| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 1995;60:319-327
© 1995 The Society of Thoracic Surgeons
Department of Cardiac Surgery, Katholieke Universiteit Leuven, Leuven, Belgium
 |
Abstract |
|---|
 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentReferences |
|---|
Methods. In 19 baboons, we compared brain protection using hypothermic circulatory arrest or RCP. Animals were placed on cardiopulmonary bypass, cooled to 18°C, underwent 1 hour of circulatory arrest or RCP, and were reperfused for 3 hours. Biochemical variables, cerebral blood flow (colored microsphere technique), and brain histology were assessed.
Results. Release of the brain-specific ischemic marker CK-BB was similar in both groups (peak values, 123 ± 97 U/L in the circulatory arrest group and 164 ± 88 U/L in the RCP group; p > 0.05), as were the arteriovenous differences in glucose uptake and lactate production (p > 0.05). During RCP, significant brain flow could not be detected (0.5 ± 0.5 mL • min-1 • 100 g-1). About 90% of the blood was shunted to the inferior caval vein, and an equilibrium in circulating microspheres was found between RCP inflow and caval vein outflow. Less than 1% of the RCP inflow returned to the aortic arch. Histologic signs of brain damage were minimal in both groups, although slightly more glial edema was found in the RCP group.
Conclusions. These data suggest that in nonhuman primates, retrograde cerebral perfusion does not perfuse the brain because of venovenous shunting.
|
Introduction |
|---|
|
TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
|---|
When Borst and associates [1] in 1964 introduced the use of hypothermic circulatory arrest (CA) for correction of aortic arch abnormalities, an important step forward was made in cardiovascular surgery. Although this technique is still commonly used, brain protection against ischemic damage remains a major drawback. Indeed, even at a temperature of 18°C, the brain cannot be safely deprived of blood for more than 45 minutes [2]. Recent studies [3] have concerned the use of retrograde cerebral perfusion (RCP) as an alternative to CA. With this technique, the brain is perfused retrogradely during hypothermia through the superior caval vein, and experimental [4, 5] as well as clinical studies [3] claim satisfactory results. In none of these studies, however, is the question addressed of whether retrograde perfusion provides adequate tissue perfusion to the brain to protect its structural and biochemical integrity. To answer this question was the aim of the present experimental study. To obtain an experimental setting as close as possible to the clinical situation, we designed an animal model using nonhuman primates because of the anatomic similarity of the venous system in all primates.
|
Material and Methods |
|---|
|
TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
|---|
Nineteen male baboons with an average weight of 9.3 kg (range, 7 to 15 kg) were premedicated with ketamine hydrochloride (Ketalar; Parke-Davis, Morris Plains, NJ), 10 mg/kg intramuscularly. After placement of an intravenous infusion line, 25 mg/kg of sodium pentobarbital (Nembutal; Abbott Laboratories, North Chicago, IL) was administered intravenously. The animal was intubated and mechanically ventilated using room air enriched with oxygen to maintain adequate blood gases. The pH was kept in the range of 7.38 to 7.45, the oxygen tension at higher than 200 mm Hg, the carbon dioxide tension in the range of 35 to 45 mm Hg, and the oxygen saturation around 99%. Anesthesia was maintained with fentanyl (Jansen Pharmaceutica, Belgium), 0.03 mg/kg every 30 minutes, and with pancuronium bromide, 0.1 mg/kg (Pavulon; Organon Teknika, Durham, NC). No glucose was administered.
One temperature probe was placed in the rectum and another, through a small hole in the skull, in the left parietal lobe of the brain. Catheters were placed in the femoral artery and vein for pressure monitoring. A urinary catheter was inserted into the bladder by way of a midline minilaparotomy to monitor urinary output. A catheter was introduced through the internal jugular vein for venous blood sampling and pressure monitoring.
Operative Technique
After the administration of an extra dose of fentanyl (0.04 mg/kg), a sternotomy was performed. The aortic arch including the cranial branches was dissected. Both caval veins were dissected, and the entry of the azygos vein was visualized. After 300 IU/kg of heparin sodium was given intravenously, the ascending aorta and both caval veins were cannulated.
