Myocardial protection in patients with acute myocardial infarction and cardiogenic shock.
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Cardiopulmonary Bypass↗
Biomedical subjects
G D Buckberg
Publications and source records attributed to G D Buckberg.
Myocardial protection: an overview.
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Animals↗
Superiority of controlled surgical reperfusion versus percutaneous transluminal coronary angioplasty in acute coronary occlusion.
Although percutaneous transluminal coronary angioplasty is successful in more than 90% of patients after acute coronary occlusion, overall mortality remains approximately 10% with higher subgroup mortality (i.e., occlusion of the left anterior descending coronary artery, multivessel disease, age older than 70 years, cardiogenic shock) and early recovery of regional wall motion is marginal. This multicenter report shows that controlled surgical reperfusion in patients with acute coronary occlusion reduces overall and subgroup mortality and restores substantial early contractility. In a survey from six institutions, 156 consecutive patients with acute coronary occlusion documented by angiography underwent surgical revascularization with controlled reperfusion using amino acid-enriched blood cardioplegic solution on total vented bypass. Ventricular wall motion was studied by echocardiography or multiple gated acquisition scan on postoperative days 5 to 7 and scored independently (0 = normal, 1 = mild hypokinesia, 2 = severe hypokinesia, 3 = akinesia, 4 = dyskinesia). Results are compared with results in 1203 patients with acute coronary occlusion treated by angioplasty in five reported medical series. Surgically treated patients were revascularized at longer ischemic intervals (6.3 versus 3.9 hours, p < 0.05) and had a greater incidence of left anterior descending occlusion (61% versus 43%, p < 0.05), multivessel disease (42% versus 22%, p < 0.05), and cardiogenic shock (41% versus 10%, p < 0.05), with 12 patients undergoing cardiopulmonary resuscitation en route to the operating room. Surgical results were superior in all categories, with overall mortality reduced from 8.7% after angioplasty to 3.9% after coronary bypass (p < 0.05). All surgical deaths occurred in patients with preoperative cardiogenic shock. Regional wall motion recovered significantly (score < 2) in 131 of 150 (87%) surgically treated patients with an average score of 0.9 +/- 0.8 (normal to mild hypokinesia) despite longer ischemic times.
Acute Disease↗
New intraoperative cardioprotective strategies for myocardial protection.
Three clinical techniques providing significant changes in the approach to myocardial protection have been reported recently. These techniques deviate from conventional practice, and they infer that normothermia is superior to hypothermia, retrograde cardioplegia is more advantageous than antegrade administration, and continuous cardioplegic delivery is preferable to intermittent dosage. Encouraging preliminary clinical results with warm-blood cardioplegia are reported, but rigid clinical and experimental testing against conventional methods is not yet available for evaluation. The ideal cardioprotective strategy has yet to be determined, but these preliminary data suggest strongly that incorporation of these techniques with conventional methods will improve intraoperative myocardial protection and provide the cardiac surgeon with an augmented arsenal of strategies that can be employed to provide increased flexibility.
Animals↗
Role of L-arginine-nitric oxide pathway in myocardial reoxygenation injury.
In view of the recent findings that NO reacts with superoxide anion to generate hydroxyl radical, the present study was conducted to ascertain the role of endogenous NO in mediating myocardial reoxygenation injury in the hypoxic piglet on cardiopulmonary bypass. Anesthetized piglets were made hypoxic (PaO2 = 20-30 mmHg) for up to 120 min, followed by reoxygenation on cardiopulmonary bypass for 30 min. Reoxygenation caused rapidly developing myocardial injury characterized by decreased contractility (expressed as end-systolic elastance) and increased lipid peroxidation (measured as conjugated dienes). Systemic venous and coronary sinus blood content of NO decreased significantly during hypoxia and increased substantially above prehypoxic levels during reoxygenation on cardiopulmonary bypass. Administration of either the antioxidants mercaptopropionyl glycine and catalase or the NO synthase inhibitor, NG-nitro-L-arginine methyl ester, to the extracorporeal circuit afforded similar and nearly complete protection against myocardial reoxygenation injury. The protective effects of NG-nitro-L-arginine methyl ester were nullified by adding an excess of L-arginine to the pump circuit, suggesting that the L-arginine-NO pathway is involved in myocardial reoxygenation injury.
