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• W2028122243 abstract "HomeStrokeVol. 43, No. 8Oxygen Imaging by MRI Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessReview ArticlePDF/EPUBOxygen Imaging by MRICan Blood Oxygen Level-Dependent Imaging Depict the Ischemic Penumbra? Ulf Jensen-Kondering, MD and Jean-Claude Baron, MD, ScD, FMedSci Ulf Jensen-KonderingUlf Jensen-Kondering From the Stroke Research Group (U.J.-K., J.-C.B.), University of Cambridge, Department of Clinical Neurosciences, Addenbrooke's Hospital, Cambridge, UK; Wolfson Brain Imaging Centre (U.J.-K.), Department of Clinical Neurosciences, University of Cambridge, UK; and INSERM U894 (J.-C.B.), Université Paris, Descartes, Sorbonne Paris Cite, Paris, France. Search for more papers by this author and Jean-Claude BaronJean-Claude Baron From the Stroke Research Group (U.J.-K., J.-C.B.), University of Cambridge, Department of Clinical Neurosciences, Addenbrooke's Hospital, Cambridge, UK; Wolfson Brain Imaging Centre (U.J.-K.), Department of Clinical Neurosciences, University of Cambridge, UK; and INSERM U894 (J.-C.B.), Université Paris, Descartes, Sorbonne Paris Cite, Paris, France. Search for more papers by this author Originally published15 May 2012https://doi.org/10.1161/STROKEAHA.111.632455Stroke. 2012;43:2264–2269Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 IntroductionMapping the ischemic penumbra (ie, the neurophysiologically silent but still viable ischemic tissue) is increasingly part of routine assessment in suspected acute stroke, although whether this approach is cost-effective is still unclear.1,2 The penumbra is characterized by both low cerebral blood flow (CBF; <20 mL · 100 g−1 · min−1) and elevated oxygen extraction fraction (OEF).3 The latter is considered a critical marker of tissue viability and is therefore a key imaging target. The penumbra was originally documented in humans using positron emission tomography (PET),2,3 a validated method to map CBF, OEF and cerebral metabolic rate of oxygen (CMRO2),4 but clinical access to PET is scarce. Consequently, MR-based diffusion and perfusion imaging (PWI) and CT-based perfusion imaging are widely used as substitutes.1 However, both methods have limitations for penumbra imaging2 and do not directly assess oxygen metabolism.A method combining the advantages of MR and the ability to map OEF would therefore be highly desirable. Blood oxygen level-dependent (BOLD) imaging has recently emerged as a possible candidate for this purpose. However, several BOLD techniques with different levels of validation, accuracy, and clinical applicability are in concurrent development, making the situation somewhat confusing. This review aims to clarify whether BOLD imaging might be of use to map oxygen in the clinical setting. We systematically review and critically discuss all studies published to date in English language, both experimental and clinical, that have applied BOLD in acute stroke. Because our focus is tissue oxygen metabolism, we do not address the T2*-weighted method to visualize leptomeningeal vessels,5 the mapping of ΔCMRO2 during physiological challenges,6 or the emerging 17O imaging method.7Principles of BOLD MRIOxyhemoglobin is diamagnetic, whereas deoxyhemoglobin (DHb) is paramagnetic. Transverse relaxation is sensitive to paramagnetic substances such as DHb,8 hence the acronym BOLD. Because high OEF results in increased DHb concentration in the end-capillaries and venules,9 it should be detectable using BOLD. Equation 1 describes the fraction of DHb (χDHb) in the microvasculature10:χDHb=1−saO2+m∗OEF∗SaO2where saO2 represents the oxygen saturation in arterial blood and m the fraction of oxygen extracted at a given point of the vascular bed. Assuming a linear oxygen extraction along the latter, theoretical maximum average m is 0.5, that is, under extreme ischemic conditions, m=0 at the arteriole and