For cardiopulmonary bypass (CPB), a Biomedicus BP-50 centrifugal pump (Medtronic, Minneapolis, MN) and a Minimax oxygenator (Medtronic) were used. Priming fluid comprised 250 mL of Geloplasma (Merieux, Benelux) and 250 mL of Plasmalyte-A (Baxter, Irvine, CA) including 1,000 IU of heparin. This resulted in a drop in hemoglobin from 12.8 ± 1.6 g/dL under control conditions to 5.6 ± 0.8 g/dL during CPB. Cardiopulmonary bypass flow rate was 2.4 L/m2, and mean arterial pressure was kept constant between 50 and 60 mm Hg. The left ventricle was vented through the apex of the heart. After 10 minutes of stabilization, cooling to a rectal temperature of 18°C was followed by 1 hour of CA (n = 6) or RCP (n = 13) according to the protocol. During RCP, a central venous pressure of 20 mm Hg was not exceeded. Retrograde cerebral perfusion inflow in both jugular veins was measured using a calibrated Bio-Medicus pump, and the return through the caval vein was measured using an electromagnetic in-line flow probe (Fig 1
). After CA or RCP, the animal was rewarmed and reperfused for 3 hours according to the protocol.
|
For biochemical analysis, blood was sampled (1) before the start of CPB, (2) after 20 minutes of full-flow CPB during normothermia, (3) after 60 minutes of CPB during hypothermia at 18°C before CA or RCP, (4) after CA or RCP and every 30 minutes during reperfusion. At these intervals, samples were taken from the internal jugular vein for analysis of the brain-specific ischemic marker CK-BB. The CK-BB value was determined by electrophoresis of the total creatine kinase fraction in the plasma (Paragon creatine kinase electrophoresis kit; Beckman Instruments, Inc, Fullerton, CA). At the same intervals, arterial blood samples were taken from the arterial line and venous blood samples from the internal jugular vein for determination of lactate and glucose levels. Brain and rectal temperatures were recorded every 10 minutes.
After the experiment, the animal was sacrificed and the brain, fixed for histologic examination according to the protocol. Perfusion fixation was performed using Karnowsky solution (2% paraformaldehyde and 2.5% glutaraldehyde in Sörensen's buffer 0.1 mmol/L). At the end of the experiment, with the aortic cannula still in place, clamps were put on the subclavian arteries distal to the vertebral branches and on the descending aorta. The brain was flushed with saline solution for about 1 minute until the returning fluid was clear. Then, with maintenance of a perfusion pressure of 50 mm Hg, the perfusate was switched to the fixative. After this procedure, the animal was decapitated, and the head was totally submerged in the fixative for at least 3 hours.
For histologic examination, nine standardized specimens were taken: right and left frontal, temporal, and parietal cortex, right and left hippocampus, and cerebellum. After fixation in OsO4 and routine embedding in Epon, 2-µm sections were stained with toluidine blue and examined using a light microscope. Ischemic lesions were scored on a scale of 0 through 4, with 0 = normal and 4 = maximal damage. The observer was unaware of the protocol followed. Different areas were investigated: cortical neurons, cortical glial cells, hippocampal CA1 to CA4 layers (the most vulnerable cell layers for ischemia of the hippocampus), gyrus dentatus, hippocampal glial cells, cerebellar Purkinje's and granular cells, glial cells of the cerebellum, white matter, and vasculature.
Cellular changes such as dark neurons, coagulative cellular degeneration, cellular edema, microvaculoation of the cytoplasm, nuclear chromatin clumping, and nuclear shrinkage were also scored on a scale of 0 through 4. For the glial cells, edema and ``status spongiosus,'' caused by astrocyte swelling resulting from ischemia, were scored in a similar way. Destabilization of the white matter and edema were graded 0 through 4. In the vasculature, residual red blood cells were traced as a possible indication of poor fixation; vascular collapse and edema surrounding the vessels were considered signs of ischemia. After all these investigations, a global grading was done to reflect the severity of the cerebral damage.
