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Malcolm J. MacDonald
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Ann Thorac Surg 1998;65:1610-1616
© 1998 The Society of Thoracic Surgeons

Original articles: cardiovascular

Myocardial Distribution of Antegrade Cold Crystalloid and Tepid Blood Cardioplegia

Ignacio G. Duarte, MDa, Steven T. Shearer, BSa, Malcolm J. MacDonald, MDa, John Parker Gott, MDa, W. Morris Brown, III, MDa, Jakob Vinten-Johansen, PhDa, Robert A. Guyton, MDa

a Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Division of Cardiothoracic Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, Georgia, USA

Accepted for publication January 12, 1998.

Address reprint requests to Dr Guyton, Division of Cardiothoracic Surgery, Department of Surgery, Crawford Long Hospital, Emory University School of Medicine, 550 Peachtree St NE, Atlanta, GA 30365-2225


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Tepid blood (TB) cardioplegia combines the improved rheologic characteristics and the augmented oxygen and substrate delivery of blood cardioplegia with the advantages of moderate hypothermia. In addition, the intramyocardial distribution of continuous TB cardioplegia may also be better than intermittent cold crystalloid (CC) cardioplegia. We sought to compare the distribution of TB and CC cardioplegia at varying infusion pressures.

Methods. In situ, isolated canine hearts were randomized to antegrade, continuous TB (28°C, n = 8) or intermittent CC (n = 8) cardioplegia infused at 50, 75, and 100 mm Hg. The regional distribution of cardioplegia at each pressure was measured by 15-µm colored microspheres. Cardioplegia distribution was measured from three areas each of the right ventricle (inflow, outflow, and apex) and the left ventricle (anterior, lateral, and posterior). Left ventricular samples were subdivided into subepicardial, midmyocardial, and subendocardial.

Results. Delivery of cardioplegia to all areas of the right and left ventricles showed a linear pressure–flow relationship over the range of pressures tested. Right ventricular distribution was two-thirds of that to the left ventricle, and left ventricular subepicardial distribution was approximately one half of subendocardial flow in both groups at all delivery pressures. However, the subendocardial to subepicardial ratio was significantly greater with TB cardioplegia than with CC cardioplegia. Transmural right ventricular cardioplegia flow was comparable in both groups. In contrast, left ventricular distribution of CC cardioplegia was greater than TB cardioplegia at all three pressures tested.

Conclusions. The pressure–flow relationship in both CC and TB cardioplegia is linear in both the right and left ventricular myocardium over clinically applicable delivery pressures. The distribution of cardioplegia to the right ventricle is not altered by increased pressure.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
The efficacy of myocardial protection provided by cardioplegic solutions in the setting of extracorporeal circulation is dependent in part on the ability to provide a balance between energy supply and demand so as to avoid ischemia and its consequences during elective cardiac arrest and subsequent reperfusion [1, 2]. As mechanical activity is the principal determinant of cardiac energy requirements, the immediate electromechanical arrest produced by cardioplegic solutions greatly diminishes myocardial oxygen demand. Cardioplegic protection, however, is also a function of its temperature [3], oxygen content [4, 5], substrate enhancement, and buffering capacity. However, the adequacy of distribution of cardioplegic solutions of any formulation determines, in large measure, the extent to which the benefits afforded by cardioplegia are exerted. The regulation of delivery and local distribution of cardioplegia to the heart arrested in diastole involves interactions between coronary perfusion pressure, oxygen content, rheologic properties determined by viscosity and the presence of formed elements in blood, the effects of temperature, and regional vascular resistance, which influences both global and regional distribution. In hearts with normal coronary arteries, vascular resistance may regulate the distribution of cardioplegia to balance energy supply with demand, but in coronary arteries with critical atherosclerotic lesions, vascular resistance may no longer play a modulatory role.

Regional and transmural heterogeneity of blood flow has been demonstrated in normal myocardium devoid of mechanically obstructive (atherosclerotic) lesions [6–9]. For example, blood flow to the right ventricular (RV) myocardium has been shown to be approximately 65% of that to the left ventricular (LV) myocardium, and subendocardial flow is approximately twice that of subepicardial flow. Spatial variations in the distribution of cardioplegic solution have been associated with regional irregularities in myocardial function, both systolic and diastolic [10].

