Ann Thorac Surg 2000;70:1901-1906
© 2000 The Society of Thoracic Surgeons
Original article: cardiovascular
Effect of hemofiltrated whole blood pump priming on hemodynamics and respiratory function after the arterial switch operation in neonates
Mitsugi Nagashima, MDa,
Yasuharu Imai, MDa,
Kazuhiro Seo, MDa,
Masatsugu Terada, MDa,
Mitsuru Aoki, MDa,
Toshiharu Shin’oka, MDa,
Masaaki Koide, MDa
a Department of Pediatric Cardiovascular Surgery, Heart Institute of Japan, Tokyo Women’s Medical University, Tokyo, Japan
Accepted for publication June 4, 2000.
Address reprint requests to Dr Nagashima, 8-1, Kawada-cho, Shinjuku-ku, Tokyo 162, Japan
e-mail: mitsugi{at}aqua.plala.or.jp
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Abstract
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Background. Primed blood might have some deleterious effects on neonates during cardiopulmonary bypass (CPB) due to unbalanced electrolytes and inflammatory mediators. We hemofiltrated pump-primed blood before CPB to reduce inflammatory mediators and to adjust pH and the concentrations of electrolytes. The current study investigated the effects of hemofiltrated whole blood priming on hemodynamics and respiratory function after CPB in neonates.
Methods. Patients who underwent the arterial switch operation in the neonatal period for transposition of the great arteries with intact ventricular septum were chosen for this study. Seventeen patients underwent CPB with hemofiltrated blood priming (group HF) and 23 patients underwent CPB with nonhemofiltrated blood priming (group N). The concentrations of electrolytes and bradykinin and high molecular weight kininogen of the primed blood before and after hemofiltration were measured. At 4 hours after completion of CPB, the left ventricular percent fractional shortening, and the relation between the mean velocity of shortening and the end-systolic wall stress (stress velocity index), were measured by echocardiogram in 7 patients in group HF and 6 patients in group N. Alveolar - arterial oxygen tension difference (AaDO2) and respiratory index (AaDO2 divided by arterial oxygen tension) were measured at several points for 48 hours after CPB in all patients.
Results. Hemofiltration of the primed blood maintained electrolytes within a physiologic level and significantly reduced the concentrations of bradykinin (5,649 ± 1,353 pg/mL versus 510 ± 35 pg/mL, p < 0.05) and high molecular weight kininogen (52.7% ± 3.2% versus 40.1% ± 3.0% of normal plasma value, p < 0.05). The percent of fractional shortening at 4 hours after completion of CPB was significantly higher in group HF (n = 7) than in group N (n = 6) (22.0% ± 0.7% versus 16.0% ± 0.4%, p < 0.01). There was also a trend toward better stress velocity index in group HF than in group N (0.81 ± 0.81 versus -2.17 ± 0.45, p = 0.09). AaDO2 and respiratory index were significantly lower in group HF than in group N for 48 hours after CPB, respectively (p < 0.05).
Conclusions. Hemofiltrated fresh whole blood used for CPB priming attenuated cardiac impairment at early reperfusion periods and reduced pulmonary dysfunction in neonates with transposition of the great arteries with intact ventricular septum. This therapeutic strategy may have an advantage in preventing lung and heart dysfunction in pediatric patients who need CPB priming with blood.
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Introduction
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The recent miniaturized oxygenators and the improvement of cardiopulmonary bypass (CPB) systems have allowed for the safer performance of cardiac operation without the need for homologous blood transfusion in selected pediatric patients [1]. However, in neonates and small infants with a body weight of less than 4 kg, homologous blood is still required to maintain the level of hematocrit needed for adequate oxygen delivery to tissues and to keep an appropriate colloidal osmotic pressure during CPB.
Even fresh blood may have high concentrations of potassium and sodium and a prediction toward metabolic acidosis. Moreover, neutrophils [2], the complement system [3], kinin-kallikrein [4], and the arachidonic acid cascade [5] in the primed blood may also be activated at the beginning of pump perfusion. These substances might have some deleterious effects on neonates at the onset of CPB when the pump is primed with blood. In July 1993, we started to hemofiltrate fresh whole blood as the pump prime with use of an ultrahemofiltrator before CPB to reduce these deleterious metabolites and inflammatory mediators as well as to adjust pH and the concentrations of electrolytes. The current study investigated the effect of hemofiltrated whole blood priming on hemodynamics and respiratory function after CPB in neonates, compared with nonhemofiltrated whole blood priming. Patients who underwent the arterial switch operation (ASO) for transposition of the great arteries with intact ventricular septum (TGA/IVS) were chosen for this study because these neonatal patients had the homogeneity of pre- and postoperative condition, age at operation, and CPB time.