m=1 at the venule level (ie, svO2=0). The OEF is closely related to CMRO2, CBF, and the oxygen content of blood by Equation 2. The oxygen content of blood is typically approximately 18 mL O2/100 mL and is the product of the hemoglobin level, saO2, and oxygen-binding capacity (approximately 1.36 mL O2/g hemoglobin).OEF=CMRO2CBF∗CaO2Thus, in situations of maximum OEF and optimal SaO2, χDHb tends to its maximum of 50%. It follows that penumbral tissue should be detectable by DHb-sensitive imaging. A rise in χDHb will lead to a drop in signal intensity on images sensitive to transverse relaxation and affected tissues will appear hypointense.Experimental and Clinical Acute Stroke Studies Using BOLD MRI TechniquesA detailed account of each study appears in the online-only Data Supplement, and only summaries are presented here. Experimental studies are only reviewed in the present review if focal ischemia or controlled cerebral hypoperfusion was induced.T2 Blood Oxygen Level-Dependent ImagingT2 sequences are sensitive to a rise in χDHb. Although the signal drop is distinct, it is very small (a few percent). Hahn-echo sequences yield greater signal reduction than Carr Purcell Meirbloom Gill multiple echoes,11 and spin-echo sequences show a smaller signal reduction than gradient echo sequences.12Six experimental10,13–17 and 1 clinical18 study have been published using T2, none relevant since 2001 (online-only Data Supplement Table I). The former consistently showed a variable drop of T2 value immediately after vessel occlusion, up to 10% depending on field strength. This was followed 30 to 60 minutes later by a steady T2 increase due to vasogenic edema within the ischemic core or if CBF fell <30 mL · 100 g−1 · min−1 (determined with the H2 clearance method),14,16 whereas T2 remained low within the noninfarcted penumbral or mildly hypoperfused areas. In the clinical study,18 T2 hypointense lesions adjacent to the subcortical core were observed, possibly representing cortical penumbra.T2*T2* is 3- to 5-fold more sensitive to BOLD-related changes than T2,16 even at lower field strengths. Apart from scanning under baseline conditions, breathing challenges have been used to enhance the sensitivity of T2* imaging to depict the penumbra.T2* in Baseline ConditionsTwo experimental19,20 and 4 clinical reports21–24 using T2* (including prebolus arrival scans from PWI) have been published (online-only Data Supplement Table II). In the former, a T2* drop of up to 8% was consistently seen, even at low fields. This was followed 1 to 2 hours later by a gradual increase in T2*, similar to the increase in T2 described previously and also due to vasogenic edema. The clinical studies reported inconsistent results,21–24 and low T2* in the appropriate area has been observed in only a handful of patients despite the widespread use of PWI. This may partly reflect the particular sensitivity of T2* to vasogenic edema. Systemic hypoxia during scanning may facilitate identification of low T2*.22 The reported lack of agreement with PET-derived OEF24 further suggests prebolus arrival T2* may not have adequate sensitivity.T2* With Breathing ChallengeFive percent CO2, a vasodilatory stimulus widely used to test cerebrovascular reactivity, increases oxygen supply relative to demand and hence induces decreases in DHb concentration. It is speculated that under this challenge only viable tissue, but not damaged tissue, will exhibit T2* increase, because cerebrovascular reactivity is abolished in the latter only. In some experimental studies, an anoxic challenge was used instead, the hypothesis being that oxygenated tissue will display a T2* drop in comparison to preanoxic images, whereas already damaged tissue will not. Another sort of challenge is to deliver normobaric 100% oxygen (oxygen challenge [OC]), the hypothesis here being that viable (penumbral) tissue will avidly take up the extra