Animals↗
Warm glutamate/aspartate-enriched blood cardioplegic solution for perioperative sudden death.
This report describes an initial experience applying warm glutamate/aspartate substrate-enriched blood cardioplegic solution to resuscitate hearts in 14 patients with witnessed perioperative arrest. Ten patients were in stable hemodynamic condition in the catheterization laboratory (n = 3) or intensive care unit when sudden irreversible fibrillation developed. It progressed to electromechanical arrest in six patients. In patients with preoperative or postoperative arrest, conventional cardiopulmonary resuscitation and defibrillation were unsuccessful and extracorporeal circulation was started 22 to 150 minutes after arrest. The left ventricle was vented, the aorta clamped, and warm (37 degrees C) aspartate/glutamate blood cardioplegic solution was given at a rate of 150 ml/min for 20 minutes. All bypass grafts were open with good flows in patients who had had coronary bypass, and coronary bypass was done in the three patients who had preoperative arrest. Eleven of 14 hearts resumed normal sinus rhythm after aortic unclamping, only two electrocardiographically proved infarctions occurred, and 13 patients had complete hemodynamic recovery with improved ejection fraction. Three patients died: one of progressive cardiogenic shock, another of mediastinitis, and the third of irreversible neurologic damage. Eleven patients were discharged from the hospital and are well after a follow-up period between 3 and 9 months. We conclude that witnessed perioperative arrest with intractable ventricular fibrillation should be treated aggressively by administering cardiopulmonary resuscitation during prompt transfer to the operating room for total vented bypass and delivery of warm substrate-enriched blood cardioplegic solution. This treatment may salvage hearts thought to be damaged irreversibly and may be a feasible approach to intractable witnessed cardiac arrest, provided cardiopulmonary resuscitation maintains satisfactory cerebral perfusion pressure.
Aged↗
The use of combined antegrade-retrograde infusion of blood cardioplegic solution in pediatric patients undergoing heart operations.
The benefits of combined antegrade-retrograde infusion of blood cardioplegic solution are becoming well known in adult coronary and valvular heart operations. Many of these advantages relate directly to the pediatric patient. They include prompt arrest and even distribution, particularly with aortic insufficiency or open aortic root, avoiding or limiting ostial cannulation, allowing uninterrupted surgical procedures, and flushing air/debris from the coronary arteries. We therefore report on the first 123 pediatric patients at the University of California, Los Angeles, to receive myocardial protection with antegrade (aortic) infusion in conjunction with retrograde (coronary sinus) infusion of blood cardioplegic solution. We employed a retroplegia catheter with a self-inflating and deflating occlusion balloon on the tip of a pressure-monitored infusion cannula that remains in the coronary sinus during the operation. Induction blood cardioplegic solution, 30 ml/kg in equally divided doses, is administered in the coronary sinus first antegrade at an aortic pressure less than 80 mm Hg, followed by retrograde infusion at less than 40 mm Hg. Maintenance cardioplegic solution (15 ml/kg) is administered every 20 minutes through one or both of the infusion cannulas, depending on the surgical procedure. Patients' ages ranged from 1 week to 16 years with a mean of 4.6 years. The following procedures were included in descending order: Fontan 20, atrioventricular valve repair/replacement (and complete atrioventricular canal) 16, aortic root/Konno/Ross 16, Rastelli 13, aortic valve repair/replacement 13, ventricular septal defect (and double-outlet right ventricle) 13, tetralogy of Fallot 10, coronary artery reimplantation/fistula repair 6, truncus arteriosus 4, arterial switch 3, bidirectional Glenn 2, sinus venosus 2, and aortopulmonary window, Senning, Stansel, interrupted aortic arch, and Ebstein's, 1 each. Aortic crossclamp times ranged from 6 to 219 minutes with a mean of 87 minutes. Myocardial oxygen consumption data for a series of six patients indicated the supplemental benefit for retrograde infusion of cardioplegic solution along with antegrade infusion, particularly in hypertrophied myocardium. Three deaths occurred (2.4% 30-day mortality), in the following patients: the first with truncus arteriosus and interrupted aortic arch, the second with complete atrioventricular canal and pulmonary hypertension, and the third with truncal valve regurgitation and replacement. There were no complications related to the retroplegia catheter. From this initial positive experience, we conclude that (1) combined antegrade-retrograde infusion of blood cardioplegic solution can be safely used in an expanding number of pediatric heart operations in all age groups, and (2) combined antegrade-retrograde infusion of blood cardioplegic solution may provide additional myocardial protection, with excellent surgical outcome, in complex congenital heart repairs.
