Superior recovery of hypertrophied rat myocardium after cardioplegic arrest.

BACKGROUND: Although cardioplegic protection of the hypertrophied heart remains a clinical challenge, we have previously observed enhanced recovery in rat hearts with pressure-overload hypertrophy induced by aortic banding. We investigated whether this unexpected result is found in other models of hypertrophy. METHODS: Hearts with hypertrophy induced by aortic banding or administration of desoxycorticosterone acetate were each compared with age-matched sham-operated and nonoperated controls. Spontaneously hypertensive rats and Wistar-Kyoto controls were also compared. We evaluated left ventricular isomyosin distribution by gel electrophoresis and recovery of isolated working rat hearts arrested at 8 degrees C for 2 hours. RESULTS: The percentage of V3 isomyosin in hearts with hypertrophy from aortic banding or administration of desoxycorticosterone acetate was increased compared with the control groups. Recovery of aortic flow in all three groups of hypertrophied hearts was at least as good or better than their respective controls. There were no significant differences in ATP or glycogen between hypertrophied and control hearts before or after arrest. CONCLUSIONS: Enhanced recovery of hypertrophied hearts is not specific to a single model. This level of recovery may be supported by induction of a "fetal genetic program," exemplified in the rat by the shift in isomyosin from predominantly V1 to the more efficient V3 isoform, which occurs in pressure-overloaded hearts.

Rapid cooling contracture with cold cardioplegia.

BACKGROUND: Cold cardioplegia can induce rapid cooling contracture. The relations of cardioplegia-induced cooling contracture to myocardial temperature or myocyte calcium are unknown. METHODS: Twelve crystalloid-perfused isovolumic rat hearts received three 2-minute cardioplegic infusions (1 mmol/L calcium) at 4 degrees, 20 degrees, and 37 degrees C in random order, each followed by 10 minutes of beating at 37 degrees C. Finally, warm induction of arrest by a 1-minute cardioplegic infusion at 37 degrees C was followed by a 1-minute infusion at 4 degrees C. Indo-1 was used to measure the intracellular Ca2+ concentration in 6 of these hearts. Additional hearts received hypoxic, glucose-free cardioplegia at 4 degrees or 37 degrees C. RESULTS: After 1 minute of cardioplegia at 4 degrees, 20 degrees, and 37 degrees C, left ventricular developed pressure rose rapidly to 54% +/- 3%, 43% +/- 3%, and 18% +/- 1% of its prearrest value, whereas the intracellular Ca2+ concentration reached 166% +/- 23%, 94% +/- 4%, and 37% +/- 10% of its prearrest transient. Coronary flow was 5.7 +/- 0.2, 8.7 +/- 0.3, and 12.6 +/- 0.6 mL/min, respectively. Warm cardioplegia induction at 37 degrees C reduced left ventricular developed pressure and [Ca2+]i during subsequent 4 degrees C cardioplegia by 16% (p = 0.001) and 34% (p = 0.03), respectively. Adenosine triphosphate and phosphocreatine contents were lower after 4 degrees C than after 37 degrees C hypoxic, glucose-free cardioplegia. CONCLUSIONS: Rapid cooling during cardioplegia increases left ventricular pressure, [Ca2+]i and coronary resistance, and is energy consuming. The absence of rapid cooling contracture may be a benefit of warm heart operations and warm induction of cardioplegic arrest.

Reducing intraoperative myocardial acidosis by continuous cardioplegic perfusion via the coronary sinus.

Continuous retrograde coronary sinus perfusion (RCSP) can deliver cardioplegic solution homogeneously to the myocardium via the disease-free venous system. However, administration of cardioplegic solution through the coronary venous system necessitates low pressure infusion which may limit the rate of cardioplegic delivery. In addition, infusion of the solution at low flow rates may not prevent the development of myocardial acidosis during arrest. To determine if RCSP is capable of limiting intraoperative myocardial acidosis, open-chest pigs, monitored by intramyocardial pH probes, underwent cardioplegic arrest with a single dose aortic root infusion followed by a 45-min period of no RCSP (Group 1), RCSP of 25 mEq/liter bicarbonate-buffered cardioplegic solution (Group 2), RCSP of blood-buffered cardioplegic solution (Group 3), and RCSP of histidine-buffered cardioplegic solution (Group 4). There were no significant differences between the groups with respect to baseline pH, with a range of 7.27 to 7.32. At the end of the 45-min arrest period, Group 2 had a statistically higher pH, 7.06 +/- 0.08, compared to Group 1, 6.74 +/- 0.08 (P less than 0.05). Hearts in Groups 3 and 4 demonstrated preservation of preischemic pH levels after 45 min of arrest, 7.29 +/- 0.07 and 7.37 +/- 0.10, respectively, significantly higher than either Group 1 or 2 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Recovery after cardioplegia in the hypertrophic rat heart.

