EFFECTS OF HYPERCARBIC ACIDOTIC REPERFUSION ON RECOVERY OF MYOCARDIAL-FUNCTION AFTER CARDIOPLEGIC ISCHEMIA IN NEONATAL LAMBS

Citation
F. Nomura et al., EFFECTS OF HYPERCARBIC ACIDOTIC REPERFUSION ON RECOVERY OF MYOCARDIAL-FUNCTION AFTER CARDIOPLEGIC ISCHEMIA IN NEONATAL LAMBS, Circulation, 90(5), 1994, pp. 321-327
Citations number
33
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
90
Issue
5
Year of publication
1994
Part
2
Pages
321 - 327
Database
ISI
SICI code
0009-7322(1994)90:5<321:EOHARO>2.0.ZU;2-G
Abstract
Background There is continued controversy over the management of pH du ring ischemia and reperfusion. Calcium overload is an integral feature of the injury resulting from ischemia and reperfusion, and hydrogen i ons are known to blunt Ca2+ influx into cells because H+ inhibits the Na+-Ca2+ exchange and the slow calcium channels. Hypercarbia is one so urce of H+, but elevated CO2 level is also known to be a potent corona ry vasodilator, which may be beneficial during early reperfusion. This study was designed to explore the effect of respiratory and metabolic acidosis during the initial phases of reperfusion after hypothermic c ardioplegic ischemia in the neonatal lamb. Methods and Results Forty i solated, blood-perfused neonatal lamb hearts underwent 2 hours of cold cardioplegic ischemia followed by reperfusion with blood with various pH values. pH was controlled either by altering the FICO2 in the vent ilating gas to the oxygenator (groups A through D) or by adding HCl to the reperfusate (group E). pH of the initial reperfusate was 6.8 in g roup A, 7.1 in group B, 7.5 in group C, and 7.8 in group D. In these g roups, pH values were maintained for the initial 5 minutes of reperfus ion and then corrected to 7.4 over 20 minutes by changing the FICO2, t o the oxygenator. In group E, HCl was added to the reperfusate to give pH 6.8 (metabolic acidosis). pH was corrected after 5 minutes of repe rfusion by administration of NaHCO3 and THAM over the next 15 minutes. At 30 and 60 minutes of reperfusion, left ventricular maximum develop ed pressure, dP/dt, -dP/dt, maximum developed pressure at V-10 (volume that gave left ventricular end-diastolic pressure of 10 mm Hg during baseline measurements), and dP/dt at V-10 were measured. Coronary bloo d flow and oxygen consumption (MVo(2)) were also measured to evaluate the metabolic recovery. Group A showed better functional recovery than groups B, C, or D (maximum dP/dt V-10: group A, 88.3+/-7.7%; group B, 69.3+/-10.8%; group C, 74.6+/-10.3%; group D, 66.1+/-9.4%; and group E, 73.7+/-13.8% at 30 minutes [P<.05]; group A, 76.1+/-13.6%; group B, 61.9+/-8.6%; group C, 63.8+/-5.4%; group D, 57.9+/-9.4%; and group E, 62.6+/-12.7% at 60 minutes [P<.05]). Coronary blood flow was higher i n group A than in other groups (A, 177.2+/-29.6%; B, 144.1+/-18.1%; C, 127.3+/-18.5%; D, 150.4+/-24.3%; and E, 106.0+/-20.0% [P<.05]). There were no significant differences in MVo(2). Conclusions These data ind icate that hypercarbic reperfusion (pH 6.8) for a short period after i schemia improved functional recovery after cold cardioplegic ischemia in neonatal lamb hearts but that metabolic acidosis to an equivalent p H did not improve postischemic function. Possible mechanisms for this effect include reduction of calcium loading to the myocardium through H+ inhibition of calcium uptake or the induction of coronary vasodilat ion by hypercarbia.