The use of blood cardioplegia, as compared with standard cold crystalloid solutions, has been advocated because of its ability to provide essential endogenous metabolic substrates and oxygen radical scavengers as well as oxygen [11, 12]. Several investigators have demonstrated improvements in myocardial metabolic recovery and early postoperative systolic and diastolic function, as well as preserved ultrastructural integrity with cold blood cardioplegia compared with cold crystalloid cardioplegia [13–15]. Better myocardial protection and postischemic function have been thought to be caused by diminished ischemia and reperfusion injuries associated with the use of blood cardioplegia. The vascular endothelium is also vulnerable to nonsurgical [16–18] and surgical [19–22] ischemic-reperfusion injury. Murphy and associates [23] recently reported that tepid blood (28°C) cardioplegia preserved endothelial function (agonist-stimulated microvascular responses) in both the RV and LV, as compared with cold crystalloid cardioplegia. They postulated that the observed failure of the cold crystalloid solution to protect the coronary microvasculature may be related in part to maldistribution of this solution owing to differences in their pressure–flow characteristics [23]. Blood cardioplegia may indeed be distributed more adequately throughout the myocardium as a result of its better rheologic properties imparting better microvascular flow characteristics, in addition to the ability of greater oxygen availability to maintain better local autoregulation as compared with cold crystalloid solutions in hearts with normal coronary arteries [24].

The current study tests the hypothesis that tepid (28°C) blood (TB) cardioplegia has better regional and global distribution than cold crystalloid (CC) cardioplegia, particularly with respect to the distribution to the RV myocardium in hearts with normal coronary arteries. Because perfusion pressure is a key determinant of cardioplegia distribution, the influence of infusion pressure (50, 75, and 100 mm Hg) on these solutions was studied.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" proposed by the National Institutes of Health (NIH publication 85-23, revised 1985).

Anesthetic techniques
Sixteen dogs weighing 19 to 26 kg were studied using an in situ, isolated heart model. Animals were premedicated with subcutaneous morphine sulfate (4 mg/kg). Anesthesia was induced with intravenous pentobarbital (20 mg/kg) and maintained with intermittent boluses (3 mg/kg) as needed. The animals were intubated endotracheally and placed on volume ventilation. Standard limb leads were applied for electrocardiographic monitoring.

Operative procedures
Through a median sternotomy, both phrenic nerves were divided, the azygous vein ligated, and Rumel tourniquets were placed around the superior vena cava and the inferior vena cava. A 14-gauge cannula (DLP, Grand Rapids, MI) was inserted into the proximal ascending aorta, and a 6F Mikro-tip catheter transducer (Millar Instruments, Houston, TX) was advanced within a sidearm of the cannula to the level of the aortic root to permit monitoring of antegrade infusion pressures. The aorta was then clamped, the Rumel tourniquets quickly secured, and the proximal superior and inferior vena cavae were incised. A previously inserted LV apical vent was opened to allow drainage of the coronary sinus and thebesian venous effluents. Hemodynamic measurements were monitored and recorded on a Hewlett-Packard physiograph (model 7758B; Andover, MA).

Cardioplegia delivery
Each animal was randomized to one of two groups: (1) antegrade, intermittent CC (1° to 4°C) cardioplegia, or (2) antegrade, continuous TB (28°C) cardioplegia. Delivery of cardioplegia was accomplished using a membrane oxygenator (Bentley 10 Plus; Baxter, Irvine, CA) and a standard roller pump (Cobe, Lakewood, CA). Crystalloid cardioplegia consisted of 1 L Isolyte, 20 mEq NaHCO3, 3 mL 50% dextrose in water, and 20 mEq KCl. The crystalloid component of blood cardioplegia consisted of 1 L Isolyte, 20 mEq NaHCO3, 3 mL 50% dextrose in water, and 100 mEq KCl for the arrest dose and 40 mEq KCl for all subsequent doses, which was delivered in a composition of 4 parts blood to 1 part crystalloid, with a final hematocrit greater than or equal to 20%. Cardioplegic arrest was always attained by an antegrade infusion of a 20-mL/kg dose of the respective cardioplegic solution at an infusion pressure of 50 mm Hg. The subsequent infusions (15 mL/kg) were randomized with respect to infusion pressure between 50, 75, and 100 mm Hg, as measured by the aortic catheter transducer. Aortic root pressure was altered by adjusting the flow rate of the cardioplegia roller pump. A 1-minute interval was allotted between doses of intermittent CC cardioplegia. Tepid blood cardioplegia was administered continuously, and the infusion pressure was altered after delivery of each volume dose.