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Material and methods
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Eligible patients for this study had a diagnosis of TGA/IVS, no other major congenital anomaly, no previous operation, age at the operation less than 28 days, and no renal failure before or after operation (creatinine level less than 1.5). Seventeen neonates who underwent ASO and CPB with hemofiltrated fresh blood priming (group HF) from July 1993 to December 1994 were compared retrospectively with 23 neonates who underwent ASO and CPB with nonhemofiltrated fresh blood priming (group N) from July 1991 to June 1993. During this period, anesthesia techniques, operative methods, and other factors including the strategy of CPB running, were not changed.
Hemofiltration for fresh whole blood priming
Citrate-phosphate-dextrose (CPD)-buffered fresh (stored for several days) whole blood (800 mL) was primed in the bypass circuit in both groups. In group HF, the primed blood was circulated in the CPB circuit for 10 minutes, and then the base line blood samples were collected. Thereafter, 3,300 mL of the HF solution (Table 1) was added to the pump circuit, and then the same volume of fluid was hemofiltrated using an ultrahemofilter (HF 1.0U, Torey, Japan) at 250 mL/min using 30 mm Hg of negative pressure. Another blood sample was then collected from the circuit for the measurement of bradykinin, high molecular weight (HMW) kininogen and electrolytes and compared with base line sample.
Surgical procedures, cardiopulmonary bypass methods, and postoperative management
One surgeon performed all operations using a standardized technique of the arterial switch operation for TGA. Anesthesia was maintained with morphine, isoflurane, and pancuronium. The circuit for CPB consisted of a pulsatile roller pump (TCW NCK component system, Tonokura, Tokyo, Japan) and a membrane oxygenator (VPCML, COBE Laboratories, Arvada, CO). Cardiopulmonary bypass was constituted with bicaval and ascending aortic cannulation, and performed with pulsatile flow at 100 to 120 mL · min-1 · kg-1. Circulatory arrest was never used. Rectal temperature was maintained at 28°C during cardiac arrest. Multidose crystalloid cardioplegias (glucose-insulin-potassium) were infused intermittently into the coronary circulation every 30 minutes. During the rewarming period, conventional ultrafiltration was performed in both groups. Hematocrit was maintained between 30% and 33% during CPB and between 35% and 40% at the completion of CPB. Most patients were weaned from CPB without any inotropic support. Some patients required less than 3 µg · kg-1 · min-1 dopamine or less than 0.03 µg · kg-1 · min-1 isoproterenol or both; care was taken to avoid left ventricular overwork in both groups. In the intensive care unit, inotropic agents (dopamine and isoproterenol) and afterload reducing agents (trinitroglycerin and phentolamine) were given as necessary to maintain normal left atrial pressure.
Measurement of cardiac and pulmonary function
Echocardiography was performed in 6 patients from group N and 7 patients from group HF at 4 hours after the termination of CPB.
The rate-adjusted mean velocity of shortening (VCFc) was calculated as percent fractional shortening (% FS) divided by rate-adjusted ejection time. The end-systolic wall stress (ESS) was calculated by following formula:
where Pes is an end-systolic pressure, Des is an end-systolic dimension and h is an end-systolic wall thickness. The relation between VCFc and ESS, which has been reported to be an afterload-adjusted, preload-independent index of contractility, was expressed as stress velocity index (SVI). Stress velocity index was defined as the number of standard deviations from the normal population of mean VCFc for the given level of ESS [6]. Thus a SVI of 0 is the normal mean value and a positive number is better than the normal mean value.
Arterial blood samples were collected for gas analysis at 2, 4, 6, 12, 24, and 48 hours after CPB. Alveolar - arterial oxygen tension difference (AaDO2) and respiratory index were calculated using the following equations:
where PACO2 is alveolar carbon dioxide tension, R is the respiratory exchange ratio, and PaO2 is arterial oxygen tension. It was assumed that R = 0.85 and PACO2 was the same as arterial carbon dioxide tension.