oxygen supplied, in turn increasing the pre-OC reduced T2* signal as compared with core and oligemia.Eleven experimental studies have used T2* with breathing challenge25–35 (online-only Data Supplement Table III). During anoxic challenge, image intensity in T2*-weighted images significantly dropped in the core, penumbra, and healthy tissue, but these changes could not clearly differentiate these tissue types without the information from diffusion-weighted imaging. CO2 challenge induced no signal change in the ischemic core, whereas both the penumbra and healthy tissue displayed a signal increase, which again could not be well differentiated with T2* weighting alone. In contrast, OC induced a larger T2-weighted image intensity increase within the penumbra than in the other tissue compartments and seemingly allowed it to be differentiated from both the core and healthy tissue.34 A 40% OC provided sufficient signal change at the same time as avoiding some unwanted effects of 100%, particularly on blood pressure.25 The findings using OC have been validated against autoradiographic 14C-2-deoxyglucose mapping.33 Two clinical studies,36,37 both using OC, which has greater clinical applicability, have been published so far. The results supported some potential for penumbra mapping suggesting this method could be widely applied in the clinical setting, although with some caveats (see “Discussion”).T2′ Blood Oxygen Level-Dependent ImagingT2′ is equivalent to T2* with the major difference that it is corrected for the spin–spin T2 effects that develop within hours due to vasogenic edema. T2, T2* and T2′ are linked through Equation 3.38 Note that this method requires generating T2 and T2* maps followed by their voxel-based inversion and subtraction.1T2′=1T2∗−1T2(with1T2′=R2′)T2′ imaging has been used in 3 experimental studies39–41 and 3 clinical studies42–44 thus far (online-only Data Supplement Table IV). Normative values for T2′ in humans and rats have also been reported.44,45 Experimentally, T2′ was generally found to be decreased in the penumbra and, as expected, provided clearer findings than T2*. In the clinical studies, T2′ maps showed low signal in affected hemisphere areas expected to have high OEF (Figure). Furthermore, the T2′ lesion appeared to predict diffusion-weighted imaging lesion growth better than PWI.44 However, quantitative analyses did not show the expected significant differences among tissue compartments,43 whereas the T2′ maps obtained in the clinical setting were noisy and artifacted and their visual assessment moderately reproducible.44Download figureDownload PowerPointFigure. T2′ in acute stroke. Patient with proximal MCA occlusion. MRI was obtained 4.8 hours after symptom onset (T0) and again on Day 7 (T1). A, ADC lesion (T0); (B) TTP lesion (T0); (C) final infarct on FLAIR (T1); (D) T2′ at T0. Reproduced from Figure 3 in Geisler BS, Brandhoff F, Fiehler J, Saager C, Speck O, Rother J, et al. Blood-oxygen-level-dependent MRI allows metabolic description of tissue at risk in acute stroke patients. Stroke. 2006;37:1778–1784 with permission. MCA indicates middle cerebral artery; ADC, apparent diffusion coefficient; TTP, time-to-peak; FLAIR, fluid-attenuated inversion recovery.Magnetic Resonance CMRO2In this approach, a 2-dimensional multiecho gradient-echo/spin-echo sequence is used to derive svO2 from R2′ and the venous blood volume fraction and in turn OEF. Relative CMRO2 is then estimated by multiplying OEF by CBF (derived from standard PWI).46 Estimates of svO2 with this method have been experimentally validated against blood oximetry obtained in the cerebral venous sinuses.47 One experimental47 and 1 clinical48 stroke studies have been published so far (online-only Data Supplement Table V). In both studies, MR-CMRO2 provided meaningful images and relative CMRO2 estimates that agreed well with the PET literature.47,48DiscussionThe