Myocardial blood flow by colored microspheres
Dye-release colored microspheres (15 ± 5 µm; Triton Technology, San Diego, CA) were used for determination of cardioplegic delivery [25, 26]. Each microsphere suspension was ultrasonicated and vortexed for 2 minutes before infusion into a glass mixing vial in-line with the cardioplegic delivery cannula, and within 15 cm of the aortic root [27]. This permitted adequate, thorough mixing of the microspheres before injection. Colored microspheres were injected 15 seconds after reaching the randomly predetermined infusion pressure for the volume dose. The color of the injected microsphere was randomized for each infusion pressure for each animal. The dose of colored microspheres given in each injection (1.5 x 106) was calculated from pilot studies to ensure that at least 400 microspheres of each color were trapped in each tissue sample for the error associated with the distribution of a finite number of particles to be reasonably small (95% of samples have errors <=10%) [28]. The total number of microspheres injected was sufficiently small to avoid changes in microvascular perfusion associated with microembolization.

Reference blood flow samples were obtained by withdrawing cardioplegia at the fixed rate of 3 mL/min from a point in the cardioplegic infusion line approximately 10 cm distal to the mixing chamber, just before the aortic root. Withdrawal of reference samples was begun 15 seconds before injection of the colored microspheres and was continued for the duration of each individual cardioplegic infusion. Reference samples were individually acquired for each microsphere infusion, representing each separate infusion pressure.

Myocardial tissue processing
After completion of all antegrade cardioplegic infusions, the arrested heart was quickly excised. Tissue samples weighing 1.0 to 2.0 g were taken from each of the following areas: RV inflow tract, RV apex, RV outflow tract, LV anterior region, LV lateral region, LV posterior region, anterior interventricular septum, and posterior interventricular septum. The LV samples were further subdivided into subepicardial, midmyocardial, and subendocardial layers. Interventricular septum samples were similarly subdivided into LV surface, midmyocardial, and RV surface samples.

Colored microspheres were extracted from each myocardial sample by digestion and analyzed spectrophotometrically. Each sample was weighed and placed into a Teflon-sealed 16-mL screw-capped glass tube. Seven milliliters of a 4-mol/L KOH solution containing 2% Tween-80 was then added to each sample for digestion of the tissue and was incubated for 3 to 5 days at room temperature with daily vortex mixing. The microspheres were recovered by filtering the suspension through an 8-µm diameter pore size Nuclepore polyester membrane (25 mm diameter) (Costar, Cambridge, MA) fitted on a nonelectrostatic vacuum filtration chamber. The glass tube was rinsed with 2 mL Tween-80 and the suspension filtered to allow for maximum recovery of microspheres. The filter was then rinsed with 70% alcohol, tightly folded, and transferred to a 1.5-mL centrifuge tube. The dye was extracted by adding 100 µL of N,N-dimethylformamide to each sample. The tube was then capped, vortexed for 30 seconds, and centrifuged (5 minutes, 2,000 g). Reference blood samples for both CC and TB cardioplegia were processed by adding 0.147 mL Tween-80 and 0.321 mL 16 mol/L KOH per milliliter of reference sample to each. Further preparation of the reference samples was then performed as described for the tissue samples.

The photometric absorption of 70 µL of the dimethylformamide solution was obtained using a diode array ultraviolet/visible spectrophotometer (DU7400; Beckman Instruments, Fullerton, CA) and the full wavelength spectrum from 300 nm to 800 nm was stored digitally. Samples were diluted as necessary to insure that absorbance was less than 1.3 absorbance units, the range within which linearity between absorbance and dye concentration is maintained according to the Beer-Lambert law. Proprietary software (Matrix Inversion for Spectrum Separation; Triton Technology) and a microprocessor were then used to perform the matrix inversion calculation for correction of color overlap in the myocardial sample spectra using prescribed wavelengths and dye standard absorption spectra. Reference blood sample absorption spectra, reference blood sample flow rate, and myocardial tissue weights were used to determine regional myocardial blood flows.