Adolescent↗
Topical cardiac hypothermia in patients with coronary disease. An unnecessary adjunct to cardioplegic protection and cause of pulmonary morbidity.
This retrospective analysis tests the hypothesis that topical cardiac hypothermia is an unnecessary adjunct to intraoperative myocardial protection and an avoidable cause of pulmonary morbidity in patients with coronary disease receiving blood cardioplegia. The hospital records of 150 nonrandomized consecutive patients undergoing elective and emergency isolated coronary revascularization were reviewed. All patients received multidose cold blood cardioplegia followed by warm blood cardioplegic reperfusion distributed through grafts. Fifty patients received iced slush, 50 received topical 4 degrees C saline, and no topical cooling was used in 50 others. Patients groups were comparable in number of grafts (3.7 versus 3.5 versus 3.5) and crossclamp time (61 versus 62 versus 61 minutes). More emergency operations were performed in the patients receiving no topical hypothermia (12/50 versus 8/50 versus 7/50). Postoperative x-ray films were reviewed by a radiologist who did not know of patient grouping. Postoperative results were comparable in hemodynamics, inotropic requirements (10/50 ice versus 8/50 saline versus 5/50 no cooling), myocardial infarction (1/50 versus 2/50 versus 2/50), and enzymes (aspartate aminotransferase myocardial band creatine kinase). No patient died. Ice topical hypothermia (versus no topical cooling) was associated with more left pleural effusions (25/50 versus 9/50; p less than 0.05), atelectasis (33/50 versus 18/50; p less than 0.05), elevated left hemidiaphragms (13/50 versus 0/50; p less than 0.05), and longer postoperative hospitalization (11.2 versus 8.5 days; p less than 0.05). Topical 4 degrees C saline reduced diaphragmatic elevation and pleural effusion (versus topical ice) but was associated with more atelectasis (34/50 versus 18/50; p less than 0.05) than no topical cooling. These data suggest that routine topical hypothermia is an unnecessary adjunct to blood cardioplegic protection in patients with coronary disease, since supplemental topical cooling does not improve postoperative hemodynamics or reduce inotropic requirements, enzyme release, or prevalence of postoperative myocardial infarction, and it increases pulmonary morbidity, which can be reduced by its avoidance.
Blood↗
Myocardial protection during surgical intervention for treatment of acute myocardial infarction.
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Journal Article↗
The inferior epigastric arteries as coronary bypass conduits. Size, preoperative duplex scan assessment of suitability, and early clinical experience.
