HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Mark F. Newman Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grocott, H. P. Articles by Newman, M. F. Search for Related Content PubMed PubMed Citation Articles by Grocott, H. P. Articles by Newman, M. F.

Ann Thorac Surg 1998;65:1645-1649
© 1998 The Society of Thoracic Surgeons

---

Original articles: cardiovascular

Cerebral Emboli and Serum S100ß During Cardiac Operations

^a Department of Anesthesiology, Duke Heart Center, Duke University Medical Center, Durham, North Carolina, USA

Accepted for publication February 1, 1998.

Address reprint requests to Dr Grocott, Duke University Medical Center, Box 3094, Durham, NC 27710
e-mail: (groco001{at}mc.duke.edu)

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. The glial protein S100ß has been used to estimate cerebral damage in a number of clinical settings. The purpose of this investigation was to determine the correlation between cerebral microemboli and S100ß levels during cardiac operations.

Methods. Transcranial Doppler ultrasonography was used to measure emboli in the right middle cerebral artery. Emboli counts (n = 111) were divided into five time periods: (1) incision to aortic cannulation; (2) aortic cannulation to cross-clamp onset; (3) cross-clamp onset to cross-clamp release; (4) cross-clamp release to decannulation; and (5) decannulation to chest closure. The level of S100ß (n = 156) was measured at baseline, at the end of cardiopulmonary bypass, then 150 and 270 minutes after cross-clamp release.

Results. The level of S100ß correlated with age, cardiopulmonary bypass time, cross-clamp time, and number of emboli at time period 2. Although cardiopulmonary bypass time was univariately associated with S100ß level, it became nonsignificant in a multivariable model that included age and cross-clamp time.

Conclusions. The correlation of S100ß level with emboli measured during cannulation (time period 2) supports the hypothesis that cannulation is a high-risk time period for cerebral injury.

	Introduction

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Central nervous system complications contribute substantially to morbidity associated with cardiopulmonary bypass (CPB). Neurocognitive complications have been reported in approximately 60% of patients at 1 week, and 30% of patients at 6 months after cardiac operation [1, 2]. There is increasing evidence that cerebral emboli account for a significant proportion of these complications. Transcranial Doppler ultrasonography has been used to detect microemboli in the middle cerebral artery of patients undergoing cardiac operation and microemboli have been correlated with adverse neurocognitive outcome [3].

The S100ß protein is present in glial and Schwann cells and is reported to have numerous functions, both in health and disease [4]. It is involved in promoting axonal growth, glial proliferation, neuronal differentiation, and calcium homeostasis [5–7]. Its presence in blood or cerebrospinal fluid (CSF) has been found after cardiac operation, stroke, subarachnoid hemorrhage, coma after cardiac arrest, and several other neurologic disorders, thus supporting its role as a marker for central nervous system injury [8–12].

Factors associated with an increase in S100ß level after cardiac operations have been poorly elucidated, with age and CPB time inconsistently related to its elevation. The purpose of this study was to determine the relationship between cerebral microemboli and serum S100ß levels during cardiac operations.

	Material and methods

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
After institutional review board approval and written informed consent, patients undergoing elective coronary artery bypass grafting were studied. Patients were premedicated with oral diazepam (0.1 mg/kg) and methadone hydrochloride (0.1 mg/kg) 90 minutes before anesthesia induction. After placement of invasive monitors, anesthesia was induced with midazolam hydrochloride (50 to 75 µg/kg) and fentanyl citrate (5 to 10 µg/kg) intravenously and maintained by continuous intravenous infusions of midazolam (0.5 µg · kg^-1 · min^-1) and fentanyl (0.05 µg · kg^-1 · min^-1). Pancuronium bromide was given, as needed, to maintain complete neuromuscular blockade.