Measurement of bradykinin and high molecular weight kininogen
Bradykinin was measured by competitive radioimmunoassay [7]. HMW kininogen was measured by chromogenic substrate method for photometric determination of prothrombin time [8]. Briefly, Fitzgerald factor deficient plasma, sulfatide, phospholipid, calcium chloride and chromogen (5-amino-2-nitrobenzoic-acid-isopropylamide) were added to the sample plasma. The activation rates of thrombin generation were measured by the change in absorbance at 405 nm. Data were represented by percent value of the normal plasma.
Statistics
All values are expressed as the mean ± standard error (SEM). Data were compared using the two-tailed unpaired Student’s t test or repeated-measures two-way analysis of variance (ANOVA). A p value less than 0.05 was considered significant.
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Results
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Patient profile and cardiopulmonary bypass values
Data are presented in Table 2. There were no significant differences in age at operation, body weight, CPB time, and aortic clamp time between groups. In both groups, all patients survived.
Substrates, electrolyte concentration, and cell counts of the primed blood
The concentrations of electrolytes, bradykinin, HMW kininogen, and cell counts of the primed blood before and after hemofiltration are shown in Table 3. Before hemofiltration, the concentrations of sodium and potassium were higher than the normal range and decreased to the normal range after hemofiltration. Total protein, albumin, and glucose concentrations were not significantly different before or after hemofiltration. The concentration of free hemoglobin was also at the same level before and after hemofiltration, suggesting that hemofiltration did not induce hemolysis. Ammonia concentration decreased significantly after hemofiltration. Bradykinin concentration was extremely elevated after 10 minutes of recirculation and hemofiltration significantly reduced (p < 0.05) its level to one-tenth the prehemofiltration value. (The average of bradykinin concentration in CPD-fresh blood is 46.2 ± 11.6 pg/mL and normal range of the bradykinin concentration is 9.6 to 21.0 pg/mL by a preliminary study.) HMW kininogen concentration decreased slightly but significantly (p < 0.05) after hemofiltration.
Hemodynamics and cardiac function
Left ventricular %FS was significantly better in group HF than group N at 4 hours after CPB (22.0% ± 0.7% versus 16.0% ± 0.4%, p < 0.01, Fig 1). There was also a trend toward better SVI in group HF than group N (0.81 ± 0.81 versus -2.17 ± 0.45, p = 0.09, Fig 2). Systemic pressure was significantly higher in group HF than group N for the first 120 minutes after completion of CPB (p < 0.05), whereas left atrial pressure was not significantly different between groups (Fig 3). At 4 hours after completion of CPB, the patients in the group HF received the same amount of inotropic support including dopamine (0.44 ± 0.32 µg · kg-1 · min-1 in group HF versus 1.20 ± 0.40 µg · kg-1 · min-1 in group N, NS) and isoproterenol (0.016 ± 0.003 µg · kg-1 · min-1 in group HF versus 0.015 ± 0.003 µg · kg-1 · min-1 in group N, NS), and equal or slightly less vasodilators, trinitroglycerin (0.094 ± 0.008 mg · kg-1 · min-1 in group HF versus 0.075 ± 0.011 mg · kg-1 · min-1 in group N, NS), and phentolamine (2.1 ± 0.8 mg · kg-1 · min-1 in group HF versus 7.1 ± 1.6 mg · kg-1 · min-1 in group N, p < 0.05) compared with group N.
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Fig 1. Fractional shortening at 3 to 4 hours after cardiopulmonary bypass. (Group HF = hemofiltrated blood priming group; Group N = nonhemofiltrated blood priming group.)
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Fig 2. Stress velocity index at 3 to 4 hours after cardiopulmonary bypass. (Group HF = hemofiltrated blood priming group; Group N = nonhemofiltrated blood priming group.)
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Fig 3. Changes in aortic (upper) and left atrial (lower) pressure after cardiopulmonary bypass. (Group HF = hemofiltrated blood priming group; Group N = nonhemofiltrated blood priming group.)