We are currently evaluating the inferior epigastric artery as an alternative arterial conduit for coronary bypass grafting. Fifty-seven inferior epigastric arteries were harvested from 47 adults. There were no differences in size between the right and left inferior epigastric arteries. Diameter was 2.5 to 3.5 mm proximally and 2 to 3 mm distally. Usable length was 6 to 16 cm (mean 11.2 +/- 0.25 cm). Grade I/IV atherosclerosis was found in one patient (2.1%). Duplex scanning was used for preoperative evaluation of the inferior epigastric arteries in 51 patients. In 21 patients the arteries were not harvested, in part because of duplex scan findings of small caliber or early bifurcation. In 30 patients the duplex findings could be compared with the surgical findings. The average length at operation was twice the length detected on duplex scan (11.2 cm versus 5.8 cm, p less than 0.001). There was a good correlation between diameter on duplex scan and that measured at operation (2.56 +/- 0.05 versus 2.62 +/- 0.07, p = not significant). Between December 1989 and May 1991, 38 patients (29 to 74 years, mean 56 years) received 42 inferior epigastric artery grafts. Proximal anastomoses were to the aorta in 17, to the vein graft hood in 20, or onto an internal mammary artery graft in 5. Distal anastomoses were to the left anterior descending artery in 2, the diagonal branch in 27, the marginal branch in 9, or the right coronary artery in 4. There were no early deaths. Complications included perioperative myocardial infarction in 1, deep sternal wound infection in 2, superficial infection at the harvest site of the inferior epigastric artery in 5, and reexploration for bleeding in 2. Because of its size and the low incidence of atherosclerosis, the inferior epigastric artery may evolve as an alternative arterial conduit for coronary bypass. Duplex scanning is a valuable noninvasive tool for preoperative evaluation of the artery's suitability. Long-term studies of patency of the inferior epigastric artery as a coronary bypass conduit are needed.
Abdominal Muscles↗
Donor hearts with impaired hemodynamics. Benefit of warm substrate-enriched blood cardioplegic solution for induction of cardioplegia during cardiac harvesting.
Brain-dead donors frequently show circulatory deterioration and often require so much inotropic support that the donor heart is of questionable value. This experimental study quantifies the cardiac metabolic consequences of brain death and the role of warm blood cardioplegic solution for induction of cardioplegia to improve the quality of potential donor hearts with impaired hemodynamics. Twelve dogs were subjected to brain death by interrupting cerebral blood flow (ligation of innominate artery, carotid arteries, and superior vena cava) and were followed up for as long as 6 hours. Each showed progressive hemodynamic deterioration, necessitating inotropic support (dopamine, calcium, and epinephrine) and large amounts of volume replacement (hetastarch; Hespan) to support the circulation (maintain mean arterial blood pressure greater than 60 mm Hg). Biopsy specimens were taken after 6 hours, or when irreversible ventricular fibrillation occurred, and were analyzed for adenosine triphosphate, creatine phosphate, glycogen, glutamate, and lactate. In six dogs the aorta was then clamped, and a 10-minute infusion of warm (37 degrees C) substrate-enriched aspartate/glutamate blood cardioplegic solution (with the dog's own blood) was given by roller pump to simulate warm induction during the harvesting process. Biopsies were then repeated. Myocardial metabolism, expressed as percent of control values, during brain death was characterized by the following: (1) moderate energy depletion (adenosine triphosphate fell 25% +/- 8%, creatine phosphate fell 55% +/- 15%; p less than 0.05 versus control: mean +/- standard error of the mean); (2) substrate depletion (tissue glutamate fell 48% +/- 9.5%, glycogen fell 66% +/- 7.5%; p less than 0.05 versus control: mean +/- standard error of the mean); and (3) evidence of anaerobic metabolism (lactate increased 374% +/- 95%; p less than 0.05 versus control: mean +/- standard error of the mean). Warm induction of blood cardioplegia in these energy- and substrate-depleted ischemic hearts showed (1) return of creatine phosphate levels to normal (113% +/- 16.8%), (2) replenishment of glutamate (201% +/- 24% of control; p less than 0.05 versus control: mean +/- standard error of the mean), and (3) 43% +/- 14% reduction in myocardial lactate content; (p less than 0.05 versus brain-dead animals). These data suggest that brain-dead donors requiring inotropic support sustain energy and substrate depletion and ischemic damage that can be reversed by a brief period of induction of cardioplegia with a warm substrate-enriched blood cardioplegic solution before harvesting.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
The inferior epigastric arteries: additional arterial conduits for aorta-coronary bypass operations?