Transcranial Doppler ultrasonography (Neurogard; Medasonics Inc, Fremont, CA) was employed using a 2-MHz pulsed-wave transcranial Doppler probe with an 18-mm sample length gated at depths of 45 to 55 mm, placed over the right middle cerebral artery before cannulation for CPB. Continuous Doppler signals were recorded throughout operation and emboli determined using an automated counting system. Emboli counts were verified off-line using both audio and video methods. Total emboli counts were analyzed according to the following intervals: time 1, incision to aortic cannulation; time 2, aortic cannulation to aortic cross-clamp onset; time 3, aortic cross-clamp onset to aortic cross-clamp release; time 4, aortic cross-clamp release to decannulation; and time 5, decannulation to chest closure.

The perfusion apparatus consisted of a membrane oxygenator (Cobe CML, Cobe Laboratories, Lakewood, CO) and a Sarns 7000 max pump (3M Inc, Ann Arbor, MI). In all patients, an ascending aortic cannula (3M Inc) and an arterial line filter (SP 3840, Pall Biomedical Products Co, Glencove, NY) were used. Nonpulsatile perfusion at 2.4 L · min^-1 · m^-2 was maintained throughout CPB. Arterial carbon dioxide tension was maintained at 35 to 40 mm Hg (uncorrected for body temperature) with an oxygen tension of 150 to 250 mm Hg. Mean arterial pressure was maintained at 50 to 90 mm Hg during CPB. Patients were cooled to 32°C during bypass and rewarmed to a nasopharyngeal temperature of 37°C (bladder temperature, 36°C) before CPB was discontinued. A crystalloid CPB prime designed to achieve a hematocrit of 0.18 or higher during CPB was used. Packed red blood cells were added when necessary to achieve the desired hematocrit.

Blood samples for S100ß determinations were taken at baseline (after induction of anesthesia but before surgical incision), at the end of CPB, and 150 and 270 minutes after cross-clamp removal. Collected blood was centrifuged (10,000 g) with the resulting supernatant immediately frozen at -70°C until analysis was completed. Serum S100ß was determined using an immunoradiometric assay (Sangtec Medical, Lund, Sweden). The assay has been described in detail previously [13].

The highest measured S100ß level (S100ßmax) (from any of the time intervals) was used for subsequent statistical comparisons; the S100ß integrated area under the time curve and the sum of the four S100ß levels were also considered for analysis but did not appear as informative. Neither S100ß nor emboli count was normally distributed, being highly positively skewed by several very high measurements. As a result, natural logarithm (ln) transformations of these measures were used to give normal distributions for subsequent statistical analysis. Because a value of zero occurred in one or both measures in certain patients (and ln(0) is indeterminate), a value of one was added to each value before transformation. The ln(1) = 0; therefore, the results would not be affected.

Tests of univariate association (Pearson correlation coefficients) were calculated between the S100ßmax and emboli counts at each of the periods. The correlation coefficient was also calculated for the total emboli count. Association was similarly tested between S100ßmax and CPB time, cross-clamp time, and age, with significance unadjusted for multiple comparisons, with a p value less than 0.05. The nonparametric Spearman correlation was also performed on the non-ln transformed values and yielded the same results. Multivariable linear regression was used to test the association between S100ß max and the factors that suggested univariate association at a p value less than 0.10.

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
The demographics and S100ß results obtained on 156 patients are presented in Table 1. Because of transcranial Doppler availability and technical limitations, emboli data were obtained on only 111 of these patients. The emboli counts and their association with S100ß levels for each of the time intervals are presented in Table 2. Both the time 2 emboli and the total emboli count were significantly correlated with S100ß level (p = 0.022, r = 0.218 and p = 0.03, r = 0.206, respectively). The S100ßmax occurred at the end of CPB in all but 7 patients, where the 150-minute sample was maximum in 6 patients, and the 270-minute post–cross-clamp release sample was maximum in 1 patient. S100ßmax ranged from 0 to 13.5 µg/L with a median, mean, and standard deviation of 2.5, 3.0, and 2.5 µg/L, respectively.

View larger version (16K): [in this window] [in a new window]   Fig 1. Univariate correlation between serum S100ß level (µg/L) and cerebral emboli during the time period (time 2) from aortic cannulation to aortic cross-clamp onset (p = 0.022, r = 0.218). Both the x-axis and y-axis are depicted on natural log scales because of the positively skewed data.