BACKGROUND: Enhanced recovery after cardioplegic arrest has been observed in rat hearts with hypertrophy induced by hemodynamic overload. We hypothesize that this is related to altered characteristics of hypertrophied myocardium-reflected by increased V(3) isomyosin and glycolytic potential-other than increased left ventricular mass. MATERIALS AND METHODS: Isolated hearts from age-matched nonoperated and sham-operated control rats and from aortic-banded, hyperthyroid, and hypothyroid rats-groups in which hypertrophy and V(3) as a percentage of left ventricular myosin vary independently-underwent 2 h of multidose cardioplegic arrest at 8 degrees C followed by reperfusion at 37 degrees C. Left ventricular V(3) isomyosin was evaluated after separation by gel electrophoresis. RESULTS: Moderate left ventricular hypertrophy was produced by aortic banding or hyperthyroidism and atrophy by hypothyroidism. V(3) isomyosin was increased in banded (28%) and hypothyroid (75%) rats compared to control (12%) and hyperthyroid rats (7%). Myocardial glycogen content closely paralleled %V(3). At 30 min of working reperfusion, functional recovery (assessed as percentage prearrest cardiac output) was 66 +/- 4 and 68 +/- 5% in control and hyperthyroid hearts and 81 +/- 2 and 80 +/- 5% in hearts from banded and hypothyroid rats (each P < 0.05 vs controls), respectively. At 30 min, hearts from banded and hypothyroid rats were also more efficient (as indexed by cardiac output at constant mean aortic pressure/myocardial oxygen consumption) than control and hyperthyroid hearts. CONCLUSIONS: The data suggest that recovery is related not to increased mass but to other changes in overload hypertrophy. Increased percentage V(3) isomyosin and glycogen reflect these changes and may themselves contribute to improved functional recovery after cardioplegic arrest, as may increased postischemic efficiency.

Warm and cold blood cardioplegia. Comparison of myocardial function and metabolism using 31p magnetic resonance spectroscopy.

BACKGROUND: Standard myocardial protection during cardiac surgery uses hypothermic arrest, but warm heart surgery, recently introduced, is now used in many centers. We hypothesized that warm continuous blood cardioplegia (WCBC) would provide better myocardial preservation than cold continuous blood cardioplegia (CCBC). METHODS AND RESULTS: In isolated cross-perfused canine hearts, left ventricular (LV) function and myocardial O2 consumption (MVO2) were measured at constant LV volume, coronary perfusion pressure, and heart rate before and after 75 minutes of arrest at 37 degrees C or 10 degrees C. Metabolism was evaluated by 31P nuclear magnetic resonance spectroscopy. LV resting tone increased transiently after arrest by CCBC but not WCBC (38 +/- 3.9 versus 2.9 +/- 0.5 mm Hg, P < .0005). Myocardial ATP changed over time differently in the groups (P < .001), declining at the outset of CCBC and returning to control levels during the recovery period after CCBC or WCBC. Intracellular pH rose from 7.17 +/- 0.03 to 7.85 +/- 0.05 during CCBC (P < .0005 versus WCBC). MVO2 declined dramatically during arrest at either temperature but to a lower value during CCBC (P < .0005). LV pressure recovered to 86.1 +/- 5.1% of its prearrest value after CCBC and to 97.2 +/- 7.8% following WCBC (P = NS). After CCBC but not WCBC, there were small but significant increases in LV end-diastolic pressure (by 1.3 mm Hg, P < .05) and in the LV relaxation constant, tau (from 37.3 +/- 1.5 to 42.3 +/- 2.4 milliseconds, P < .05). CONCLUSIONS: The increase in intracellular pH during CCBC is largely accounted for by physicochemical factors. Group differences in ATP over time may be related to rapid cooling contracture during CCBC. The data suggest that CCBC mildly impairs LV function but that WCBC preserves function and metabolism at or near prearrest levels.