Statistical analysis
Statistical analysis of the determined mean regional cardioplegic delivery rates were performed using SAS Software (Cary, NC). Analysis of variance, with Bonferroni correction for multiple comparisons, two-way analysis of variance, and Wilcoxon rank sum test were used to evaluate degrees of differences in a region with respect to delivery pressure of each cardioplegic solution and between cardioplegic solutions. Results are expressed as mean ± standard error of the mean (mL · g-1 · min-1). Differences were considered significant when p was less than or equal to 0.05.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
Cardioplegic flow rates to the whole heart at 50, 75, and 100 mm Hg are summarized in Table 1. Generally, cardioplegic flow rate to the whole heart increased linearly with increasing pressure in both CC and TB groups. In the CC group, cardioplegic flow increased by approximately 44% each when pressures were increased from 50 to 75 mm Hg and from 75 to 100 mm Hg. In the TB group, average myocardial cardioplegic flow rate increased by 31% when pressure was increased from 50 to 75 mm Hg, and average flow increased by 44% when pressure was increased from 75 to 100 mm Hg.


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  		Table 1. Whole-Heart Cardioplegic Delivery (mL/min) per Infusion Pressurea

 
Interventricular septum
Average cardioplegic flow to the anterior interventricular septum tended to increase at each increment in pressure. In the CC group, myocardial cardioplegic flow rate was significantly greater at 100 mm Hg, and this greater flow was similar in the RV, mid, and LV regions of the anterior septum. Flow to the septum was significantly greater in the CC group than in TB at 50 mm Hg, but was similar in the two groups at 75 and 100 mm Hg. Similar results were observed in the posterior interventricular septum.

Right ventricle
Increasing delivery pressure from 50 to 75 and 100 mm Hg increased myocardial flow rates to the entire RV in both CC and TB groups; CC and TB cardioplegic flow rates at 100 mm Hg were significantly higher than those at 50 mm Hg, but not at 75 mm Hg (Fig 1). There was a marked heterogeneity of flow between the inflow tract, the outflow tract, and the apical region in the CC group. Mean flow to the apical region was approximately 24% less than that to the inflow tract at all three infusion pressures. Cardioplegic flow to the outflow tract was similar to that in the other two regions. In contrast, there was no significant difference in flow distribution to the apical region, outflow tract, and inflow tract at any delivery pressure with TB cardioplegia (Fig 2). There was no significant difference in total cardioplegic flow between CC and TB groups.



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  		Fig 1. Average flows to the whole right ventricle were similar for both cold crystalloid (CC) and tepid blood (TB) cardioplegia (A), but cold crystalloid flow to the left ventricle was significantly greater than tepid blood at 75 mm Hg delivery pressure (p = 0.05) (B).

 


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  		Fig 2. Right ventricular (RV) transmural flow (inflow [IT], outflow [OT], and apex [AP]) for cold crystalloid (CC) (A) and tepid blood (TB) (panel B) cardioplegia. RVAP flow significantly less than RVIT flow across the range of infusion pressures in the cold crystalloid group (p = 0.011).

 
Left ventricle
In the LV, cardioplegic flow rate increased with increasing pressure in both CC and TB groups (Fig 1b). In the CC group, flow increased by 44% when pressure increased from 50 to 75 mm Hg, whereas flow increased by 46% from 75 to 100 mm Hg. In the TB group, cardioplegic flow increased in the LV by 34% and 46%, respectively. Flow rate for CC tended to be greater than that for TB cardioplegia at each delivery pressure, but this difference reached statistical significance only at 75 mm Hg delivery pressure. The distribution of flow within anterior, lateral, and posterior regions of the LV was similar for both groups.

Endocardial versus epicardial
The distribution of cardioplegia within the LV was significantly greater to the subendocardium than to the subepicardium in both groups at all three pressures, with a subendocardium to subepicardium ratio exceeding 2 (Fig 3). In the CC group, both subendocardial and subepicardial cardioplegic flow increased significantly at 100 mm Hg compared with 50 mm Hg, but the ratio remained similar. In contrast, subepicardial flow in the TB group did not change significantly throughout the range of infusion pressures, although subendocardial blood flow increased significantly at each pressure increment. However, the subendocardium to subepicardium ratio was significantly greater in the TB cardioplegia group compared to the CC group at both 50 and 100 mm Hg.



