Rabbit ventricular myocyte volume changes as a direct result of crystalloid cardioplegia in congestive heart failure induced by aortic regurgitation

Objectives: We hypothesized that the cell volume of ventricular myocytes is olated from hearts in volume-overload congestive failure would respond diff erently to hypothermic cardioplegia than would sham-operated cohorts. Methods: Adult rabbits underwent either valvotomy and aortic regurgitation- induced heart failure or sham surgery, Congestive failure was confirmed cli nically and by means of echocardiography. Cell volumes of isolated myocytes were measured by digital video microscopy. After equilibration in 37 degre es C physiologic solution, cells were suprafused with 9 degrees C standard or low-Cl- St Thomas' Hospital solution followed by reperfusion in 37 degre es C physiologic solution. Results: Exposure to cold St Thomas' Hospital solution for 20 minutes cause d sham myocytes to swell by 8% (n = 9); cell volumes fully recovered on nor mothermic reperfusion. In contrast, congestive failure myocytes (n = 9) mai ntained their cell volume in cold St Thomas' Hospital solution and during r eperfusion. Lowering the [K+][Cl-] product of SI Thomas' Hospital solution by partially replacing Cl- with an impermeant anion prevented cellular edem a in the sham group (n = 8) but caused a 4% swelling in failure myocytes (n = 10) on reperfusion. Osmotically shrinking the failure cells (n = 9) conv erted their behavior to that of sham cells. Conclusions: In the absence of ischermia, congestive failure myocytes are l ess sensitive to cardioplegia-induced edema than sham cells. Low-Cl- cardio plegia, which prevents edema and protects the normal heart, induced swellin g and may be detrimental in myopathic hearts. Differences in volume regulat ion in failure and sham myocytes may be due to activation of volume-sensiti ve channels that are turned off by osmotic shrinkage.