Experimental Protocols
The CA group comprised 6 animals. Circulatory arrest was followed by 3 hours of reperfusion on CPB. In this group, biochemical studies and brain histology were performed as already described. Organ blood flow at 37°C and 18°C was measured in 3 animals. The RCP group comprised 13 animals divided into two subgroups.
Three animals underwent RCP with 3 hours of reperfusion on CPB. Biochemical measurements and brain histology were performed as already described, and organ blood flow was measured at 37°C and 18°C before RCP. Ten animals had RCP without reperfusion. In these experiments, reperfusion was not performed to allow brain flow measurements using microspheres during RCP. (Reperfusion would induce dislodging of microspheres by antegrade reperfusion, provided microspheres entered the brain tissue during RCP). In all these experiments, microspheres were injected only during RCP to avoid the presence of any microspheres in the brain tissue before RCP. Shunting was studied during RCP by serial sampling at inflow and outflow lines of the RCP system and calculating the equilibrium of circulating microspheres in these lines.
|
Results |
|---|
|
TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
|---|
. The corresponding data for the RCP group were similar to those obtained in the CA group (p > 0.05) and are not shown. Cooling was associated with a rise in glucose and lactate levels, but the arteriovenous difference in concentration remained close to zero. Glucose uptake and lactate production occurred at the end of CA and RCP, disappeared at 30 minutes of reperfusion, and then reappeared on further reperfusion and rewarming. Similar patterns were found in the CA and the RCP group (data not shown).
|
. There was a slight rise during cooling on CPB (p < 0.05, analysis of variance for repeated measures). With antegrade reperfusion after the period of CA or RCP, a minor but significant rise in the release of this enzyme compared with the prearrest levels was found (p < 0.05, analysis of variance for repeated measures). Peak values were 123 ± 97 U/L in the CA group and 164 ± 88 U/L in the RCP group (p > 0.05). During the postarrest reperfusion phase, there were no differences between the CA and RCP groups in terms of CK-BB release.
|
. In most organs, flow was not significantly altered by hypothermia, but in the brain, it was significantly reduced (p < 0.05). Global brain flow decreased from 81 ± 32 mL • min-1 • 100 g-1 to 31 ± 17 mL • min-1 • 100 g-1 (p < 0.05.) This reduction was consistent in the different areas examined: cortical gray and white matter, hippocampus, cerebellum, and medulla oblongata.
|
. The highest values were found in the medulla oblongata, but these calculated flows remained less than 2 mL • min-1 • 100 g-1.
|
). A small amount of microspheres could be detected in the blood collected from the aortic arch.
|
. Comparable values were found in the RCP inflow and the caval vein lines (p > 0.05). Values obtained in blood samples originating from the aortic arch showed severe deoxygenation and desaturation and a decrease in pH (p < 0.05 versus RCP inflow and inferior caval vein samples).
|
.
|
As indices of glial damage, we scored edema, chromatin clumping, and status spongiosus. In this category, the rating was higher than in cellular damage, and there was a tendency toward higher scores in the RCP group. Status spongiosus scored significantly higher in the RCP group than in the CA group (p < 0.05).
In the white matter, again edema was detected. However, myelin destruction was never observed. In the vasculature, a rather high incidence of perivascular edema and collapsed blood vessels was noted but was comparable in both groups. The presence of red blood cells, a reflection of poor fixation, was hardly ever observed.
Figure 6 shows representative photomicrographs from the cerebral cortex of 3 baboons: a control baboon without brain ischemia (pilot study) (Fig 6A), a baboon in the CA group (Fig 6B), and a baboon from the RCP group (Fig 6C). Note that the multiangularly shaped neurons are well delineated and have a large nucleus. Note also the granular structure of the cytoplasm. Glial cells are smaller, reveal almost no cytoplasm, and have a prominent nucleus. The dendrites are well delineated. Blood vessels are open and do not contain red blood cells. The aspect of the cortex is homogeneous. After 60 minutes of CA and 3 hours of reperfusion, perivascular edema, some dark neurons, and microvacuolation of the cytoplasm are present, but no real cellular damage can be recognized. After 60 minutes of RCP with 3 hours of reperfusion, the glial edema is more prominent (so-called status spongiosus), and there is edema in cortical and glial cells. Some chromatin clumping is also present, but there are no signs of real cell death.
