Multi-dose crystalloid cardioplegia preserves intracellular sodium homeostasis in myocardium.

The goal of this study was to assess the effect of multi-dose St Thomas' cardioplegia on intracellular sodium homeostasis in a rat heart model. A new magnetic resonance method was applied which enable us to detect intracellular Na changes without chemical shift reagents. Three groups of isolated rat hearts were subjected to 51 min of ischemia and 51 min of reperfusion at 37 degrees C: Group 1-three infusions of St Thomas' cardioplegia every 17 min for 2 min (n=7); Group 2-single-dose infusion of cardioplegia at the beginning of stop-flow ischemia (n=8); and Group 3-clamp ischemia (n=3) without cardioplegia administration. Performance of the heart was assessed by rate-pressure product relative to the pre-ischemic level (RPP). An NMR method was applied which continuously detects the Na(i) concentration in the heart, using the ability of bound sodium to exhibit triple-quantum transitions and the growth of the corresponding signal when sodium ions pass from extracellular to intracellular space. Clamp ischemia without cardioplegia and 50 min of reperfusion left the heart dysfunctional, with Na(i) growth from the pre-ischemic level of 13.9+/-1.2 mM to 34.9+/-1.3 mM and 73. 9+/-1.9 mM at the end of ischemia and reperfusion, respectively. During single-dose cardioplegia the corresponding values for Na(i) were 30.2+/-1 mM and 48.5+/-1.7 mM (RPP=29%). Multiple infusions of cardioplegic solution resulted in a remarkable preservation of the heart's intracellular Na concentration with a non-significant increase in Na(i) during ischemia and only 16.7+/-1 mM, (P=0.01), after subsequent reperfusion (RPP=85%). The time course of Na(i) changes in the rat heart model demonstrates a prominent potential of multi-dose St Thomas' cardioplegia in preserving intracellular sodium homeostasis at 37 degrees C. The growth of Na(i) concentration during ischemia, as an indicator of the viability of the myocytes, can have a prognostic value for the heart's performance during reperfusion.

Sodium TQF NMR and intracellular sodium in isolated crystalloid perfused rat heart.

The feasibility of monitoring intracellular sodium changes using Na triple quantum filtered NMR without a chemical shift reagent (SR) was investigated in an isolated rat heart during a variety of interventions for Na(i) loading. Perfusion with 1 mM ouabain or without K+ present in the perfusate for 30 min produced a rise of the Na TQF signal with a plateau of approximately 190% and approximately 228% relative to the preintervention level, respectively. Stop-flow ischemia for 30 min resulted in a TQF signal growth of approximately 147%. The maximal Na TQF signal increase of 460% was achieved by perfusion without K+/Ca2+, corresponding to an elimination of the Na transmembrane gradient. The observed values of Na NMR TQF growth in the physiological and pathological ranges are in agreement with reported data by other methods and have a linear correlation with intracellular sodium content as determined in this study by Co-EDTA method and by sucrose-histidine washout of the extracellular space. Our data indicate that the increase in Na TQF NMR signal is determined by the growth of Na(i), and the extracellular Na contribution to the total TQF signal is unchanged at approximately 64%. In conclusion, Na TQF NMR without using SR offers a unique and noninvasive opportunity to monitor alterations of intracellular sodium. It may provide valuable insights for developing cardioprotective strategies and for observing the effects of pharmaceutical treatments on sodium homeostasis.

Effects of specific sodium/hydrogen exchange inhibitor during cardioplegic arrest.

BACKGROUND: The accumulation of intracellular sodium during myocardial ischemia couples an inappropriate calcium influx and depressed cardiac recovery during subsequent reperfusion. The effects of the selective sodium/ hydrogen exchange inhibitor HOE 694 are evaluated during myocardial ischemia and reperfusion. METHODS: Ten isolated rat hearts were subjected to a 2-minute infusion of St. Thomas' cardioplegia +/- 1 mumol/L HOE 694 followed by 50 minutes' normothermic (37 degrees C) global ischemia. Intracellular sodium accumulation was continuously measured using triple quantum filtered 23Na nuclear magnetic resonance spectroscopy without chemical shift reagents. Hemodynamic variables were assessed before and after ischemia. RESULTS: The addition of 1 mumol/L HOE 694 to St. Thomas cardioplegic solution (n = 5) attenuated the accumulation of intracellular sodium after 50 minutes' ischemia (160.5% +/- 9.1% versus 203.4% +/- 10.9% [mean +/- standard error], HOE 694 versus control, respectively; p = 0.014) and after the initial reperfusion period (first 30 minutes) (288.7% +/- 10.2% versus 335.9% +/- 10.3%; p = 0.008). HOE 694-treated hearts showed significantly improved postischemic recovery of left ventricular developed pressure (53.5% +/- 8.4% versus 26.4% +/- 6.6%; p = 0.036) and rate-pressure product (40.2% +/- 6.9% versus 13.2% +/- 5%; p = 0.014). Postischemic recovery of coronary flow was not significantly different between the two groups (68.6% +/- 5.9% versus 55.5% +/- 4.6%, HOE 694 versus control, respectively; p = 0.11). CONCLUSIONS: The addition of 1 mumol/L HOE 694 to cardioplegic solution attenuates the increase of intracellular sodium during myocardial ischemia and early reperfusion. This is coupled with an improved recovery of contractile function, possibly as a result of decreased sodium and calcium overload of ischemic myocardium.

