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颈动脉压力感受器卸载诱发的反射性血浆高血糖和高渗状态。

Reflex plasma hyperglycemia and hyperosmolality evoked by unloading of the carotid baroreceptors.

作者信息

Järhult J, Holmberg J, Lundvall J

出版信息

Acta Physiol Scand. 1977 Sep;101(1):105-11. doi: 10.1111/j.1748-1716.1977.tb05988.x.

DOI:10.1111/j.1748-1716.1977.tb05988.x
PMID:906854
Abstract

Hemorrhage is usually accompanied by a considerable increase in the plasma osmolality and glucose concentration due to an augmented release of glucose from the liver. In the present cat experiments an attempt was made to investigate the possible role of different vascular receptors in mediating this hyperglycemic (hyperosmolar) response. Bilateral vagotomy or stimulation of the carotid chemoreceptors by perfusion of the carotid sinus with venous blood at normal pressure only slightly increased the arterial plasma glucose concentration. On the other hand, when the sinus nerves were cut in the vagotomized animal, thereby simulating complete unloading of the carotid baroreceptors, the arterial plasma glucose concentration rose by about 8 mM/L and the arterial plasma osmolality by about 10 mOsm/kg H2O. Perfusion of the carotid baroreceptors with arterial blood at different levels of hypotension showed that the baroreceptor-induced hyperglycemia was graded in relation to the pressure level. Regional hypotension of the liver, pancreas, intestine, kidneys or brain did not significantly affect plasma glucose concentration or osmolality. We conclude that the reflex release of glucose from the liver during hemorrhage mainly is initiated from the unloading of arterial baroreceptors.

摘要

出血通常伴随着血浆渗透压和葡萄糖浓度的显著升高,这是由于肝脏释放葡萄糖增加所致。在目前的猫实验中,试图研究不同血管受体在介导这种高血糖(高渗)反应中的可能作用。双侧迷走神经切断术或通过在正常压力下用静脉血灌注颈动脉窦刺激颈动脉化学感受器,仅使动脉血浆葡萄糖浓度略有升高。另一方面,当在迷走神经切断的动物中切断窦神经,从而模拟颈动脉压力感受器的完全卸载时,动脉血浆葡萄糖浓度升高约8 mM/L,动脉血浆渗透压升高约10 mOsm/kg H₂O。用不同程度低血压的动脉血灌注颈动脉压力感受器表明,压力感受器诱导的高血糖与压力水平呈分级关系。肝脏、胰腺、肠道、肾脏或大脑的局部低血压对血浆葡萄糖浓度或渗透压没有显著影响。我们得出结论,出血期间肝脏中葡萄糖的反射性释放主要是由动脉压力感受器的卸载引发的。

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