View larger version (16K): [in this window] [in a new window]   Fig 2. Univariate correlation between serum S100ß level (µg/L) and age (years) (p = 0.002, r = 0.248). The y-axis is depicted on a natural log scale because of the positively skewed data.

View larger version (17K): [in this window] [in a new window]   Fig 3. Univariate correlation between serum S100ß level (µg/L) and cross-clamp time (min) (p = 0.0001, r = 0.406). The y-axis is depicted on a natural log scale because of the positively skewed data.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

There are several possible explanations for S100ß level elevations after cardiac operations. Cerebral damage may lead to increased release of S100ß into the cerebral extracellular fluid, which then enters the circulation through focal breaches in the blood/brain barrier caused by emboli-induced ischemia. It may also increase in cerebral extracellular fluid, flow into the CSF, then drain into the cerebral and systemic venous circulations, without any interruption in the blood/brain barrier. The increases may also occur because of generalized increases in permeability of the blood/brain barrier caused by CPB [16], which would cause increased serum markers without any cellular cerebral damage. It is likely, however, that all of these mechanisms contribute to increases in serum S100ß level. Each may produce, however, a different time course and pattern of S100ß level elevation.

The kinetics of S100ß release into the circulation may have important implications in its ability to diagnose cerebral damage. Timing of increases in S100ß levels is different after various cerebral insults performed in animals. Increases after traumatic injury were seen much earlier than increases after focal ischemia in rats [17]. In the study by Johnsson and colleagues [8] on humans and cardiac operations, late increases corresponded to neurologic abnormalities. Further work is needed to define the optimal timing of diagnostic tests as little extended sampling data exist in patients undergoing cardiac operations.

Because of the association between emboli and S100ß levels, this study lends some support to the hypothesis that cerebral damage (measurable by S100ß level elevations) occurs as a result of cerebral emboli and that areas of the brain injured by microemboli release S100ß from damaged glial cells. Although it may not indicate neuronal damage directly, S100ß level elevations and neuronal damage associations have been investigated in both animal [17] and human studies. Human studies have included examining the relationship between S100ß level elevations and neuronal damage seen in acute stroke [9], head injury [18], transient ischemic attacks [10], subarachnoid and intracerebral hemorrhage [10], coma after cardiac arrest [11], as well as Alzheimer’s disease [19] and Down’s syndrome [12]. In this study we chose to measure S100ß primarily based on its availability and published experience. There is a possibility that using a more specific indicator of neuronal injury, such as neuron-specific enolase, may have shown better correlation with emboli. However, the ability of S100ß to determine cerebral injury and outcome after stroke has recently been demonstrated to be better than that of neuron-specific enolase [9]. One cannot discount the ability of S100ß to correlate with cerebral injury solely on the basis of its presumed lack of specificity for neuronal injury.

Cerebral microemboli have been demonstrated to be associated with neurocognitive dysfunction after cardiac operations [20]. The mechanism for this dysfunction is likely attributable to small but numerous areas of focal cerebral ischemia as a result of embolic occlusion of the cerebral vessels. This, however, has never been definitely proven, although one group of researchers has demonstrated microvascular occlusion in postmortem brain samples [3].

By dividing the emboli analysis into time periods based on cannulation and CPB events, we may have helped define an at-risk period for brain injury. Cannulation is a time when large numbers of emboli are generated. Our association with emboli number during cannulation (time 2) and S100ß level elevations is consistent with this. We speculate that during cannulation more damaging particulate emboli are produced, leading to more severe and prolonged occlusion of cerebral vessels with subsequent brain injury. Gaseous emboli, which are produced throughout CPB but especially after cross-clamp removal, may cause more temporary occlusion without the same degree of injury. Because of limitations in currently available transcranial Doppler technology, we were not able to differentiate quantitatively between particulate or gaseous emboli; therefore, we cannot confidently conclude that particulate emboli were responsible for the S100ß level elevations.