Antegrade cold blood cardioplegia is not demonstrably advantageous over cold crystalloid cardioplegia in surgery for congenital heart disease.

OBJECTIVE: The superiority of blood cardioplegia in pediatric cardiac surgery has not previously been challenged in a controlled clinical trial. The purpose of this study was to compare antegrade cold blood versus cold crystalloid cardioplegia in pediatric cardiac surgery. METHODS: One hundred thirty-eight pediatric patients (mean age 32 months; 95% CL 24.2 to 39.8 months; range 1 day to 15 years) were prospectively randomized to receive either cold blood (4:1 dilution, blood/Plegisol, potassium chloride 15 mEq/L; n = 62) or cold crystalloid (Plegisol; n = 76) cardioplegic solution during a variety of operations for congenital heart disease. Multiple doses of cold (4 degrees C) cardioplegic solution was administered antegradely in addition to topical cooling during ischemic arrest. Myocardial recovery and outcome measures were assessed by five clinical end points: (1) inotropic support, (2) echocardiographic assessment of ventricular function, (3) overall complication rate, (4) length of stay in the intensive care unit, and (5) 30-day survival. Multiple logistic regression and multivariate analysis of variance were used to investigate which of the following clinical determinants were contributory: (1) cardioplegia, (2) urgency of operation, (3) aortic crossclamp time, (4) age, and (5) cyanosis. Population data did not differ between the two cardioplegia groups (p > 0.05). RESULTS: The most important clinical determinant of studied end points was the aortic crossclamp time (p < 0.05). The type of cardioplegic solution (blood vs crystalloid) was less important (p > 0.05). The only statistically significant difference between blood and crystalloid cardioplegia for the measured clinical end points was the level of intraoperative inotropic support (p < 0.05), although this did not correlate with any significant differences in measured ventricular function. CONCLUSION: Our results suggest no clear clinical advantage of antegrade cold blood cardioplegia over crystalloid cardioplegia during hypothermic cardioplegic arrest in pediatric cardiac surgery. The aortic crossclamp time was the strongest predictor of measured outcomes.

Sodium alterations in isolated rat heart during cardioplegic arrest.

Triple-quantum-filtered (TQF) Na nuclear magnetic resonance (NMR) without chemical shift reagent is used to investigate Na derangement in isolated crystalloid perfused rat hearts during St. Thomas cardioplegic (CP) arrest. The extracellular Na contribution to the NMR TQF signal of a rat heart is found to be 73 +/- 5%, as determined by wash-out experiments at different moments of ischemia and reperfusion. With the use of this contribution factor, the estimated intracellular Na ([Na+]i) TQF signal is 222 +/- 13% of preischemic level after 40 min of CP arrest and 30 min of reperfusion, and the heart rate pressure product recovery is 71 +/- 8%. These parameters are significantly better than for stop-flow ischemia: 340 +/- 20% and 6 +/- 3%, respectively. At 37 degrees C, the initial delay of 15 min in [Na+]i growth occurs during CP arrest along with reduced growth later (approximately 4.0%/min) in comparison with stop-flow ischemia (approximately 6.7%/min). The hypothermia (21 degrees C, 40 min) for the stop-flow ischemia and CP dramatically decreases the [Na+]i gain with the highest heart recovery for CP (approximately 100%). These studies confirm the enhanced sensitivity of TQF NMR to [Na+]i and demonstrate the potential of NMR without chemical shift reagent to monitor [Na+]i derangements.

Sand aspiration: a case report.

There have been few documented cases of sand aspiration. The authors report on a 3-year-old boy who suffered severe respiratory compromise secondary to sand aspiration. Emergency intubation and subsequent bronchoscopy were required to relieve airway obstruction. The patient did well and suffered no long-term sequelae.