[Additional myocardial protection by normothermic cardioplegic reperfusion]. / Dopolnitel'naia zashchita miokarda s pomoshch'iu normotermicheskoi kardioplegicheskoi reperfuzii.

Three series of experiments were conducted on a model of an isolated working rat heart to study the efficacy of variants of cardioplegic myocardial protection in exposure to 30-minute total ischemia at 37 degrees C: (1) preischemic administration of potassium solution (K(+)-30 mM, Mg(2+)-1.6 mM, osmolarity 330 MOSM/1); ischemia, unmodified reperfusion; (2) preischemic administration of this solution, ischemia, postischemic administration of this solution for 5 minutes (normothermic cardioplegic reperfusion), putting in a working regimen; (3) the regimen of the experiments is the same as in series 2, but normothermic cardioplegic reperfusion was carried out with a modified potassium-magnesium solution (K(+)-15 mM, Mg(2+)-15 mM, osmolarity 360 MOSM/1). The values of functional restoration, rate and total discharge of the enzyme LDH into the perfusate were compared. Restoration of functional values (aortic pressure, aortic output, cardiac index) according to the experimental series: 3 greater than 2 greater than 1. LDH discharge into the perfusate: 3 less than 2 less than 1. The results of the study provide evidence that reperfusion damage may be lessened by normothermic cardioplegic reperfusion; the highest effect was produced by a solution with specially selected properties: electrolyte composition and high osmolarity.

[The effect of normothermic cardioplegic reperfusion with phosphocreatine on the recovery of the cardiac functional indices after total ischemia]. / Vliianie normotermicheskoi kardioplegicheskoi reperfuzii s fosfokreatinom na vosstanovlenie funktsional'nykh pokazatelei serdtsa posle total'noi ishemii.

Experiments were conducted on a model of an isolated functioning rat heart to study myocardial protection by normothermic cardioplegic reperfusion (NCR) with phosphocreatine (PC) in 30-minute total ischemia at 37 degrees C. Five series of experiments were performed: (1) cardioplegia (K+ 30 mM/l, Mg2+ 15 nM/l, osmolarity 330 MOSM/l), ischemia, NCR not applied; (2) the same solution was introduced in the preischemic period, ischemia, NCR (K+ 15 mM/l, Mg2+ 15 mM/l, osmolarity 360 MOSM/l); (3) with the same experimental schedule, PC (10 mmol/l) was added to the cardioplegic solution in the preischemic period; (4) in a similar experiment PC was added in the stage of NCR; (5) PC administered in the preischemic stage and in NCR. Restoration of heart functional parameters, rate and ejection of lactate dehydrogenase into the perfusate were compared. The results of the experiment bear evidence that NCR protects the myocardium from reperfusion damage in normothermic ischemia. The optimal cardioprotective effect of PC is produced when it is administered in the preischemic stage. PC added to the solution for NCR has no positive effect on the restoration of heart functional parameters.

[Alterations of the myocardium and adrenergic nerves of the isolated rat heart under conditions of total ischemia and normothermic cardioplegic reperfusion]. / Izmeneniia miokarda i adrenergicheskikh nervov izolirovannogo serdtsa krys pri total'noi ishemii i normotermicheskoi kardioplegicheskoi reperfuzii.

The increase of the ischemic period from 30 to 60 min did not enhance the degree of the contractural myocardial damage in connection with progression of "no reflow" phenomenon. Endogenous catecholamines do not play a decisive role in genesis of ischemic (reperfusion) heart damage. Cardioplegic reperfusion with a high K+ content results in a considerable loss of mediator from the adrenergic nerve fibres thus leading to the partial isolated heart desympathization.

[Effectiveness of protecting the myocardium against ischemia with a normothermic cardioplegic solution and creatine phosphate]. / Effektivnost' zashchity miokarda ot ishemii normotermicheskim kardioplegicheskim rastvorom s kreatinfosfatom.

The protective effects of cardioplegic solutions (CS) containing creatine phosphate (CP) were studied in a rat heart model of cardiopulmonary bypass and ischemic cardiac arrest. Isolated rat hearts were subjected to a 3-minute coronary infusion with CS containing CP in normothermic (37 degrees C) and hypothermic (4-6 degrees C) regimes. In the normothermia group, the postischemic functional recovery was 70-75% of the preischemic control value, while the cellular ATP and CP content was reduced but insignificantly. By contrast, in the hypothermia group, the postischemic functional recovery was markedly depressed, with the tissue high-energy phosphate content being appreciably lowered. The data obtained confirm high efficacy of CP-containing cardioplegic solutions administered under normothermia conditions.

[Is the damaging action of catecholamines on the myocardium realized via hyperstimulation of the beta receptors?]. / Realizuetsia li povrezhdaiushchee deistvie katekholaminov na miokard cherez giperstimuliatisiiu beta-retseptorov?

Experiments on an isolated rat heart were made to compare the damaging action on the myocardium of catecholamines (noradrenaline, adrenaline and isoproterenol) differing in the affinity for beta-receptors. The damage to myocardial cells was evaluated from the release into the perfusate of intracellular enzymes (creatine phosphokinase and lactate dehydrogenase) and the number of contracture damaged myocytes. Noradrenaline exerted the most powerful damaging action on the myocardium at a concentration of 10(-6) M. Perfusion of the heart with isoproterenol at concentrations of 10(-6) M and 10(-5) M did not lead to the affection of cardiomyocytes. It was isoproterenol concentration exceeding noradrenaline concentration 100 times that produced an increase in the rate of the release of the enzymes to the perfusate and a rise of the number of contractures in the myocardium, with the above increase being less than that provoked by adrenaline and noradrenaline (10(-6) M). It is concluded that the mechanism of the cardiotoxic effect of catecholamines cannot be reduced only to their effect on myocardial beta-receptors.