experimental and clinical literature reviewed infers that as predicted, all technical variants of BOLD MRI are able to detect elevated OEF as reduced intensity on T2 and T2* images. However, several factors common to essentially all BOLD techniques dim this apparent success. First, as discussed, vasogenic edema may develop as early as 2 hours after occlusion49 and obliterate the OEF-related changes, although it can theoretically be corrected using T2′ imaging. Second, local hematocrit may drop in low-flow areas50 and lead to an overestimation of OEF.51 Third, as further discussed subsequently, changes in cerebral blood volume that occur in stroke also influence the BOLD signal.52 Finally, decreased perfusion pressure slightly increases precapillary oxygen loss,53 altering the constant m in Equation 1. Although some of these issues may be partly circumvented by carrying out side-to-side comparisons, doing so gives up absolute quantification.Although T2 BOLD can in principle pick up T2 changes of a few percent, parenchymal T2 hypointensities have so far been reported in 1 clinical article of 9 patients only.18 There are 2 main reasons for this: (1) T2 relaxation is field strength-dependent54 and most experimental reports have used very high fields that are not clinically available yet; and (2) the absolute T2 changes are very small, and clinically available sequences might not be sensitive enough. It is thus questionable if this technique will ever translate to the clinical setting.In contrast, the T2* effect is in principle detectable at clinically available field strengths, yet the convincing T2* changes reported in animal studies are rarely reported in humans, and the 1 study testing T2* against PET found no correlation with OEF.24 Apart from T2* susceptibility artifacts, for example, on the brain surface, and artifacts from by magnetic field inhomogeneity, obliteration of T2* by early vasogenic edema probably largely explains this discrepancy, because clinical MR is rarely started within the first hour after symptom onset. A more promising alternative may therefore be T2′, which corrects for such spin–spin effects.T2* imaging with anoxic challenge appears to enable differentiation of core, penumbra, and healthy tissue better than CO2 breathing does, but neither is likely to ever have clinical application in stroke because both endanger the highly oxygen-dependent penumbra. In comparison, OC appears promising because it seems to differentiate penumbra from core, although perhaps less efficiently from oligemia as well, and is clinically applicable. However, several aspects of the method still need to be addressed and might confound its reliability. Particularly, the induced T2* changes are small in humans (approximately 2%), and the changes in OEF induced by hyperoxia can be difficult to disentangle from other effects that also cause T2* changes, namely (1) CBF increases in ischemic tissue; (2) hypercapnia; (3) local changes in hematocrit; and (4) local changes in cerebral blood volume, especially because cerebral blood volume may be elevated in penumbra, locally increasing the apparent response to OC due to a higher concentration of DHb. In addition, in this method, OC is delivered to the subject for diagnostic purposes, yet normobaric hyperoxia may influence the fate of the penumbra.55 Nevertheless, the T2* OC method clearly deserves further investigations.The T2′ method has shown potential in delineating hypoxic tissue although its ability to differentiate core, penumbra, and oligemia has not been clearly demonstrated. Preliminary clinical results show the expected signal changes and a reasonably good match with hypoperfusion and final infarct and T2′ may actually depict the penumbra better than PWI.44 However, T2′ is characterized by substantial image noise (Figure) because even small changes in T2* and T2 can lead to large changes in computed