›› 2011, Vol. 31 ›› Issue (11): 1560-.doi: 10.3969/j.issn.1674-8115.2011.11.012

• Original article (Basic research) • Previous Articles     Next Articles

Acute hyperglycemia on vessel function of normal rats

ZHENG Jun1,2, WANG Yuan1, LIANG Yun-xing1, ZHONG Mei-fang3, YANG Jie4, CHEN Hong1   

  1. 1.Department of Pharmacology, Basic Medical College, Shanghai Jiaotong University, Shanghai 200025, China；2.Department of Endocrinology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200001, China；3.Shanghai Institute of Health Sciences, Shanghai Jiaotong University School of Medicine, Shanghai 201318, China；4.Department of Biochemistry and Molecular Cell Biology, Basic Medical College, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2011-11-28 Published:2011-11-29
  • Supported by:

    National Natural Science Foundation of China, 30971154；Shanghai Municipal Health Bureau Foundation, 2007167

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Abstract:

Objective To investigate the influence and possible mechanism of acute hyperglycemia on vessel function of normal rats. Methods The isolated thoracic aorta of Wistar rats (n=5) were taken for determination of vascular function in vitro. Vascular rings were incubated with high glucose solution containing 25, 50 and 100 mmol/L glucose (high glucose group) or hyperosmotic solution containing 25, 50 and 100 mmol/L mannitol (hyperosmotic control group) for 10 min, and blank control group was also established. The contraction response to phenylephrine (PE) and relaxation response to acetylcholine (Ach) of vessels were examined with tension transducer, and the relative production of reactive oxygen species (ROS) and nitric oxide (NO) of vascular rings was determined with DCF method and DAF-FM fluorescent probe respectively. Results There was no significant difference in the contraction response to 1 μmol/L PE among blank control group, high glucose group and hyperosmotic control group (P>0.05). Compared with blank control group, the relaxation response to 1 μmol/L acetylcholine in high glucose group and hyperosmotic control group decreased with the increase of glucose concentrations and osmotic pressure （P<0.05）, and the decrease of relaxation response in hyperosmotic control group was more significant than that in high glucose group (P<0.05). The relative production of NO in high glucose group and hyperosmotic control group and the relative production of ROS in high glucose group were significantly higher than those in blank control group （P<0.05 or P<0.01）, while there was no significant difference in the relative production of ROS between hyperosmotic control group and blank control group （P>0.05）. Conclusion Acute high glucose leads to concentration-dependent reduction in vasodilatation, which may be associated with the endothelial damage caused by increased ROS production. Excessive NO production induced by hyperosmosis may also serve as free radicles to damage blood vessels.

Key words: acute hyperglycemia, osmotic pressure, vessel function, reactive oxygen species, nitric oxide