|
|
Comment |
|---|
|
TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
|---|
Brain Ischemia During CA and RCP
Although anaerobic metabolism of glucose associated with lactate production is a marker of ischemic events affecting the brain, it is not a specific one [7]. During our experiments, glucose uptake and lactate production were noted only after CA was induced and reperfusion started. Absolute levels of glucose and lactate increased during cooling on CPB, but the arteriovenous difference remained close to zero. Previous studies [8] revealed such a rise in circulating glucose induced by hypothermia, which is probably due to the inhibition of the pancreatic secretory process. During CA or RCP at 18°C, anaerobic glucose metabolism and lactate production occurred to the same extent in both groups. Although lactate production is not a specific marker, it might be indicative of brain ischemia, which undoubtedly occurs during CA.
The enzyme CK-BB, on the other hand, is used as a specific marker of brain damage [7]. Indeed, CK-BB cannot be traced in the circulation and is produced in the brain tissue only after cerebral damage. It shows up in the cerebrospinal fluid after approximately 30 minutes, and in some studies [8, 9], a positive correlation was noted between the appearance of the enzyme and the extent of the injury. Release of the enzyme into the serum indicates damage to the blood-brain barrier as a result of ischemia [7]. Its appearance is described during routine cardiac operations [10], although to a much lesser extent than during CA when possibly brain damage occurs [9]. In studies in children, peak CK-BB values have been found at 127 to 180 minutes of reperfusion after CA, with complete disappearance of the enzyme after 24 hours. A correlation has been made between duration of arrest and peak concentration of the enzyme [8].
In our study, the biochemical variables lactate production and CK-BB release revealed a minor degree of brain ischemia. The results were similar in both groups. Although increased CK-BB levels are indicative of brain damage, the amount of CK-BB release in our experiments was low compared with circumstances where major brain cell injury occurs. Although clinical studies [8] describe peak CK-BB release between 2 and 3 hours of reperfusion, we found peak concentrations at approximately 90 minutes of reperfusion with a plateau until the end of the experiment.
Also, histologic studies of the brain after CA or RCP did not reveal critical ischemic damage. To show minor ischemic lesions at the cellular and subcellular level, perfusion fixation of the brain is obligatory [11]. Using such a technique, two main findings characterizing ischemia can be demonstrated: edema of the various structures and shrinkage of the cells. This was found in the neurons and the glial cells of the brain, although neuronal cells showed more coagulative changes and astrocyte swelling. The appearance of dark neurons is the first sign of ischemic aggression. Together with microvacuolation, it is a sign of a minimal ischemic lesion and is completely reversible. Cellular edema and coagulative changes in the neuron with clumping of the chromatin indicate more severe ischemic damage. In both groups, these signs were present but to a minor degree (maximum score of 2). These finding are reversible. Signs of real cell death such as nuclear shrinkage and pyknosis were almost absent.
The reaction of the glial cells to ischemia was characterized by different forms and grades of edema. The damage was more pronounced than in the neuronal cells, but probably the edema would disappear with longer reperfusion. Typical findings in the glial cells were cellular edema with swollen cell bodies and status spongiosus, which is a more severe form of edema. The white matter also showed edema, but no real destruction was noticed. Edema was present around blood vessels with collapse of the vessels. In previous studies [12], complete absence of histologic damage after CA of 70 minutes was reported, but the reperfusion period was 6 hours. A longer period of CA revealed cell necrosis and brain hemorrhage. Other studies [13] also report minor cell changes after CA.
Brain Perfusion During RCP
In previous experimental studies in dogs, Usui and colleagues [4, 5] obtained flow values between 10 and 20 mL • min-1 • 100 g-1 in the brain during RCP. The optimal perfusion pressure was found to be around 20 mm Hg. These data are different from ours, although we also used a perfusion pressure of 20 mm Hg. Using the colored microsphere technique, we could not detect brain flow values higher than 1 mL • min-1 • 100 g-1. Only in the medulla oblongata were flows between 1 and 2 mL • min-1 • 100 g-1 detected.