T2′ (Equation 3). Furthermore, T2*-weighted images are prone to substantial distortions, introducing additional errors. Although acquisition time for T2′ is not particularly long, head motion can lead to misalignment of the T2 and T2* images and hence additional T2′ noise. These drawbacks probably explain the reported modest interobserver agreement,44 which in turn calls into question the method's robustness for clinical applications, although deeper training in image reading might improve detection of artifacts and distortions. Regardless, this technique is clearly worth further investment.To date, 1 group only has published on the use of MR CMRO2, and <20 patients have been reported since it first appeared in 2003. Calculated relative CMRO2 for tissue at risk has been in agreement with historical PET data in both rodents and humans, lending support to the validity of the method. However, absolute quantification of OEF and CMRO2 still appears elusive, and the MR sequence used to estimate OEF suffers from poor signal-to-noise ratio. In addition, quantification of CBF with PWI is notoriously difficult, which together with the risk for misalignment of OEF with CBF images may introduce additional errors in CMRO2 estimates. Finally, based on the images published so far, the spatial resolution of the method appears limited.So far, indirect validation has been reported against the H2 clearance CBF method,14,1614C-2-deoxyglucose autoradiography,33 and sinus vein oxymetry47 for T2 BOLD, T2* with OC and MR CMRO2, respectively, and only the prebolus T2* technique has been directly compared with PET.24 However, back-to-back PET and MR in hyperacute stroke is extremely challenging, and accordingly scans in the latter study were acquired relatively late after stroke. Novel “hybrid” PET/MR systems, which allow simultaneous acquisition of both modalities, may prove useful in this respect. In any scenario, however, validation of hyperacute BOLD against PET will remain challenging, even in animal models. Thus, although using nonhuman primates would be optimal with 15O-PET,56 these models are extremely cumbersome and expensive and raise ethical issues. 15O-PET is feasible in rodents57 but is hampered by poor spatial resolution due to the highly energetic 15O positron. Alternatively, a PET hypoxia tracer such as 18F-fluoromisonidazole could be considered, but it has specific drawbacks.58ConclusionsAlthough T2 mapping was successfully used in animal studies and indirectly validated, its clinical translation is unlikely due to small signal at clinically available fields. T2*-weighted imaging has proven unreliable in acute stroke, including poor correlation with PET, probably from contamination by early vasogenic edema. T2′ mapping corrects for this effect and seems promising but appears limited by image noise and processing artifacts. T2*-weighted imaging with anoxic challenge or CO2 breathing is of experimental interest but clinical applications are unlikely. MR CMRO2 is in principle attractive but has methodological issues and has not been formally validated. T2*-weighted imaging with OC has yielded particularly interesting and promising results, but its signal may be affected by cerebral blood volume changes and formal validation is still missing, whereas its clinical value and applicability remain uncertain. Overall, therefore, BOLD MRI is promising to depict the penumbra but still requires formal validation and, although still difficult to predict, is unlikely to replace diffusion-weighted/PWI for clinical applications, at least in the near future.AcknowledgmentsWe thank T.A. Carpenter, PhD, for editing the article.Sources of FundingU.J.