The univariate association of serum S100ß level with CPB time is similar to that described by previous investigators [13]. It has not been a consistent finding in all studies, however [15]. The patient numbers in our study allowed multivariate analysis to be performed, after which the CPB time association became nonsignificant, being replaced by cross-clamp duration. The stronger cross-clamp duration correlation may be related to the fact that a large percentage of time on bypass is spent with the cross-clamp applied. As our CPB technique is nonpulsatile, with longer cross-clamp times there is a longer period of time in which the CPB flow is nonpulsatile. One can speculate that this is more damaging because of its nonphysiologic characteristics. Before and particularly after cross-clamp release, some physiologic pulsation occurs as the heart regains its normal rhythm during the rewarming phase before discontinuation of CPB. Longer cross-clamp times also occur during more complex operations when more bypass grafts are carried out, although the number of grafts was not a significant association with S100ß level increases. Almost every graft requires a new aortic proximal anastomotic site, which in itself can lead to further emboli production from an atheromatous aorta.

The association of S100ß level increases and advancing age is a very important finding. Age-related changes in S100ß levels have been described in several reports. Kato and colleagues [21] described selective increases in S100ß protein level in aging rats. Sheng and associates [22] showed similar increases in brain tissue S100ß level in humans. Van Engelen and colleagues [23] described aging-associated increases in S100ß level in CSF, suggesting that age-specific normal values should be used to diagnose accurately increases in CSF S100ß level. Unlike tissue and CSF measurements, age-related changes in baseline serum S100ß level have both been described previously. Previous studies that reported S100ß level elevations after cardiac operations have not had sufficient enrollment to account for any age-related effects in multivariable analysis. Taggart and colleagues [15] did show a weak but significant association with age. Our association was much stronger. Age is known to be a risk factor for increased neurologic injury [24] and is the most important predictor of stroke in a recent prospective analysis of stroke during coronary artery bypass grafting [25]. It is thought that advanced atherosclerosis contributes to this risk in the elderly, but an age-related change in the CBF response to mean arterial pressure has also been demonstrated, suggesting that the elderly may experience periods of cerebral hypoperfusion during hypotension earlier than younger patients [26].

Although the release of S100ß may indeed indicate that damage to brain has occurred, the limitation of using S100ß level to estimate injury is that it is an astroglial protein and only indirectly related to neuronal injury. Although no neurocognitive outcomes are reported here, its association with cerebral microemboli has been described previously [20]. Correlation of S100ß level with definitive neurologic or neurocognitive dysfunction in cardiac operations has yet to be performed in any large-scale study, although one small study reports such a correlation [8]. Until such a study is performed, one must be cautious at assuming the degree to which S100ß can measure definitive neurologic outcomes during cardiac operations.

In summary, we demonstrated a positive correlation between elevations in serum S100ß level and cerebral emboli, advanced age, and duration of cross-clamp during coronary artery bypass grafting.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This work was supported by National Institutes of Health grants NIH GM08600-02 and NIH R01-AG09663.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

