Meerson F Z, Vorontsova E Ia, Pshennikova M G
Biull Eksp Biol Med. 1983 Nov;96(11):11-3.
The effects of administering high glucose concentration (22 mM) or uridine, a cofactor of glycogen synthesis (2 X 10(-4) M), into the perfusion medium on the post-stress disturbances of the rat isolated atrium extensibility and contractile function were studied. Stress decreased the extensibility of the atrial myocardium and caused the depression of the developing systolic pressure in the isometric regime of contraction. These disturbances could be completely eliminated by a 4-fold increase of glucose concentration compared with physiological concentration, namely from 5.5 to 22 mM. The same radical effect was attained under unchanged glucose concentration by addition of uridine (2 X 10(-4) M) into the solution. The data evidence that the disturbances in glycogen resynthesis and glycolysis play an important role in the occurrence of post-stress disturbances of heart contractile function and hold promise for uridine use with a view of elimination of the stress-induced and ischemic heart injuries.
研究了在灌注介质中加入高葡萄糖浓度（22 mM）或糖原合成的辅助因子尿苷（2×10⁻⁴ M）对大鼠离体心房伸展性和收缩功能应激后紊乱的影响。应激降低了心房心肌的伸展性，并导致等长收缩状态下收缩压上升幅度的降低。与生理浓度相比，将葡萄糖浓度提高4倍，即从5.5 mM提高到22 mM，可完全消除这些紊乱。在葡萄糖浓度不变的情况下，通过向溶液中加入尿苷（2×10⁻⁴ M）也能达到同样的显著效果。数据表明，糖原再合成和糖酵解的紊乱在心脏收缩功能应激后紊乱的发生中起重要作用，并且尿苷有望用于消除应激诱导的和缺血性心脏损伤。