-K. is supported by the Deutsche Forschungsgemeinschaft (DFG Je 598/1-1).DisclosuresNone.FootnotesThe online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STROKEAHA.111.632455/-/DC1.Correspondence to Jean-Claude Baron, MD, ScD, FMedSci, Stroke Research Group, University of Cambridge, Department of Clinical Neurosciences, Addenbrooke's Hospital Box 83, Cambridge CB2 2QQ, UK. E-mail [email protected]ac.ukReferences1. Donnan GA, Baron JC, Ma H, Davis SM. Penumbral selection of patients for trials of acute stroke therapy. Lancet Neurol. 2009; 8: 261– 269.CrossrefMedlineGoogle Scholar2. Heiss WD. The concept of the penumbra: can it be translated to stroke management?Int J Stroke. 2010; 5: 290– 295.CrossrefMedlineGoogle Scholar3. Furlan M, Marchal G, Viader F, Derlon JM, Baron JC. Spontaneous neurological recovery after stroke and the fate of the ischemic penumbra. Ann Neurol. 1996; 40: 216– 226.CrossrefMedlineGoogle Scholar4. Baron JC, Frackowiak RS, Herholz K, Jones T, Lammertsma AA, Mazoyer B , et al. Use of PET methods for measurement of cerebral energy metabolism and hemodynamics in cerebrovascular disease. J Cereb Blood Flow Metab. 1989; 9: 723– 742.CrossrefMedlineGoogle Scholar5. Hermier M, Nighoghossian N, Derex L, Wiart M, Nemoz C, Berthezene Y , et al. Hypointense leptomeningeal vessels at T2*-weighted MRI in acute ischemic stroke. Neurology. 2005; 65: 652– 653.CrossrefMedlineGoogle Scholar6. Jain V, Langham MC, Floyd TF, Jain G, Magland JF, Wehrli FW. Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia. J Cereb Blood Flow Metab. 2011; 31: 1504– 1512.CrossrefMedlineGoogle Scholar7. Delapaz R, Gupte P. Potential application of (1)O MRI to human ischemic stroke. Adv Exp Med Biol. 2011; 701: 215– 222.CrossrefMedlineGoogle Scholar8. Ogawa S, Lee TM, Kay AR, Tank DW. Brain magnetic resonance imaging with contrast dependent on blood oxygenation. Proc Natl Acad Sci U S A. 1990; 87: 9868– 9872.CrossrefMedlineGoogle Scholar9. Baron JC, Bousser MG, Rey A, Guillard A, Comar D, Castaigne P. Reversal of focal ‘misery-perfusion syndrome' by extra–intracranial arterial bypass in hemodynamic cerebral ischemia. A case study with 15O positron emission tomography. Stroke. 1981; 12: 454– 459.LinkGoogle Scholar10. Grohn OH, Lukkarinen JA, Oja JM, van Zijl PC, Ulatowski JA, Traystman RJ , et al. Noninvasive detection of cerebral hypoperfusion and reversible ischemia from reductions in the magnetic resonance imaging relaxation time, T2. J Cereb Blood Flow Metab. 1998; 18: 911– 920.CrossrefMedlineGoogle Scholar11. Kennan RP, Zhong J, Gore JC. Intravascular susceptibility contrast mechanisms in tissues. Magn Reson Med. 1994; 31: 9– 21.CrossrefMedlineGoogle Scholar12. Bandettini PA, Wong EC, Jesmanowicz A, Hinks RS, Hyde JS. Spin-echo and gradient-echo EPI of human brain activation using bold contrast: a comparative study at 1.5 T. NMR Biomed. 1994; 7: 12– 20.CrossrefMedlineGoogle Scholar13. Calamante F, Lythgoe MF, Pell GS, Thomas DL, King MD, Busza AL , et al. Early changes in water diffusion, perfusion, T1, and T2 during focal cerebral ischemia in the rat studied at 8.5 T. Magn Reson Med. 1999; 41: 479– 485.CrossrefMedlineGoogle Scholar14. Grohn OH, Kettunen MI, Penttonen M, Oja JM, van Zijl PC, Kauppinen RA. Graded reduction of cerebral blood flow in rat as detected by the nuclear magnetic resonance relaxation time T2: a theoretical and experimental approach. J Cereb Blood Flow Metab. 2000; 20: 316– 326.CrossrefMedlineGoogle Scholar15. Grohn OH, Lukkarinen JA, Silvennoinen MJ, Pitkanen A, van Zijl PC, Kauppinen RA. Quantitative magnetic resonance imaging assessment of cerebral ischemia in rat using on-resonance T(1) in the rotating frame. Magn Reson Med. 1999; 42: 268– 276.CrossrefMedlineGoogle Scholar16. Kavec M, Grohn OH, Kettunen MI, Silvennoinen MJ, Penttonen M, Kauppinen RA. Use of spin echo T(2) BOLD in assessment of cerebral misery perfusion at 1.5 T. MAGMA. 2001; 12: 32– 39.CrossrefMedlineGoogle Scholar17. van der Toorn A, Verheul HB, Berkelbach van der Sprenkel JW, Tulleken CA, Nicolay K. Changes in metabolites and tissue water status after focal ischemia in cat brain assessed with localized proton MR spectroscopy. Magn Reson Med. 1994; 32: 685– 691.CrossrefMedlineGoogle Scholar18. Ida M, Mizunuma K, Hata Y, Tada S. Subcortical low intensity in early cortical ischemia. AJNR Am J Neuroradiol. 