1. Borowicz L., Goldsborough M., Selenes O., McKhann G. Neuropsychological changes after cardiac surgery: a critical review. J Cardiothorac Vasc Anesth 1996;10:105-112.[Medline]
2. Nussmeier N. Adverse neurologic events: risks of intracardiac versus extracardiac surgery. J Cardiothorac Vasc Anesth 1996;10:31-37.[Medline]
3. Moody D., Bell M., Challa V., Johnson W., Prough D. Brain microemboli during cardiac surgery or aortography. Ann Neurol 1990;28:477-486.[Medline]
4. Fano G., Biocca S., Fulle S., Mariggio M., Belia S., Calissano P. The S-100: a protein family in search of a function. Prog Neurobiol 1995;46:71-82.[Medline]
5. Fano G., Mariggio M., Angelella P., Antonica N., Fulle S., Calissano P. The S-100 protein causes an increase of intracellular calcium and death of PC12 cells. Neuroscience 1993;53:919-925.[Medline]
6. Haglid K., Yang Q., Hamberger A., Bergman S., Widerberg A., Danielson N. S-100ß stimulates neurite outgrowth in the rat sciatic nerve grafted with acellular muscle transplants. Brain Res 1997;753:196-201.[Medline]
7. Selinfreund R., Barger S., Pledger W., Van Eldik L. Neurotrophic protein S100ß stimulates glial cell proliferation. Proc Natl Acad Sci 1991;88:3554-3558.[Abstract/Free Full Text]
8. Johnsson P., Lindqvist C., Lindgren A., et al. Cerebral complications after cardiac surgery assessed by S-100 and NSE levels in blood. J Cardiothorac Vasc Anesth 1995;9:694-699.[Medline]
9. Missler U., Wiesmann M., Friedrich C., Kaps M. S-100 protein and neuron-specific enolase concentrations in blood as indicators of infarction volume and prognosis in acute ischemic stroke. Stroke 1997;28:1956-1960.[Abstract/Free Full Text]
10. Persson L., Hardemark H., Gustafsson G., et al. S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system. Stroke 1987;18:911-918.[Abstract/Free Full Text]
11. Karkela J., Book E., Kaukinen S. CSF and serum brain-specific creatine kinase isoenzyme (CK-BB), neuron-specific enolase (NSE) and neural cell adhesion molecule (NCAM), as prognostic markers for hypoxic brain injury after cardiac arrest in man. J Neurol Sci 1993;116:100-109.[Medline]
12. Griffin W., Stanley L., Ling C., et al. Brain interleukin-1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease. Proc Natl Acad Sci 1989;86:7611-7615.[Abstract/Free Full Text]
13. Westaby S., Johnsson P., Parry A., et al. Serum S-100 protein: a potential marker for cerebral events during cardiopulmonary bypass. Ann Thorac Surg 1996;61:88-92.[Abstract/Free Full Text]
14. Taggart D., Bhattacharya K., Meston N., et al. Serum S-100 protein concentration after cardiac surgery: a randomized trial of arterial line filtration. Eur J Cardiothorac Surg 1997;11:645-649.[Abstract]
15. Taggart D., Mazel J., Bhattacharya K., et al. Comparison of serum S-100B levels during CABG and intracardiac operations. Ann Thorac Surg 1997;63:492-496.[Abstract/Free Full Text]
16. Laursen H., Bodker A., Andersen K., Waaben J., Husum B. Brain oedema and blood-brain barrier permeability in pulsatile and nonpulsatile cardiopulmonary bypass. Scand J Thorac Cardiovasc Surg 1986;20:161-166.[Medline]
17. Hardemark H.-G., Ericsson N., Kotwica Z., et al. S-100 protein and neuro-specific enolase in CSF after experimental traumatic or focal ischemia brain damage. J Neurosurg 1989;71:727-731.[Medline]
18. Ingebrigtsen T., Romner B. Serial S-100 protein serum measurements related to early magnetic resonance imaging after minor head injury. J Neurosurg 1996;85:945-948.[Medline]
19. Mrak R., Sheng J., Griffin W. Correlation of astrocytic S100ß expression with dystrophic neurites in amyloid plaques of Alzheimer’s disease. J Neuropath Exp Neurol 1996;55:273-279.[Medline]
20. Pugsley W., Klinger L., Paschalis C., et al. Microemboli and cerebral impairment during cardiac surgery. Vasc Surg 1990;24:34-43.
21. Kato K., Suzuki F., Morishita R., Asano T., Sato T. Selective increase in S-100ß protein by aging in rat cerebral cortex. J Neurochem 1990;54:1269-1274.[Medline]
22. Sheng J., Mrak R., Rovnaghi C., Kozlowska E., Van Eldik L., Griffin S. Human brain ßS100 and ßS100 mRNA expression increases with age: pathogenic implications for Alzheimer’s disease. Neurobiol Aging 1996;17:359-363.[Medline]
23. Van Engelen B., Lamers K., Gabreels F., Wevers R., van Geel W., Borm G. Age-related changes in neuron-specific enolase, S-100 protein, and myelin basic protein concentrations in cerebrospinal fluid. Clin Chem 1992;38:813-816.[Abstract/Free Full Text]
24. Heyer E., Delphin E., Adams D. Cerebral dysfunction after cardiac operations in elderly patients. Ann Thorac Surg 1995;60:1716-1722.[Abstract/Free Full Text]
25. Newman M., Wolman R., Kanchuger M., et al. Multicenter preoperative stroke risk index for patients undergoing coronary artery bypass surgery. Circulation 1996;94(Suppl 2):74-80.
26. Newman M., Kramer D., Croughwell N., et al. Differential age effects of mean arterial pressure and rewarming on cognitive dysfunction after cardiac surgery. Anesth Analg 1995;81:236-242.[Abstract]

