[Effect of agents that act in the area of cholinergic synapses on the glycolysis process in an ischemic extremity]. / Vliianie sredstv, deistvuiushchikh v oblasti kholinergicheskikh sinapsov, na protsess glikoliza v ishemizirovannoi konechnosti.

Glycolysis intensity in an intact and ischemized muscle of a limb was decreased by prozerin and carbacholine in experiments on 230 noninbred rats with 2 models of acute ischemia. A less pronounced decrease was caused by benzohexonium, cholinesterase and dipyroxim. Meanwhile atropine blocked the glycolysis.

[Glycogen metabolism in ischemic organs]. / Osobennosti obmena glikogena v ishemizirovannykh organakh.

Acute ischemia was created by placing a tourniquet on the extremity or on a clamp on the kidney limb for a period corresponding to the critical metabolism level in the test tissue study. Restoration of circulation in the ischemic kidney led to the excessive accumulation of glucose high-molecular polymer of the glycogen type. The character of its branching in the molecule determined by the iodine complex spectrum pointed to the changes in the processes of glycogen biosynthesis. Lactate of the ischemic kidney could be used for the glycogenesis requirements. This anomalous glycogen was shown to be actively uptaken by the kidney tissue. Glycogen accumulation in the muscle tissue following acute ischemia failed to exceed the normal level, and its structure was unchanged.