The discrepancy in results could be due to the different animal species used or to the different methods of flow measurement. The venous cerebral circulation is quite different in canine and primate species. In the venous drainage system of the brain in primates, three different systems can be recognized: the superficial cerebral veins, the deep cerebral veins, and the venous sinuses. The superficial cerebral veins drain the blood from the cerebral cortex and the underlying white matter into the venous sinuses. Deep cerebral veins drain the blood in a centripetal direction from the deep white matter, the basal ganglia, and the diencephalon toward the lateral ventricles. Large subependymal veins empty into the internal cerebral veins and together form the great cerebral vein (of Galen). This large vein empties into the dural sinuses. Both sinuses and veins lack valves.
The system of the cerebral venous sinuses is very complex. The upper part consisting of the sinuses sagittalis superior, sagittalis inferior, rectus occipitalis, and transversus comes together in the confluens sinuum; the inferior part comes together in the sinus cavernosus. The blood from these sinuses leaves the skull through the internal jugular vein. The external jugular vein, which is much smaller, drains the blood from the facial structures. An anterior jugular vein, which is very small, is usually present; it originates at the chin, drains the superficial structures of the face, and forms an arcus venosus juguli with the vein on the other side. It also branches to the external jugular vein. These three veins with the subclavian vein form the brachiocephalic trunk.
Between the internal and external jugular systems are different venovenous anastomoses: the plexus venosus caroticus internus, rete foraminis ovalis and plexus pterygoideus, plexus venosus canalis ovalis, and a direct anastomosis between both jugular veins through the retromandibular and posterior auricular veins. The jugular system is connected with the thoracic wall through an extended venous plexus around the spinal cord. Arteriovenous anastomoses are present at the level of the pia mater.
In dogs, the venous system is similar to that in humans but is not as well developed and as complex. There is no double-outflow system as in humans; the maxillary vein drains the blood from the whole head [14]. Therefore, the connection between the great maxillary vein, which was used in the experiments of Usui and associates [4, 5] for RCP, and the deep venous system of the brain is more direct. Venovenous anastomoses also exist, but are not as numerous and are less pronounced.
During RCP, we observed massive shunting most probably by way of the large connection between the internal and external jugular veins, the connections between these veins and the venous system of the spinal cord, the connections between the superficial venous sinuses and the external jugular vein (vena emissaria), and between other smaller plexuses. In total, more than 20 direct venovenous anastomoses are described in humans [15].
Another possible explanation for the discrepancy in flow data may be related to the use of hydrogen clearance by Usui and co-workers [4, 5]. The disadvantages of this technique are that flow is registered only in a small part of the brain and that the introduction of the electrode into the brain tissue can cause trauma to the tissue. This eventually induces false-positive or false-negative results [16]. The microsphere technique is widely accepted for organ flow measurements and allows a high spatial resolution. This technique is considered the best available for the assessment of brain flow in experimental conditions [16]. A disadvantage of the microsphere technique in our setting is that reperfusion after microsphere injection during RCP will dislodge the microspheres from the brain tissue provided RCP perfuses the brain. This forced us to terminate the experiment at the end of RCP in a subset of animals, excise the brain, and analyze the brain tissue for microsphere content. As mentioned already, this resulted in a very low microsphere content, which represented flows of less than 2 mL • min-1 • 100 g-1. During antegrade brain perfusion, regional flow in the different brain structures could be assessed, with similar results as in previous studies [13]. After cooling to 18°C, brain flow decreased significantly in all these regions. This reflects a severe reduction in oxygen consumption, which provides adequate brain protection during CA of 60 minutes, as was shown histologically.
Shunting During RCP
A remarkable finding during RCP in our experiments was that the largest fraction of RCP inflow returns through the inferior caval vein. The possible venovenous anastomoses responsible for this shunting have already been discussed. The least fraction of RCP inflow, however, returned through the aortic arch. This return cannot completely be considered outflow after brain tissue perfusion because microspheres are traced in this severely deoxygenated blood. Arteriovenous shunts at the level of the pia mater are probably responsible for this shunting. Studies in primates [17] describe functional arteriovenous shunts with a diameter of 70 µm in the pia mater and spinal cord. Massive venovenous shunting can be proved by an equilibrium of circulating microspheres in the inflow and outflow lines of the RCP system.