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  		Fig 3. Left ventricular endocardium to epicardium flow ratio for cold crystalloid (CC) and tepid blood (TB) cardioplegia. The ratio was significantly greater for tepid blood than cold crystalloid at 50 and 100 mm Hg (p = 0.05 and p = 0.03, respectively). This relationship for each solution was unchanged by altering infusion pressure.

 
Right ventricle versus left ventricle
The relative distribution of cardioplegia between RV and LV is represented as the RV/LV ratio in Figure 4. Generally, RV flow was less than LV flow on a per gram basis, averaging between 60% and 70% of the flow rate to the LV myocardium. The RV/LV ratio for TB cardioplegia tended to be greater than for CC, but this was not statistically significant. The ratio of cardioplegic distribution between the RV and LV did not change significantly with the three delivery pressures.



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  		Fig 4. Relative interventricular distribution of cold crystalloid (CC) and tepid blood (TB) cardioplegia on a per gram basis. RV flow was approximately 66% of LV flow for both cardioplegia solutions and independent of delivery pressures. No significant differences exist between the two groups at any pressure.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
Cardioplegia [7], like coronary blood flow in the normal beating myocardium, is distributed nonhomogeneously in the arrested heart [6]. However, the heterogeneous distribution of continuous TB cardioplegia, particularly with respect to distribution to the RV, remains undetermined. Improved myocardial distribution may, in part, account for the observed beneficial effects of TB cardioplegia in comparison with intermittent CC cardioplegia observed in our previous study [23]. Accordingly, we sought to quantify the distribution of CC and TB cardioplegia administered antegrade at varying infusion pressures. Delivery of both CC and TB cardioplegia to the RV and LV myocardium showed a relatively linear relationship with perfusion pressure; this linearity is in contrast to the biphasic flow pattern of blood flow under autoregulatory control, with a pressure-independent phase between 60 and 120 mm Hg, and pressure-dependent phases both above and below this autoregulatory plateau. This linear pressure–flow relationship suggests a loss of vascular-mediated regulation of cardioplegic flow involving either a maximum vasodilation or maximum vasoconstriction. In addition, the delivery of CC cardioplegia to the LV myocardium tended to be greater than TB cardioplegia at each perfusion pressure. With both formulations, myocardial delivery of cardioplegia to the RV was less than that to the LV. In the LV myocardium, there is an apparent subendocardial luxury perfusion with both formulations, because the subendocardial to subepicardial flow ratio was greater than 1 at each pressure, but TB cardioplegia had greater subendocardial distribution than CC cardioplegia. This "luxury" distribution to the subendocardium in normal hearts may not hold for hearts with coronary artery disease in which the presence of flow-limiting stenoses may impede the distribution of cardioplegia of either formulation to the subendocardium specifically. In the current study, the relative contributions of hypothermia versus tepid temperature or the differences in cardioplegic composition to regional distribution were not determined. In addition, the delivery of cardioplegia may be impeded in hypertrophied hearts even in the presence of normal coronary arteries.

In general, the myocardial distribution of CC cardioplegia was greater than that for TB cardioplegia at each pressure. These higher flow rates for CC cardioplegia were likely the result of lower viscosity properties and lower microvascular resistances, the latter also facilitated by the absence of formed elements in the crystalloid solution. In addition, as CC has a diminished oxygen carrying capacity in comparison with blood cardioplegia, the greater flow rate in comparison with TB cardioplegia may be a regulatory mechanism (vasodilation) geared to maintaining an appropriate tissue oxygen supply–demand balance. Hypothermia, however, is associated with diminished flow rates because of increased viscosity, increased coronary vascular resistance, and diminished myocardial oxygen demand. In the present study, we did not pharmacologically achieve maximal vasodilation, nor did we determine the vascular reserve to ascertain whether a fixed resistance was operative in these hearts. However, the linearity of the pressure–flow relationship over the pressure range tested is consistent with a fixed vascular resistance.