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Respiratory function
AaDO2 and respiratory index, which represent gas exchange in the lung, were significantly improved in group HF compared with group N for 48 hours after CPB (ANOVA, p < 0.05, respectively) (Fig 4). In both groups, there were significant increases in AaDO2 and respiratory index at 6 to 12 hours after CPB (ANOVA, p < 0.05), followed by a gradual recovery toward normal level. However, in group HF, these gas exchange indices started to recover earlier than in group N. The duration of mechanical ventilation was significantly shorter in group HF than in group N (2.7 ± 0.3 days in group HF versus 4.1 ± 0.4 days in group N, p < 0.01).
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Fig 4. Changes in alveolar - arterial oxygen tension difference (upper) and respiratory index (lower) after cardiopulmonary bypass. (AaDO2 = alveolar - arterial oxygen tension difference; Group HF = hemofiltrated blood priming group; Group N = nonhemofiltrated blood priming group.)
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Comment
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Cardiopulmonary bypass is associated with edema formation, particularly in small infants and neonates, as a consequence of an inflammatory reaction. Cardiopulmonary bypass causes activation of inflammatory cascades, such as complement [3], kinin-kallikrein [4], and the coagulation system [9], as well as stimulation of neutrophils and platelets [2]. These systemic inflammatory responses also elevate the levels of the substances that are capable of increasing vascular permeability, such as bradykinin [4], C3a, C5a [4, 10], tumor necrosis factor-
, interleukin-1 (IL-1), IL-8 [11], and so on, resulting in edema formation and organ dysfunction. Finn and colleagues [12] reported that the recirculation of primed blood caused an increase in the concentrations of C3a, terminal complement complex (C5b-9), and IL-8 in a simulated CPB model. The current study also demonstrated that the concentration of bradykinin in the primed blood increased dramatically after only 10 minutes of recirculation within the pump circuit. The inflammatory mediators that are formed in the primed blood may aggravate edema formation during CPB. Unbalanced electrolytes, including high concentrations of sodium and potassium in the primed blood, also may cause organ dysfunction. The effect of the components of the pump prime is greatly influential on neonates because the ratio of pump prime to blood volume is more than 1.0 to 2.0. Ratcliffe and coworkers [13] demonstrated that pump priming fluid had a significant effect on levels of metabolites, such as glucose, lactate, and other electrolytes during and even early after CPB in infants.
In 1990, Ridley and coworkers [14] tried to reduce the detrimental metabolite load and to adjust the unphysiologic concentration of the electrolytes by hemofiltration for the primed blood. They demonstrated that this technique maintained the level of electrolytes within physiologic range and minimized the changes in blood glucose and lactate in pediatric patients during and early after CPB. Our study demonstrated that hemofiltration of priming blood reduced the inflammatory mediators and adjusted the concentrations of electrolytes, resulting in the attenuation of hemodynamic impairment and pulmonary dysfunction after CPB in neonates with TGA/IVS.
We used a hemofilter with a membrane that has a higher hydraulic permeability than the hemodialysis membrane. This membrane is designed to remove substances with a molecular weight (MW) of less than 65 kDa. Because many inflammatory mediators have a molecular weight less than 65 kDa, they could be potentially removed by hemofiltration. A "modified ultrafiltration," which was advocated by Naik and colleagues [15] in 1991 and performed for 10 to 15 minutes after CPB, has been reported to successfully reduce complement and cytokines. High-volume, zero-balanced hemofiltration during the rewarming period has been shown to reduce C3a and tumor necrosis factor in pediatric patients who underwent open heart operation [16]. In this study also, small molecules, such as ammonia (MW = 17), creatinine (MW = 113), and bradykinin (MW = 1,060), were removed by this hemofilter, whereas albumin (MW = 68,000) was not.
The mechanisms by which hemofiltration of priming blood attenuates heart and lung dysfunction after CPB have not yet been elucidated. We speculate that hemofiltration of priming blood may reduce inflammatory mediators from the priming fluid. The reduction of initial inflammatory response in the early period of CPB may attenuate subsequent inflammatory reactions, rather than directly removing all of the inflammatory mediators by hemofiltration of priming blood. It is also inferred that the recirculation of the primed blood and the subsequent hemofiltration may consume the molecular substrates of inflammation. In the present study, a significant decrease in the concentration of HMW kininogen in the primed blood after hemofiltration was probably due to its consumption by and adherence to a foreign body, not by dilution nor removal through the hemofilter, because the total protein and albumin concentrations did not change significantly before or after hemofiltration and the molecular weight of HMW kininogen is 78 kDa, which is not removed. Another explanation is that a long recirculation of primed blood before CPB may improve the biocompatibility of the artificial surface. It has been reported that the electron microscopic findings of the hollow fiber in reused dialysis membrane were covered by protein layers [17]. Moreover, elevation of the level of C3a has been demonstrated to be attenuated in patients treated with reused dialysis membranes than those treated with a new membrane [18]. Thus, at the onset of CPB, this protein layer may also suppress the inflammatory contact activation of the patient’s own blood.