1994; 15: 1387– 1393.MedlineGoogle Scholar19. De Crespigny AJ, Wendland MF, Derugin N, Kozniewska E, Moseley ME. Real-time observation of transient focal ischemia and hyperemia in cat brain. Magn Reson Med. 1992; 27: 391– 397.CrossrefMedlineGoogle Scholar20. Roussel SA, van Bruggen N, King MD, Gadian DG. Identification of collaterally perfused areas following focal cerebral ischemia in the rat by comparison of gradient echo and diffusion-weighted MRI. J Cereb Blood Flow Metab. 1995; 15: 578– 586.CrossrefMedlineGoogle Scholar21. Tamura H, Hatazawa J, Toyoshima H, Shimosegawa E, Okudera T. Detection of deoxygenation-related signal change in acute ischemic stroke patients by T2*-weighted magnetic resonance imaging. Stroke. 2002; 33: 967– 971.LinkGoogle Scholar22. Wardlaw JM, von Heijne A. Increased oxygen extraction demonstrated on gradient echo (T2*) imaging in a patient with acute ischaemic stroke. Cerebrovasc Dis. 2006; 22: 456– 458.CrossrefMedlineGoogle Scholar23. Morita N, Harada M, Uno M, Matsubara S, Matsuda T, Nagahiro S , et al. Ischemic findings of T2*-weighted 3-Tesla MRI in acute stroke patients. Cerebrovasc Dis. 2008; 26: 367– 375.CrossrefMedlineGoogle Scholar24. Donswijk ML, Jones PS, Guadagno JV, Carpenter TA, Moustafa RR, Fryer TD , et al. T2*-weighted MRI versus oxygen extraction fraction PET in acute stroke. Cerebrovasc Dis. 2009; 28: 306– 313.CrossrefMedlineGoogle Scholar25. Baskerville TA, Deuchar GA, McCabe C, Robertson CA, Holmes WM, Santosh C , et al. Influence of 100% and 40% oxygen on penumbral blood flow, oxygen level, and T2*-weighted MRI in a rat stroke model. J Cereb Blood Flow Metab. 2011; 31: 1799– 1806.CrossrefMedlineGoogle Scholar26. de Crespigny AJ, Wendland MF, Derugin N, Vexler ZS, Moseley ME. Rapid MR imaging of a vascular challenge to focal ischemia in cat brain. J Magn Reson Imaging. 1993; 3: 475– 481.CrossrefMedlineGoogle Scholar27. Dijkhuizen RM, Berkelbach van der Sprenkel JW, Tulleken KA, Nicolay K. Regional assessment of tissue oxygenation and the temporal evolution of hemodynamic parameters and water diffusion during acute focal ischemia in rat brain. Brain Res. 1997; 750: 161– 170.CrossrefMedlineGoogle Scholar28. Harris NG, Lythgoe MF, Thomas DL, Williams SR. Cerebrovascular reactivity following focal brain ischemia in the rat: a functional magnetic resonance imaging study. Neuroimage. 2001; 13: 339– 350.CrossrefMedlineGoogle Scholar29. Jones RA, Muller TB, Haraldseth O, Baptista AM, Oksendal AN. Cerebrovascular changes in rats during ischemia and reperfusion: a comparison of BOLD and first pass bolus tracking techniques. Magn Reson Med. 1996; 35: 489– 496.CrossrefMedlineGoogle Scholar30. Lythgoe MF, Thomas DL, Calamante F, Pell GS, King MD, Busza AL , et al. Acute changes in MRI diffusion, perfusion, T(1), and T(2) in a rat model of oligemia produced by partial occlusion of the middle cerebral artery. Magn Reson Med. 2000; 44: 706– 712.CrossrefMedlineGoogle Scholar31. Ono Y, Morikawa S, Inubushi T, Shimizu H, Yoshimoto T. T2*-weighted magnetic resonance imaging of cerebrovascular reactivity in rat reversible focal cerebral ischemia. Brain Res. 1997; 744: 207– 215.CrossrefMedlineGoogle Scholar32. Robertson C, McCabe C, Lopez-Gonzalez MDR, Brennan D, Gallagher L, Holmes WM , et al. Co-registration of T2*-weighted MRI with [14C]-2-deoxyglucose autoradiography to validate delineation of the ischaemic penumbra. J Cereb Blood Flow Metab. 2009; 29: S87– S92.MedlineGoogle Scholar33. Robertson CA, McCabe C, Gallagher L, Lopez-Gonzalez Mdel R, Holmes WM, Condon B , et al. Stroke penumbra defined by an MRI-based oxygen challenge technique: 1. Validation using [14C]2-deoxyglucose autoradiography. J Cereb Blood Flow Metab. 