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Abdominal Muscles↗
Myocardial temperature management during aortic clamping for cardiac surgery. Protection, preoccupation, and perspective.
The temperature of the heart and the duration of aortic clamping are the two aspects of myocardial protection that receive the greatest amount of attention during many cardiac operations. Preoccupation with profound cardiac cooling has given rise to the development of multiple devices to keep the heart as cold as possible. This report is written to put into perspective the roles of hypothermia and aortic clamping in the overall strategy of myocardial protection. I also wish to (1) suggest that intraoperative myocardial damage is determined more by "how the heart is protected" than by "how long the aorta is clamped or how cold the heart is made," (2) question whether the benefits of deep cardiac hypothermia are sufficient to offset the monetary costs and morbidity that may result from its use, and (3) suggest that using all the measures currently available to prevent, avoid, and reverse ischemic and reperfusion damage is preferable to preoccupation with profound cardiac cooling.
Aorta↗
Studies of myocardial protection in the immature heart. III. Models of ischemic and hypoxic/ischemic injury in the immature puppy heart.
This study compares the metabolic and functional effects of three different models of ischemia in the immature heart. The intent was (1) to develop a model of energy-depleted and functionally depressed heart to be used in subsequent studies of myocardial protection and (2) to characterize the biochemical changes following different interventions. Forty-five minutes of normothermic global ischemia produced severe depletion of adenosine triphosphate and creatine phosphate (greater than 70%) but was associated with 85% +/- 10% recovery of left ventricular function. Postischemic functional depression (less than 30% recovery) could be produced by either (1) extending the ischemic duration to 60 minutes or (2) preceding 45 minutes of ischemia by 60 minutes of hypoxic stress (oxygen tension 25 to 30 mm Hg). Neither of these more severe interventions caused more profound depletion of adenosine triphosphate or creatine phosphate, but hypoxic stress produced marked tissue depletion of glutamate (52%) and aspartate (48%) before aortic clamping. Longer ischemia or preceding hypoxia led to greater myocardial accumulation of lactate (greater than 250 versus 104 mumol/gm dry weight) and succinate (18 versus 11 mumol/gm dry weight) during aortic clamping, p less than 0.05 versus 45 minutes of ischemia) and greater postischemic depression and amino acid (greater than 65% aspartate depletion) and carbohydrate (greater than 50% glycogen depletion) metabolism, p less than 0.05 versus simple ischemia. These findings suggest that more severe ischemic/hypoxic models are needed in immature hearts to produce functional depression, and the biochemical analyses suggest the characteristics of metabolic defects that must be corrected to resuscitate these hearts during surgical correction of congenital defects.
Adenosine Triphosphate↗
Studies of myocardial protection in the immature heart. IV. Improved tolerance of immature myocardium to hypoxia and ischemia by intravenous metabolic support.