This article has been cited by other articles:

				J. W. Hammon Extracorporeal Circulation: Perfusion System Card. Surg. Adult, January 1, 2008; 3(2008): 350 - 370. [Full Text]

				R. C. Groom and Cardiovascular Disease Study Group A Systematic Approach to the Understanding and Redesigning of Cardiopulmonary Bypass Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2005; 9(2): 159 - 161. [Abstract] [PDF]

				E. Iriz, F. Kolbakir, H. Akar, B. Adam, and H. T. Keceligil Comparison of Hydroxyethyl Starch and Ringer Lactate as a Prime Solution Regarding S-100{beta} Protein Levels and Informative Cognitive Tests in Cerebral Injury Ann. Thorac. Surg., February 1, 2005; 79(2): 666 - 671. [Abstract] [Full Text] [PDF]

				R. Motallebzadeh, R. Kanagasabay, M. Bland, J. C. Kaski, and M. Jahangiri S100 protein and its relation to cerebral microemboli in on-pump and off-pump coronary artery bypass surgery Eur. J. Cardiothorac. Surg., March 1, 2004; 25(3): 409 - 414. [Abstract] [Full Text] [PDF]

				M. Schoenburg, B. Kraus, A. Muehling, U. Taborski, H. Hofmann, G. Erhardt, S. Hein, M. Roth, P. R. Vogt, G. F. Karliczek, et al. The dynamic air bubble trap reduces cerebral microembolism during cardiopulmonary bypass J. Thorac. Cardiovasc. Surg., November 1, 2003; 126(5): 1455 - 1460. [Abstract] [Full Text] [PDF]

				T. Ueno, Y. Iguro, H. Yamamoto, R. Sakata, Y. Kakihana, and K. Nakamura Serial measurement of serum S-100B protein as a marker of cerebral damage after cardiac surgery Ann. Thorac. Surg., June 1, 2003; 75(6): 1892 - 1897. [Abstract] [Full Text] [PDF]

				E. A. Hessel II and L. H. Edmunds Jr. Extracorporeal Circulation: Perfusion Systems Card. Surg. Adult, January 1, 2003; 2(2003): 317 - 338. [Full Text]

				M. A. Ozatik, O. Tarcan, A. Kale, G. Askon, M. Balco, A. Undar, D. S. Kucukaksu, E. Sener, and O. Tasdemir Do S100{beta} protein level increases due to inflammation during cardiopulmonary bypass occur without any neurological deficit? Perfusion, September 1, 2002; 17(5): 335 - 338. [Abstract] [PDF]

				G. S. Aldea, L. O. Soltow, W. L. Chandler, C. M. Triggs, C. R. Vocelka, G. I. Crockett, Y. T. Shin, W. E. Curtis, and E. D. Verrier Limitation of thrombin generation, platelet activation, and inflammation by elimination of cardiotomy suction in patients undergoing coronary artery bypass grafting treated with heparin-bonded circuits J. Thorac. Cardiovasc. Surg., April 1, 2002; 123(4): 742 - 755. [Abstract] [Full Text] [PDF]

