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Administration of putrescine, a polyamine, to rats leads to endothelial injury manifesting itself by an increased number of endothelial cells circulating in blood. Moreover, putrescine affects the metabolism of the arterial wall itself, primarily by increasing the activity of phosphomonoesterases I and II and by decreasing the activities of Krebs cycle enzymes, both of which are phenomena that can be regarded as "preatherogenic" changes 5, 6, 8, 11 preceding the onset of pathological processes in the arterial wall. Putrescine significantly decreases aortic ATPase (adenylpyrophosphatase) both in the acute and chronic phases of experiment. Ultrastructural changes after 16 weeks of putrescine administration manifested themselves in increased proliferation and smooth muscle cell injury eosinophil inflitration into the adventitia. The findings support the hypothesis that high levels of PA in homocysteinemic patients and those on chronic dialysis are a common denominator accelerating atherosgenesis in these subjects.

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Chronic administration of methionine to rats induced endothelial lesion manifested by increased endothelaemia and metabolic changes indicative of pathological processes involving the vessel wall. These changes did not spontaneously return to values observed in control animals. Long-term administration of antiatherosclerotic drugs Pyridinolcarbamate and Phtalazinole II normalized metabolic disorder in the aortic wall and reduced endothelaemia to normal values.

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The uptake of 42K, 86Rb and 201Tl by non-ischaemic and ischaemic myocardium was determined in rats with coronary artery ligature lasting 10, 30, 60 and 120 min, and in control rats without ischaemia. Whereas the myocardial concentration of 201Tl and 42K in control rats was similar and higher than that of 86Rb, 201Tl was superior to the other two radionuclides due to its significantly higher accumulation in non-ischaemic myocardium and the higher ratio of non-ischaemic to ischaemic radioactivity. The 86Rb accumulation in non-ischaemic myocardium and non-ischaemic/ischaemic ratio began to decrease from its maximum at 10 min. 201Tl, 42K and 86Rb blood levels in intact animals decreased rapidly after intravenous injection to low and nearly stabilized values at 5 min. Na+K+-ATPase activity in the ischaemic myocardium was high in the acutely ischaemic myocardium and decreased to below control levels after 4 h of ischaemia; changes in activity could not influence the low uptake of potassium analogues in fresh ischaemic myocardium.

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The authors tested metipranolol (Trimepranol Spofa) for its effect in the ischaemic focus in the dog. Electrodes were sutured on the left ventricular myocardial surface and a ligature was prepared on the descending branch of the left coronary artery. One week after the operation the artery was ligated without chest opening, and electrograms were recorded. Twenty-four hours after the ligation the activity of creatine phosphokinase was determined and the histological changes were examined in samples of myocardial tissue underlying the individual electrodes. The findings in control dogs and in dogs treated with Trimepranol were compared. Trimepranol manifested itself by an early decrease of heart rate and decrease of ST segments elevations in the electrograms from the myocardial surface. Twenty-four hours after coronary artery ligation no Q waves developed in a half of the sites under the exploring electrodes in the peripheral zone and there was higher preservation of CK activity in the corresponding tissue specimens. Moreover in the treated dogs the occurrence of early ventricular arrhythmias was reduced. The study proved a protective effect of the beta-blocking agent Trimepranol in the peripheral zone of the ischaemic focus in canine myocardium.

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The protective effect of hydroxymercurifluorescein (Mercurascan, MSC) on the ischemic myocardium was evaluated in dogs. MSC was given 17 min after ligation of the descending branch of the left coronary artery in closed-chest animals. The favorable effect of this drug was confirmed (1) by an immediate decrease of ST-segment elevation in electrograms from epicardial electrodes, (2) by a reduced number of Q waves 24 h after the ligation, and (3) by the preservation of CPK activity in the sites with moderate early ST-segment elevations. Microscopic examination also confirmed this. We conclude that MSC given shortly after coronary artery occlusion in dogs protects some cells in the border zone of ischemic focus from the development of necrosis. The membrane stabilizing effect or neutralization of proteolytic enzymes are the suggested explanations for the mechanism of MSC action.

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The effect of the anabolic hormone 19-nortestosterone propionate (Superanabolon Spofa) on the metabolism of chronically ischaemic striated muscle (anterior tibial m.) was studied in a described model in the rat. Metabolic changes were estimated in terms of the activities of a number of enzymes in muscle fibres. Enzyme activities (AcP, ATPase, CE, LDH, MDH) were determined both biochemically and histochemically excepting SDH, which was determined only by the histochemical way. Morphological changes were investigated by routine histology. Administration of 19-nortestosterone propionate prevented enzymatic changes which are typical for chronic ischaemia, primarily the decrease in the activities of dehydrogenases of Krebs' cycle tricarboxylic acides (MDH, SDH). In addition, the ratio of red to white muscle fibres increased. Administration of anabolic hormone has a similar favourable action on ischaemic muscle as training, studied previously.

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