In the clinical setting, RCP is administered through the superior caval vein. In our study, however, we used bilateral internal jugular vein cannulation to avoid possible interference of competent valves that exist in the venous system [18, 19]. In primates, the existence of such valves is controversial [3, 18, 19]. However, failed RCP because of competent valves at the level of the internal jugular vein has been reported [20]. Our results show that selective cannulation of the internal jugular vein distal from the semilunar valve is still associated with massive shunting. Therefore, we conclude that shunting occurs at the level of the multiple venovenous anastomoses between deep and superficial venous drainage systems of the head.
|
Footnotes |
|---|
|
TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
|---|
Address reprint requests to Dr Flameng, Department of Cardiac Surgery, University Clinic Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.
|
References |
|---|
|
TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  P. J. Shah, A. L. Estrera, C. C. Miller III, T.-Y. Lee, A. D. Irani, R. Meada, and H. J. Safi Analysis of Ascending and Transverse Aortic Arch Repair in Octogenarians Ann. Thorac. Surg., September 1, 2008; 86(3): 774 - 779. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. De Paulis, A. Salica, D. Maselli, R. Scaffa, A. Bellisario, and L. Weltert Initial Experience of an Arterial Shunt for Bilateral Antegrade Cerebral Perfusion During Hypothermic Circulatory Arrest Ann. Thorac. Surg., February 1, 2008; 85(2): 624 - 627. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Pretre and M. I. Turina Deep Hypothermic Circulatory Arrest Card. Surg. Adult, January 1, 2008; 3(2008): 431 - 442. [Full Text]
|
|
|
|
|
|
D. K. Harrington, F. Fragomeni, and R. S. Bonser Cerebral Perfusion Ann. Thorac. Surg., February 1, 2007; 83(2): S799 - S804. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Yang, Z. Li, Y. Yang, R. Zhu, R. Summers, R. Deslauriers, and J. Ye Increased pressure during retrograde cerebral perfusion provides better preservation of the Na+, K+-ATPase activity Perfusion, November 1, 2006; 21(6): 319 - 324. [Abstract] [PDF]
|
|
|
|
 |
|
 K. Kitahori, S. Takamoto, H. Takayama, Y. Suematsu, M. Ono, N. Motomura, T. Morota, and K. Takeuchi A novel protocol of retrograde cerebral perfusion with intermittent pressure augmentation for brain protection J. Thorac. Cardiovasc. Surg., August 1, 2005; 130(2): 363 - 370. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R.S. Bonser and D.K. Harrington Editorial comment Eur. J. Cardiothorac. Surg., July 1, 2005; 28(1): 102 - 103. [Full Text] [PDF]
|
|
|
|
|
|
S. A. Kucuker, M. A. Ozatik, A. Saritas, and O. Tasdemir Arch repair with unilateral antegrade cerebral perfusion Eur. J. Cardiothorac. Surg., April 1, 2005; 27(4): 638 - 643. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Ye, Z. Li, Y. Yang, L. Yang, A. Turner, M. Jackson, and R. Deslauriers Use of a pH-stat strategy during retrograde cerebral perfusion improves cerebral perfusion and tissue oxygenation Ann. Thorac. Surg., May 1, 2004; 77(5): 1664 - 1670. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Hagl, N. Khaladj, M. Karck, K. Kallenbach, R. Leyh, M. Winterhalter, and A. Haverich Hypothermic circulatory arrest during ascending and aortic arch surgery: the theoretical impact of different cerebral perfusion techniques and other methods of cerebral protection Eur. J. Cardiothorac. Surg., September 1, 2003; 24(3): 371 - 378. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Murkin Retrograde cerebral perfusion: more risk than benefit? J. Thorac. Cardiovasc. Surg., September 1, 2003; 126(3): 631 - 633. [Full Text] [PDF]
