Selizarova N O, Eliseev V V, Krylova I B
Patol Fiziol Eksp Ter. 1994 Oct-Dec(4):11-3.
The Langendorf isolated rat hearts underwent 30-minute total ischemia followed by 60-minute reperfusion. Adenosine, inosine or guanosine was added at a concentration of 50 mumol/l into the perfusate in the first 30 minutes. The nucleotides significantly increased the developed pressure and the maximum left ventricular contractility rate. The most effective agent was adenosine which also made blood flow higher. Guanosine was more effective than adenosine and inosine in protecting the heart from ischemic contracture. At the same time adenosine augmented the arrhythmogenic effect of reperfusion, by significantly elevating the cardiac levels of diene conjugates and malonic dialdehyde. It is suggested that the arrhythmogenic effect of adenosine is the result of activated lipid peroxidation due to adenosine exchange via the xanthine reaction during nucleotide-induced vasodilation.
采用Langendorf离体大鼠心脏模型,先进行30分钟全心缺血,再进行60分钟再灌注。在最初30分钟内,将浓度为50 μmol/L的腺苷、肌苷或鸟苷添加到灌注液中。这些核苷酸显著增加了心脏收缩压和左心室最大收缩速率。最有效的药物是腺苷,它还能使血流量增加。在保护心脏免受缺血性挛缩方面,鸟苷比腺苷和肌苷更有效。同时,腺苷通过显著提高心脏中二烯结合物和丙二醛的水平,增强了再灌注的致心律失常作用。提示腺苷的致心律失常作用是核苷酸诱导血管舒张过程中,通过黄嘌呤反应进行腺苷交换导致脂质过氧化激活的结果。