The composition of the hemofiltration solution is also an important variable. In the present study, no calcium-containing solution was used for the hemofiltration of priming blood, to maintain low level of Ca2+ during cooling and early reperfusion periods. A low concentration of Ca2+ during cooling [19] and early reperfusion periods [20] has been shown to attenuate cardiac dysfunction after ischemia-reperfusion. In addition, low Ca2+ during CPB may reduce the activation of neutrophils and macrophages. It has been documented in vitro that low concentrations of extracellular Ca2+ inhibits the release of superoxide of both neutrophils [21] and macrophages [22]. The hemofiltration solution we used had a glucose level that was higher than physiologic range, although it had the same concentration of glucose as fresh whole CPD-blood. Hyperglycemia during CPB may exacerbate neurologic damage after cardiac operation [23]. Neurologic damages were never seen in the patients in this present study, however, presumably because no circulatory arrest was used. Further investigation will be required to find an optimal hemofiltration solution for preserving organs function during and after CPB in pediatric patients.
The pattern of the postoperative gas exchange in this study, which typically showed an impairment at approximately 6 to 12 hours after CPB and then gradual improvement, was comparable with the findings from Boston Children’s group regarding the postoperative change in cardiac index in neonatal patients who underwent an arterial switch operation [24]. That group reported that cardiac index reached a nadir at 9 to 12 hours after aortic unclamping. They speculated that the mechanism is related to ischemia-reperfusion and adhesion molecules. Hennein and coworkers [25] reported that the blood concentrations of the proinflammatory cytokines including IL-6 and IL-8 peaked at approximately 6 to 12 hours after CPB in patients who underwent coronary arterial bypass grafting and was correlated with myocardial function. Our clinical findings regarding the lung function after CPB may also account for cytokine production.
In conclusion, this study demonstrated that hemofiltration of the primed fresh whole blood could manipulate electrolytes of the primed blood within physiologic range and remove or reduce some deleterious substances from the primed fluid. In addition, this technique attenuated myocardial impairment at the early reperfusion period and reduced pulmonary dysfunction as well as the duration of mechanical ventilation in neonates with TGA/IVS. Although the mechanisms of these beneficial effects have yet to be clarified, this therapeutic strategy may confer an advantage in preventing postoperative lung and heart dysfunction in pediatric patients who require blood pump priming with open heart operation.
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Acknowledgments
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We thank Dr Sperling for reviewing the manuscript and Drs Akazawa and Uchita for collecting data and samples.
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References
|
|---|
-
Kawaguchi A., Bergsland J., Subramanian S. Total bloodless open heart surgery in the pediatric age group. Circulation 1984;70:I30-I37.
-
Coleman R.W. Platelet and neutrophil activation in cardiopulmonary bypass. Ann Thorac Surg 1990;49:32-34.[Abstract]
-
Hammerschmidt D.E., Stroncek D.F., Bowers T.K., et al. Complement activation and neutropenia occurring during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1981;81:370-377.[Abstract]
-
Pang L.M., Stalcup S.A., Lipset J.S., Hayes C.J., Bowman F.J., Mellins R.B. Increased circulating bradykinin during hypothermia and cardiopulmonary bypass in children. Circulation 1979;60:1503-1507.[Abstract/Free Full Text]
-
Faymonville M.E., Deby D.G., Larbuisson R., et al. Prostaglandin E2, prostacyclin, and thromboxane changes during nonpulsatile cardiopulmonary bypass in humans. J Thorac Cardiovasc Surg 1986;91:858-866.[Abstract]
-
Colan S.D., Borow K.M., Neumann A. Left ventricular end-systolic wall stress-velocity of fiber shortening relation: a load-independent index of myocardial contractility. J Am Coll Cardiol 1984;4:715-724.[Abstract]
-
Ando T., Shimamoto K., Nakahashi Y., et al. Blood kinin measurement by sensitive kinin radioimmunoassay and its clinical application. In: Fritz H., Dietze G., eds. Recent progress on kinins. Basel, Switzerland: Birkhauser Verlag, 1982:222-232.