2011; 31: 1778– 1787.CrossrefMedlineGoogle Scholar34. Santosh C, Brennan D, McCabe C, Macrae IM, Holmes WM, Graham DI , et al. Potential use of oxygen as a metabolic biosensor in combination with T2*-weighted MRI to define the ischemic penumbra. J Cereb Blood Flow Metab. 2008; 28: 1742– 1753.CrossrefMedlineGoogle Scholar35. Shen Q, Huang S, Du F, Duong TQ. Probing ischemic tissue fate with bold fMRI of brief oxygen challenge. Brain Res. 2011; 1425: 132– 141.CrossrefMedlineGoogle Scholar36. Dani KA, Santosh C, Brennan D, McCabe C, Holmes WM, Condon B , et al. T2*-weighted magnetic resonance imaging with hyperoxia in acute ischemic stroke. Ann Neurol. 2010; 68: 37– 47.CrossrefMedlineGoogle Scholar37. Dani K, Lopez R, Santosh C, Brennan C, McGabe C, Holmes W , et al. Oxygen challenge MRI provides a measure of the underlying haemodynamic and metabolic state of the tissue. International Stroke Conference 2011. 2011; 42: e287.Google Scholar38. Hoppel BE, Weisskoff RM, Thulborn KR, Moore JB, Kwong KK, Rosen BR. Measurement of regional blood oxygenation and cerebral hemodynamics. Magn Reson Med. 1993; 30: 715– 723.CrossrefMedlineGoogle Scholar39. Jensen UR, Liu JR, Eschenfelder C, Meyne J, Zhao Y, Deuschl G , et al. The correlation between quantitative T2′ and regional cerebral blood flow after acute brain ischemia in early reperfusion as demonstrated in a middle cerebral artery occlusion/reperfusion model of the rat. J Neurosci Methods. 2009; 178: 55– 58.CrossrefMedlineGoogle Scholar40. Grune M, van Dorsten FA, Schwindt W, Olah L, Hoehn M. Quantitative T*(2) and T′(2) maps during reversible focal cerebral ischemia in rats: separation of blood oxygenation from nonsusceptibility-based contributions. Magn Reson Med. 1999; 42: 1027– 1032.CrossrefMedlineGoogle Scholar41. Zhang J, Chen YM, Zhang YT. Blood-oxygenation-level-dependent-(BOLD-) based R2′ MRI study in monkey model of reversible middle cerebral artery occlusion. J Biomed Biotechnol. 2011; 2011: 318– 346.CrossrefGoogle Scholar42. Fiehler J, Geisler B, Siemonsen S" @default.
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• W2028122243 title "Oxygen Imaging by MRI" @default.
• W2028122243 cites W1963604937 @default.
• W2028122243 cites W1967505584 @default.
• W2028122243 cites W1967749348 @default.
• W2028122243 cites W1977288387 @default.
• W2028122243 cites W1983782549 @default.
• W2028122243 cites W1986475040 @default.
• W2028122243 cites W1986574952 @default.
• W2028122243 cites W1988609700 @default.
• W2028122243 cites W1991960473 @default.
• W2028122243 cites W1992906729 @default.
• W2028122243 cites W2018315879 @default.
• W2028122243 cites W2023571526 @default.
• W2028122243 cites W2024156895 @default.
• W2028122243 cites W2027683350 @default.
• W2028122243 cites W2032153246 @default.
• W2028122243 cites W2033539732 @default.
• W2028122243 cites W2035809927 @default.
• W2028122243 cites W2040405635 @default.
• W2028122243 cites W2048415901 @default.
• W2028122243 cites W2052453732 @default.
• W2028122243 cites W2055162855 @default.
• W2028122243 cites W2055217296 @default.
• W2028122243 cites W2058208915 @default.
• W2028122243 cites W2059377466 @default.
• W2028122243 cites W2062983361 @default.
• W2028122243 cites W2064533924 @default.
• W2028122243 cites W2065999262 @default.
• W2028122243 cites W2071714163 @default.
• W2028122243 cites W2076809978 @default.
• W2028122243 cites W2078369663 @default.
• W2028122243 cites W2079716456 @default.
• W2028122243 cites W2079842952 @default.
• W2028122243 cites W2080370764 @default.
• W2028122243 cites W2083510208 @default.
• W2028122243 cites W2084206570 @default.
• W2028122243 cites W2089551181 @default.
• W2028122243 cites W2090005971 @default.
• W2028122243 cites W2094636057 @default.
• W2028122243 cites W2101399987 @default.
• W2028122243 cites W2106324086 @default.
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