Thirteen immature puppies (2 to 4 kg) underwent 1 hour of acute hypoxia (oxygen tension 25 to 30 mm Hg), followed by 45 minutes of normothermic global ischemia on total vented bypass with normal blood reperfusion. Ventricular function was assessed by inscribing Starling function curves and measuring stroke work indices before hypoxia and after reperfusion. Seven puppies (control) received normal saline infusion at 4 ml/kg/hr. Six other puppies received a 4 ml/kg/hr intravenous infusion of glutamate/aspartate, glucose-insulin-potassium, mercaptopropionyl glycine, carnitine, and catalase during hypoxia and reperfusion. In control hearts, acute hypoxia depleted myocardial glutamate and aspartate by 52% (p less than 0.05 versus prehypoxia) and 48% (p less than 0.05 versus prehypoxia) and caused severe hemodynamic deterioration (55% decrease of stroke work index) (p less than 0.05 versus prehypoxia); three of seven (43%) required premature institution of bypass. Postischemic left ventricular function recovered to only 40% of control levels (p less than 0.05 versus prehypoxia). In contrast, intravenous metabolic infusions maintained tissue glutamate (p less than 0.05 versus control group) and aspartate (p less than 0.05 versus control group) in treated hearts during hypoxia and allowed cardiac index to rise 20% (p less than 0.05 versus prehypoxia); all treated hearts tolerated 1 hour of hypoxia, and stroke work recovered 70% (p less than 0.05 versus control group) of stroke work index after subsequent ischemia. Impaired tolerance of immature hearts to acute hypoxia and subsequent ischemia is due to substrate depletion. This impairment can be reduced by intravenous metabolic support during hypoxia and reperfusion and leads to improved recovery of postischemic function.
Animals↗
Studies of myocardial protection in the immature heart. V. Safety of prolonged aortic clamping with hypocalcemic glutamate/aspartate blood cardioplegia.
This study tests the hypothesis that multidose, hypocalcemic aspartate/glutamate-enriched blood cardioplegia provides safe and effective protection during prolonged aortic clamping of immature hearts. Of 17 puppies (6 to 8 weeks of age, 3 to 5 kg) placed on vented cardiopulmonary bypass, five were subjected to 60 minutes of 37 degrees C global ischemia without cardioplegic protection and seven underwent 120 minutes of aortic clamping with 4 degrees C multidose aspartate/glutamate-enriched blood cardioplegia ([Ca++] = 0.2 mmol/L), preceded and followed by 37 degrees C blood cardioplegic induction and reperfusion. Five puppies underwent blood cardioplegic perfusion for 10 minutes without intervening ischemia to assess the effect of the cardioplegic solution and the delivery techniques. Left ventricular performance was assessed 30 minutes after bypass was discontinued (Starling function curves). Hearts were studied for high-energy phosphates and tissue amino acids. One hour of normothermic ischemia resulted in profound functional depression, with peak stroke work index only 43% of control (0.7 +/- 0.1 versus 1.7 +/- 0.2 gm x m/kg, p less than 0.05). There was 70% depletion of adenosine triphosphate (7.6 +/- 1 versus control 20.3 +/- 1 mumol/gm dry weight, p less than 0.05) and 75% glutamate loss (6.6 +/- 1 versus control 26.4 +/- 3 mumol/gm, p less than 0.05). In contrast, after 2 hours of aortic clamping with multidose blood cardioplegia preceded and followed by 37 degrees C blood cardioplegia, there was complete recovery of left ventricular function (peak stroke work index 1.6 +/- 0.2 gm x m/kg) and maintenance of adenosine triphosphates, glutamate, and aspartate levels at or above control levels adenosine triphosphate 18 +/- 2 mumol/gm, aspartate 21 +/- 1 versus control 2 mumol/gm, and glutamate 25.4 +/- 2 mumol/gm). Puppy hearts receiving blood cardioplegic perfusion without ischemia had complete recovery of control stroke work index. We conclude that methods of myocardial protection used in adults, with amino acid-enriched, reduced-calcium blood cardioplegia, can be applied safely to the neonatal heart and allow for complete functional and metabolic recovery after prolonged aortic clamping.
Adenosine Triphosphate↗
Overdose reperfusion of blood cardioplegic solution. A preventable cause of postischemic myocardial depression.