In both the CC and TB groups, delivery of cardioplegia to all the regions analyzed increased linearly with increasing infusion pressure. Aldea and colleagues [7] previously demonstrated a curvilinear relationship between normothermic blood cardioplegic flow and perfusion pressures in the range of 5 to 60 mm Hg after pharmacologically induced maximum vasodilation. Below a perfusion pressure of approximately 40 mm Hg, a slight but consistent curvilinearity was observed associated with a slight nonlinear change in vascular resistance; at pressures greater than 40 mm Hg, the pressure–flow relationship was relatively linear. This same curvilinearity at pressures less than 40 mm Hg was also observed with crystalloid cardioplegia, arguing against an autoregulatory mechanism for this nonlinear profile. The linear increase in cardioplegic flow observed at infusion pressures greater than 50 mm Hg for both TB and CC cardioplegia is consistent with the results of Aldea and colleagues [7], and suggests a fixed vascular resistance, with flow regulated primarily by delivery pressure across this range of pressures. The fixed resistance at these higher infusion pressures may be the result of the vasoconstrictor effects of hypothermia in the CC group, or the vascular response to the hyperkalemia in the two solutions. In any event, either autoregulatory control of flow was lost with both solutions or the inflection point of autoregulation was lost.

Significant heterogeneity of cardioplegic delivery to the RV was observed in the CC group, with diminished flow specifically to the apical segment. In contrast, TB cardioplegia was delivered uniformly throughout the RV myocardium. With respect to the distribution of the cardioplegic solutions between the two ventricles, both TB and CC cardioplegia demonstrated approximately two-thirds flow to the RV relative to the LV. This approximates the differences in myocardial blood flow between the normally working RV and LV, although the workload of the RV is on the order of 30% of that of the LV. However, in the arrested heart in which cardiac work is not generated and hence does not contribute to blood and oxygen demands, the RV/LV ratio of less than 1.0 per gram of myocardium most likely reflects the increased capillary density present in the LV myocardium, particularly in the subendocardium. This lesser distribution of cardioplegia to the RV myocardium was not altered by increasing perfusion pressure. Thus, these data may suggest that the improved RV protection previously reported with TB cardioplegia by Murphy and coworkers [23] does not appear to be the result of simply increased perfusion.

Cardioplegic flow was approximately twofold greater in the subendocardium than in the subepicardium in both groups. The increased endocardial flow may be related to the greater capillary density and decreased capillary resistance as compared with the epicardial surface [3]. As previously described, vascular resistance appeared fixed throughout the range of infusion pressures, as reflected by a fairly constant endocardium to epicardium ratio in both groups. This ratio was significantly greater in the TB group compared with the CC group at both 50 and 100 mm Hg infusion pressure. This difference between continuous TB and CC cardioplegia was primarily the result of decreased subepicardial flow rather than increased subendocardial flow in the TB group as compared with the CC group, as endocardial flows were similar in both groups. These data may suggest that the subepicardial vasculature specifically may have retained some degree of vasoactivity to redistribute flow to the subendocardium, although on a transmural basis overall myocardial flow was pressure-dependent.

In conclusion, the benefits provided by antegrade TB cardioplegia hypothesized previously by Murphy and associates [23] are most likely the result of factors other than improved regional distribution. Autoregulation of transmural cardioplegic flow appeared to be absent with both groups of cardioplegia, although some degree of vasodilator capacity may be present in the subepicardial vessels of the blood cardioplegic group. Although the relative distribution between the LV and RV was similar between the two solutions, the homogeneous distribution of TB cardioplegia throughout the RV may afford improved preservation of the RV, particularly at the apex, as compared with CC cardioplegia. The generally similar flows between the two groups implies adequate delivery of TB at these infusion pressures. If vascular resistance is fixed with both CC and TB cardioplegia, greater infusion pressures would be necessary to ensure more adequate delivery beyond coronary artery stenoses or to hypertrophied myocardium. The need to increase perfusion pressure to improve delivery of cardioplegia must be balanced by the vulnerability of ischemic myocardium to perfusion (cardioplegia) and reperfusion injuries.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
We are grateful for the assistance of Ms Jill Robinson, Ms Sara Katzmark, and Ms L. Susan Schmarkey. This study was supported in part by the Carlyle Fraser Heart Center.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

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