				D. B. Mark and M. F. Newman Protecting the Brain in Coronary Artery Bypass Graft Surgery JAMA, March 20, 2002; 287(11): 1448 - 1450. [Full Text] [PDF]

				A. T. Tang, M. Devbhandari, and S. K Ohri Complete Myocardial Revascularization in Severe Arteriopathy Asian Cardiovasc Thorac Ann, December 1, 2001; 9(4): 315 - 317. [Abstract] [Full Text] [PDF]

				R. W. Kim, D. C. Mariconda, G. Tellides, G. S. Kopf, M. L. Dewar, Z. Lin, and J. A. Elefteriades Single-clamp technique does not protect against cerebrovascular accident in coronary artery bypass grafting Eur. J. Cardiothorac. Surg., July 1, 2001; 20(1): 127 - 132. [Abstract] [Full Text] [PDF]

				R. E. Anderson, L.-O. Hansson, O. Nilsson, J. Liska, G. Settergren, and J. Vaage Increase in serum S100A1-B and S100BB during cardiac surgery arises from extracerebral sources Ann. Thorac. Surg., May 1, 2001; 71(5): 1512 - 1517. [Abstract] [Full Text] [PDF]

				M. I. Dar, T. Gillott, F. Ciulli, and G. J. Cooper Single aortic cross-clamp technique reduces S-100 release after coronary artery surgery Ann. Thorac. Surg., March 1, 2001; 71(3): 794 - 796. [Abstract] [Full Text] [PDF]

				M. S. Ali, M. Harmer, and R. Vaughan Serum S100 protein as a marker of cerebral damage during cardiac surgery Br. J. Anaesth., August 1, 2000; 85(2): 287 - 298. [Abstract] [Full Text] [PDF]

				R. E. Anderson, L.-O. Hansson, J. Liska, G. Settergren, and J. Vaage The effect of cardiotomy suction on the brain injury marker S100{beta} after cardiopulmonary bypass Ann. Thorac. Surg., March 1, 2000; 69(3): 847 - 850. [Abstract] [Full Text] [PDF]

				J. W. Hammon Jr and D. Stump COMMENTARY: BIOCHEMICAL MARKERS OF BRAIN INJURY AFTER CARDIAC SURGERY J. Thorac. Cardiovasc. Surg., January 1, 2000; 119(1): 130 - 131. [Full Text] [PDF]

				S. Westaby, K. Saatvedt, S. White, T. Katsumata, W. van Oeveren, N. K. Bhatnagar, S. Brown, and P. W. Halligan IS THERE A RELATIONSHIP BETWEEN SERUM S-100{beta} PROTEIN AND NEUROPSYCHOLOGIC DYSFUNCTION AFTER CARDIOPULMONARY BYPASS? J. Thorac. Cardiovasc. Surg., January 1, 2000; 119(1): 132 - 137. [Abstract] [Full Text] [PDF]

				M. Herrmann, A. D. Ebert, D. Tober, J. Hann, and C. Huth A contrastive analysis of release patterns of biochemical markers of brain damage after coronary artery bypass grafting and valve replacement and their association with the neurobehavioral outcome after cardiac surgery Eur. J. Cardiothorac. Surg., November 1, 1999; 16(5): 513 - 518. [Abstract] [Full Text] [PDF]

				M. Takahashi, A. Chamczuk, Y. Hong, and G. Jackowski Rapid and Sensitive Immunoassay for the Measurement of Serum S100B Using Isoform-specific Monoclonal Antibody Clin. Chem., August 1, 1999; 45(8): 1307 - 1311. [Full Text] [PDF]

				R. E. Anderson, L.-O. Hansson, and J. Vaage Release of S100B during coronary artery bypass grafting is reduced by off-pump surgery Ann. Thorac. Surg., June 1, 1999; 67(6): 1721 - 1725. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Mark F. Newman Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grocott, H. P. Articles by Newman, M. F. Search for Related Content PubMed PubMed Citation Articles by Grocott, H. P. Articles by Newman, M. F.