
We hypothesized that the ability of prior hyperglycemia to suppress the sympatho-adrenal response would depend on the type of stress. To test this hypothesis, hyperglycemia was induced in chronically catheterized rats, before submitting them to either hypoxia (7.5% O2) or handling stress. Central venous blood samples were drawn for the determination of plasma glucose, epinephrine (EPI), norepinephrine (NOR) and insulin concentrations. Hypoxia caused significant increases in plasma EPI and NOR concentrations (deltaEPI = + 2.95+/-0.68 nmol/l, deltaNOR = + 12.45+/-1.29 nmol/l). Hyperglycemia, antecedent to hypoxia, dose dependently reduced the sympatho-adrenal response. In contrast, the sympatho-adrenal response to handling stress was not affected by even marked antecedent hyperglycemia (deltaEPI = + 2.48+/-0.46 nmol/l, deltaNOR = + 3.12+/-0.69 nmol/l at glucose = 20.7+/-0.6 mmol/l; vs. deltaEPI = + 2.48 + 0.58 nmol/l, deltaNOR= +2.97+/-0.11 nmol/l at glucose = 6.77+/-0.17 mg/dl). Thus, antecedent hyperglycemia suppresses the hypoxia-induced activation of both the sympathetic nerves and the adrenal medulla, but not the activation induced by handling. We conclude that the ability of hyperglycemia to suppress sympathetic activation depends on the stress producing the activation. We therefore speculate that hypoxic stress has a metabolic component to its central activation that handling stress does not.
我们推测,既往高血糖抑制交感 - 肾上腺反应的能力将取决于应激的类型。为了验证这一假设,我们在长期插管的大鼠中诱导高血糖,然后使其遭受低氧(7.5% O₂)或处理应激。采集中心静脉血样本以测定血浆葡萄糖、肾上腺素(EPI)、去甲肾上腺素(NOR)和胰岛素浓度。低氧导致血浆EPI和NOR浓度显著升高(ΔEPI = + 2.95±0.68 nmol/l,ΔNOR = + 12.45±1.29 nmol/l)。低氧之前的高血糖呈剂量依赖性地降低交感 - 肾上腺反应。相比之下,即使是明显的既往高血糖也不会影响对处理应激的交感 - 肾上腺反应(葡萄糖浓度为20.7±0.6 mmol/l时,ΔEPI = + 2.48±0.46 nmol/l,ΔNOR = + 3.12±0.69 nmol/l;葡萄糖浓度为6.77±0.17 mg/dl时,ΔEPI = + 2.48 + 0.58 nmol/l,ΔNOR = +2.97±0.11 nmol/l)。因此,既往高血糖可抑制低氧诱导的交感神经和肾上腺髓质的激活,但不抑制处理诱导的激活。我们得出结论,高血糖抑制交感激活的能力取决于产生激活的应激。因此,我们推测低氧应激在其中枢激活方面具有处理应激所没有的代谢成分。