Статті в журналах: "Cerebral clearance"

1

Ito, Shingo, Kohta Matsumiya, Sumio Ohtsuki, Junichi Kamiie та Tetsuya Terasaki. "Contributions of Degradation and Brain-to-blood Elimination Across the Blood—Brain Barrier to Cerebral Clearance of Human Amyloid-β Peptide(1-40) in Mouse Brain". Journal of Cerebral Blood Flow & Metabolism 33, № 11 (21 серпня 2013): 1770–77. http://dx.doi.org/10.1038/jcbfm.2013.125.

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The purpose of the present study was to estimate the relative contributions of degradation and brain-to-blood elimination processes to the clearance of microinjected human amyloid-β peptide(1-40) (hAβ(1-40)) from mouse cerebral cortex, using a solid-phase extraction method together with a newly developed ultraperformance liquid chromatography/tandem mass spectrometry (UPLC/MS/MS) quantitation method for intact hAβ(1-40). The clearance rate constant of hAβ(1-40) in mouse cerebral cortex was determined to be 3.21 × 10−2/min under conditions where the saturable brain-to-blood elimination process across the blood–brain barrier (BBB) was expected to be saturated. Thus, this clearance rate constant should mainly reflect degradation. The [125I]hAβ(1-40) elimination rate across the BBB under nonsaturating conditions was determined to be 1.48 × 10−2/min. Inhibition studies suggested that processes sensitive to insulin and phosphoramidon, which inhibit neprilysin, insulin-degrading enzyme, and endothelin-converting enzyme, are involved not only in degradation, but also in elimination of hAβ(1-40). In conclusion, our results suggest a dominant contribution of degradation to cerebral hAβ(1-40) clearance, and also indicate that a sequential process of degradation and elimination of degradation products is involved in cerebral hAβ(1-40) clearance.

2

Zhou, Yuan, Wei Cai, Zilong Zhao, Tristan Hilton, Min Wang, Jason Yeon, Wei Liu, et al. "Lactadherin promotes microvesicle clearance to prevent coagulopathy and improves survival of severe TBI mice." Blood 131, no. 5 (February 1, 2018): 563–72. http://dx.doi.org/10.1182/blood-2017-08-801738.

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Key Points Lactadherin promotes the clearance of circulating microvesicles through phagocytosis. Promoting microvesicle clearance prevents coagulopathy, reduces cerebral edema, and improves neurological function in severe TBI mice.

3

YAMADA, Tsutomu, Tetsuji AWATA, and Takefumi MATSUO. "Significance of Antithrombin III Clearance in Cerebral Stroke." Journal of Japan Atherosclerosis Society 13, no. 4 (1985): 905–9. http://dx.doi.org/10.5551/jat1973.13.4_905.

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4

Voorhees Iii, William D., John A. DeFord, Mark W. Bleyer, J. A. Marchosky, and C. J. Moran. "Continuous monitoring of cerebral perfusion by thermal clearance." Neurological Research 15, no. 2 (April 1993): 75–82. http://dx.doi.org/10.1080/01616412.1993.11740113.

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5

Ko, Sang-Bae, H. Alex Choi, Raimund Helbok, J. Michael Schmidt, Neeraj Badjatia, Jan Claassen, E. Sander Connolly, Stephan A. Mayer, and Kiwon Lee. "Quantitative analysis of hemorrhage clearance and delayed cerebral ischemia after subarachnoid hemorrhage." Journal of NeuroInterventional Surgery 8, no. 9 (August 14, 2015): 923–26. http://dx.doi.org/10.1136/neurintsurg-2015-011903.

