DIRECT EFFECTS OF OXYGENATED CRYSTALLOID OR BLOOD CARDIOPLEGIA ON ISOLATED MYOCYTE CONTRACTILE FUNCTION

The majority of myocardial protective techniques performed in the Unit ed States incorporate hypothermic hyperkalemic blood or crystalloid ca rdioplegia. Oxygenated blood cardioplegia has not been compared with o xygenated crystalloid cardioplegia in an isolated myocyte model of hyp othermic, hyperkalemic cardioplegic arrest in which direct measurement s of contractile function and myocyte swelling can he made, Accordingl y, isolated myocyte contractile function and myocyte profile surface a rea were examined after hypothermic arrest with oxygenated crystalloid or blood cardioplegia. Methods: Isolated left ventricular pig myocyte s were randomly assigned to undergo cardioplegic arrest for 2 hours at 4 degrees C. Either oxygenated crystalloid or blood cardioplegia was used, After 2 hours, myocytes were reperfused with standard cell mediu m at 37 degrees C and contractile function was examined, A control gro up, of myocytes was maintained in cell medium at 37 degrees C for 2 ho urs, Myocyte velocity of shortening (micrometers per second) was exami ned at baseline and after beta-adrenergic stimulation (isoproterenol, 25 nmol/L), Velocity of shortening declined equally from baseline cont rol values (65 +/- 2 mu m/sec) in the groups subjected to oxygenated c rystalloid cardioplegia and blood cardioplegia (37 +/- 2 mu m/sec and 42 +/- 1 mu m/sec, respectively; p < 0.05), Results: Although beta-adr energic stimulation caused a significant increase in velocity of short ening in an myocyte groups, the increase was less pronounced in myocyt es subjected to crystalloid cardioplegia (157 +/- 6 mu m/sec) and bloo d cardioplegia (159 +/- 6 mu m/sec) than in normothermic control myocy tes (205 +/- 7 mu m/sec; p < 0.05). Myocyte profile surface area, an i ndex of cell volume, was measured in all myocyte groups, Myocyte surfa ce area increased equally after cardioplegic arrest and rewarming In b oth cardioplegia groups (crystalloid 4119 +/- 53 mu m(2); blood 3924 /- 48 mu m(2)); surface areas in both cardioplegia groups were signifi cantly greater than in the normothermic control group (3158 +/- 39 mu m(2), p < 0.05). Conclusion: Equivalent effects of oxygenated crystall oid and blood cardioplegia were observed with respect to myocyte contr actile function, inotropic responsiveness, and intracellular volume re gulatory processes.