|
|
|
|
|
|
D.K. Harrington, M. Bonser, A. Moss, M.T.E. Heafield, M.J. Riddoch, and R.S. Bonser Neuropsychometric outcome following aortic arch surgery: a prospective randomized trial of retrograde cerebral perfusion J. Thorac. Cardiovasc. Surg., September 1, 2003; 126(3): 638 - 644. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. F. Duebener, I. Hagino, K. Schmitt, T. Sakamoto, C. Stamm, D. Zurakowski, H.-J. Schafers, and R. A. Jonas Direct visualization of minimal cerebral capillary flow during retrograde cerebral perfusion: an intravital fluorescence microscopy study in pigs Ann. Thorac. Surg., April 1, 2003; 75(4): 1288 - 1293. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. B. Griepp Cerebral protection during aortic arch surgery J. Thorac. Cardiovasc. Surg., March 1, 2003; 125(90030): S36 - 38. [Full Text] [PDF]
|
|
|
|
|
|
R. Pretre and M. I. Turina Deep Hypothermic Circulatory Arrest Card. Surg. Adult, January 1, 2003; 2(2003): 401 - 412. [Full Text]
|
|
|
|
|
|
D. Spielvogel, M. N. Mathur, and R. B. Griepp Aneurysms of the Aortic Arch Card. Surg. Adult, January 1, 2003; 2(2003): 1149 - 1168. [Full Text]
|
|
|
|
|
|
A. L. Estrera, C. C. Miller III, T. T.T. Huynh, E. E. Porat, and H. J. Safi Replacement of the ascending and transverse aortic arch: determinants of long-term survival Ann. Thorac. Surg., October 1, 2002; 74(4): 1058 - 1065. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Tasdemir, A. Saritas, S. Kucuker, M. A. Ozatik, and E. Sener Aortic arch repair with right brachial artery perfusion Ann. Thorac. Surg., June 1, 2002; 73(6): 1837 - 1842. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. S. Bonser, C. H. Wong, D. Harrington, D. Pagano, M. Wilkes, T. Clutton-Brock, and M. Faroqui Failure of retrograde cerebral perfusion to attenuate metabolic changes associated with hypothermic circulatory arrest J. Thorac. Cardiovasc. Surg., May 1, 2002; 123(5): 943 - 950. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. Li, L. Yang, M. Jackson, R. Summers, M. Donnelly, R. Deslauriers, and J. Ye Increased pressure during retrograde cerebral perfusion in an acute porcine model improves brain tissue perfusion without increase in tissue edema Ann. Thorac. Surg., May 1, 2002; 73(5): 1514 - 1521. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Harrington, C. H. Wong, and R. S. Bonser Neurological Complications of Aortic Surgery Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2002; 6(1): 7 - 16. [Abstract] [PDF]
|
|
|
|
|
|
T. Hirotani, T. Kameda, S. Shirota, and T. Kumamoto Reply J. Thorac. Cardiovasc. Surg., March 1, 2002; 123(3): 587 - 587. [Full Text]
|
|
|
|
|
|
W. A. L. Soong, S. Uysal, and D. L. Reich Cerebral Protection During Surgery of the Aortic Arch Seminars in Cardiothoracic and Vascular Anesthesia, November 1, 2001; 5(4): 286 - 292. [Abstract] [PDF]
|
|
|
|
|
|
K. Ueno, S. Takamoto, T. Miyairi, T. Morota, K. Shibata, A. Murakami, and Y. Kotsuka Arterial blood gas management in retrograde cerebral perfusion: the importance of carbon dioxide Eur. J. Cardiothorac. Surg., November 1, 2001; 20(5): 979 - 985. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. L. Reich, S. Uysal, M. A. Ergin, and R. B. Griepp Retrograde cerebral perfusion as a method of neuroprotection during thoracic aortic surgery Ann. Thorac. Surg., November 1, 2001; 72(5): 1774 - 1782. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. P. Ehrlich, C. Hagl, J. N. McCullough, N. Zhang, H. Shiang, C. Bodian, and R. B. Griepp Retrograde cerebral perfusion provides negligible flow through brain capillaries in the pig J. Thorac. Cardiovasc. Surg., August 1, 2001; 122(2): 331 - 338. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
< |