Reperfusion of warm blood cardioplegic solution is useful in minimizing reperfusion damage after ischemia. This study tests the hypothesis that overzealous administration of blood cardioplegic solution at reperfusion counteracts these benefits and can lead to a prevalence of depressed ventricular performance and mortality similar to that seen after normal blood reperfusion. Thirty-one dogs underwent 45 minutes of 37 degrees C global ischemia on vented bypass. Six received normal blood reperfusion and 25 were reperfused with a warm aspartate/glutamate-enriched blood cardioplegic solution; of these, eight received high-dose (3600 +/- 600 ml) and 17 received limited-dose (1180 +/- 120 ml) blood cardioplegic reperfusion over 10 to 20 minutes. High-dose blood cardioplegic perfusion (5100 +/- 200 ml) without prior ischemia was tested in an additional five dogs. High-dose blood cardioplegia without preceding ischemia did not alter ventricular function (peak stroke work index 96% of control). After ischemia, normal blood reperfusion (no cardioplegia) resulted in marked left ventricular dysfunction (peak stroke work index 36% of control, p less than 0.05 versus control) and a 33% mortality rate (2/6 died). High-dose cardioplegic reperfusion yielded marginal recovery of stroke work index (40% of control, p less than 0.05 versus control) and a 25% mortality rate (2/8 died). In contrast, limited-dose reperfusion of blood cardioplegic solution allowed 100% survival (17/17) and restored stroke work index to 90% of control (1.3 versus 1.45 gm.m/kg). We conclude that reperfusion damage can be avoided by initial reoxygenation with limited doses of substrate-enriched blood cardioplegic solution. Conversely, high-dose reperfusion of blood cardioplegic solution offsets this benefit, reduces recovery substantially, and may be lethal.
Animals↗
Studies of controlled reperfusion after ischemia. XIX. Reperfusate composition: benefits of blood cardioplegia over fluosol DA cardioplegia during regional reperfusion--importance of including blood components in the initial reperfusate.
HYPOTHESIS: Initial reoxygenation with blood cardioplegic solution produces better regional recovery than with Fluosol DA cardioplegic solution (Green Cross Corporation, Osaka, Japan) because blood cardioplegia ensures delivery of important blood components (i.e., plasma and red blood cells) that limit reperfusion damage. METHODS: Twenty-five dogs underwent 2 hours of ligation of the left anterior descending coronary artery followed by controlled reperfusion at 50 mm Hg through an internal mammary graft on total vented bypass. Five dogs received normal blood reperfusion, 10 dogs received a 20-minute reperfusion with Fluosol DA 20% cardioplegic solution, and 10 others received a blood cardioplegic reperfusate of identical composition (i.e., pH, calcium, potassium, glucose, osmolarity). Regional oxygen consumption was measured during reperfusion, and segmental shortening (ultrasonic crystals), tissue water content, and histochemical damage (triphenyltetrazolium chloride stain) were assessed 2 hours later. RESULTS: Reperfusion with normal blood failed to restore contractile function (3% systolic shortening), caused severe edema (81% water content), and caused marked histochemical damage (48% triphenyltetrazolium chloride nonstaining). Hearts reperfused with Fluosol DA cardioplegic solution did not take up as much oxygen as hearts receiving blood cardioplegic reperfusion (37 versus 54 ml/100 gm, p less than 0.05). Blood cardioplegia was superior to Fluosol DA cardioplegia in recovery of segmental contractility (69% versus 34% systolic shortening, p less than 0.05), produced less edema (79.5% versus 80.9% water content, p less than 0.05), and produced less histochemical damage with triphenyltetrazolium chloride (11% versus 40% area of nonstaining/area at risk, p less than 0.05). CONCLUSIONS: Initial reperfusion with a blood cardioplegic solution ensures better oxygen utilization, superior recovery of regional contractility, and less tissue damage than Fluosol DA cardioplegic reperfusion. These data emphasize the importance of including blood components (plasma or red blood cells) in the oxygenated cardioplegic reperfusate to limit reperfusion injury.
Adenosine Triphosphate↗