-
Dati F., Barthels M., Conard J., et al. Multicenter evaluation of a chromogenic substrate method for photometric determination of prothrombin time. Thromb Haemost 1987;58:856-865.[Medline]
-
Plötz F.B., van Oeveren W., Bartlett R.H., Wildevuur C.R. Blood activation during neonatal extracorporeal life support. J Thorac Cardiovasc Surg 1993;105:823-832.[Abstract]
-
Kalfin R.E., Engelman R.M., Rousou J.A., et al. Induction of interleukin-8 expression during cardiopulmonary bypass. Circulation 1993;88:401-406.
-
Millar A.B., Armstrong L., van der Linden J., et al. Cytokine production and hemofiltration in children undergoing cardiopulmonary bypass. Ann Thorac Surg 1993;56:1499-1502.[Abstract]
-
Finn A., Morgan B.P., Rebuck N., et al. Effects of inhibition of complement activation using recombinant soluble complement receptor 1 on neutrophil CD11B/CD18 and L-selectin expression and release of interleukin-8 and elastase in simulated cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996;111:451-459.[Abstract/Free Full Text]
-
Ratcliffe J.M., Wyse R.K.H., Hunter S., Alberti K.G.M.M., Elliott M.J. The role of the priming fluid in the metabolic response to cardiopulmonary bypass in children of less than 15kg body weight undergoing open-heart surgery. Thorac Cardiovasc Surgeon 1988;36:65-74.[Medline]
-
Ridley P.D., Ratcliffe J.M., Alberti K.G.M.M., Elliott M.J. The metabolic consequences of a washed cardiopulmonary bypass pump-priming fluid in children undergoing cardiac operations. J Thorac Cardiovasc Surg 1990;100:528-537.[Abstract]
-
Naik S.K., Knight A., Elliott M.J. A prospective randomized study of a modified technique of ultrafiltration during pediatric open-heart surgery. Circulation 1991;84(Suppl 3):422-431.
-
Journois D., Israel-Biet D., Pouard P., et al. High-volume, zero-balanced hemofiltration to reduce delayed inflammatory response to cardiopulmonary bypass in children. Anesthesiology 1996;85:965-976.[Medline]
-
Strokov A.G., Poz I.L., Baeva L.B., et al. Experience with the multiple use of dialyzers. Ter Arkh 1994;66:60-65.[Medline]
-
Chan M.K., Lau N. Optimal reuse of cuprammonium rayon hollow-fiber dialyzers. Int J Artif Organ 1989;12:223-228.
-
Aoki M., Nomura F., Kawata H., Mayer J.E., Jr Effect of calcium and preischemic hypothermia on recovery of myocardial function after cardioplegic ischemia in neonatal lambs. J Thorac Cardiovasc Surg 1993;105:207-212.[Abstract]
-
Samouilidou E.C., Levis G.M., Darsinos J.T., Pistevos A.C., Karli J.N., Tsiganos C.P. Effect of low calcium on high-energy phosphates and sarcolemmal Na+/K(+)-ATPase in the infarcted-reperfused heart. Biochim Biophys Acta 1991;1070:343-348.[Medline]
-
Khalfi F., Gressier B., Brunet C., et al. Involvement of the extracellular calcium in the release of elastase and the human neutrophils oxidative burst. Cell Mol Biol 1996;42:1211-1218.
-
Forman H.J., Nelson J. Effect of extracellular calcium on superoxide release by rat alveolar macrophages. J Appl Physiol 1983;54:1249-1253.[Abstract/Free Full Text]
-
Hindman B. Con: glucose priming solutions should not be used for cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1995;9:605-607.[Medline]
-
Wernovsky G., Wypij D., Jonas R.A., et al. Postoperative course and hemodynamic profile after the arterial switch operation in neonates and infants. A comparison of low-flow cardiopulmonary bypass and circulatory arrest. Circulation 1995;92:2226-2235.[Abstract/Free Full Text]
-
Hennein H.A., Ebba H., Rodriguez J.L., et al. Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization. J Thorac Cardiovasc Surg 1994;108:626-635.[Abstract/Free Full Text]
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Top
Abstract
Introduction