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ObjectiveInitial hemorrhage burden is an independent predictor for delayed cerebral ischemia (DCI) in patients with aneurysmal subarachnoid hemorrhage (aSAH). However, the association between clot clearance and DCI still remains to be elucidated.MethodsQuantitative analysis of hemorrhage volume and clot clearance was made in 116 consecutive patients who were scanned within 24 h from onset. Cisternal plus intraventricular hemorrhage volume (CIHV) was calculated as clot volume from the initial scans and scans performed up to 7 days after onset. Clot clearance was calculated as a percentage of residual clot volume compared with the clot volume on the initial scan. Initial clot volume and clot clearance were dichotomized to evaluate the association with DCI.ResultsIncluded patients were aged 55.5±15.2 years with a female preponderance (65.5%, (76/116)). The group with higher initial clot volume (≥17.2 mL) had higher odds for DCI (OR 4.3, 95% CI 1.3 to 14.0, p=0.015). However, the rate of DCI was not different between high and low clot clearance groups (26.7% vs 31.0%, p=0.66). Clot clearance rate was similar in patients with and without DCI up to day 7 after onset.ConclusionsThe quantitative clot clearance rate is not an independent predictor for DCI.

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Zampella, Edward, Richard B. Morawetz, Holt A. McDowell, H. E. van Zeiger, Pamela D. Varner, Robert D. McKay, and James H. Halsey. "The Importance of Cerebral Ischemia during Carotid Endarterectomy." Neurosurgery 29, no. 5 (November 1, 1991): 727–31. http://dx.doi.org/10.1227/00006123-199111000-00014.

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Abstract The importance of cerebral ischemia produced by carotid clamping during carotid endarterectomy remains controversial. In an effort to determine the importance of cerebral ischemia during carotid endarterectomy. 369 patients undergoing 431 consecutive carotid endarterectomies were studied by Xenon-133 (133Xe) clearance and electroencephalogram (EEG) monitoring. None of the patients was shunted during the procedures. The severity of ischemia as indicated by 133 Xe clearance from the ipsilateral hemisphere during 20 to 30 minutes of carotid occlusion did not predict the appearance of complications in this group of patients (x2 = 1.417: P = 0.841). There was a highly significant relationship between the depth of cerebral ischemia as demonstrated by 133Xe clearance and the appearance of abnormalities on the EEG (x2 = 42.043, P < 0.0001). In the subgroup of patients developing abnormalities as shown by EEG. there was a negative correlation (x2 = 17.495; P < 0.002) between reduction in blood flow and the appearance of complications, in that the higher the blood flow during occlusion the more likely the patient developing EEG changes would develop complications.

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EISENHUT, M. "Causes of reduced immune complex clearance in cerebral malaria." Parasite Immunology 31, no. 2 (February 2009): 59. http://dx.doi.org/10.1111/j.1365-3024.2008.01074.x.

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8

Asgari, Mahdi, Diane de Zélicourt, and Vartan Kurtcuoglu. "Possible contribution of astrocyte networks to cerebral metabolite clearance." Neurology, Psychiatry and Brain Research 22, no. 1 (March 2016): 15. http://dx.doi.org/10.1016/j.npbr.2015.12.034.

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Rosu, Gabriela-Camelia, Bogdan Catalin, Tudor Adrian Balseanu, Mogoanta Laurentiu, Margaritescu Claudiu, Samir Kumar-Singh та Pirici Daniel. "Inhibition of Aquaporin 4 Decreases Amyloid Aβ40 Drainage Around Cerebral Vessels". Molecular Neurobiology 57, № 11 (11 серпня 2020): 4720–34. http://dx.doi.org/10.1007/s12035-020-02044-8.

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Abstract Aquaporin-4 (AQP4) is located mainly in the astrocytic end-feet around cerebral blood vessels and regulates ion and water homeostasis in the brain. While deletion of AQP4 is shown to reduce amyloid-β (Aβ) clearance and exacerbate Aβ peptide accumulation in plaques and vessels of Alzheimer’s disease mouse models, the mechanism and clearing pathways involved are debated. Here, we investigated how inhibiting the function of AQP4 in healthy male C57BL/6 J mice impacts clearance of Aβ40, the more soluble Aβ isoform. Using two-photon in vivo imaging and visualizing vessels with Sulfurodamine 101 (SR101), we first showed that Aβ40 injected as a ≤ 0.5-μl volume in the cerebral cortex diffused rapidly in parenchyma and accumulated around blood vessels. In animals treated with the AQP4 inhibitor TGN-020, the perivascular Aβ40 accumulation was significantly (P < 0.001) intensified by involving four times more vessels, thus suggesting a generalized clearance defect associated with vessels. Increasing the injecting volume to ≥ 0.5 ≤ 1 μl decreased the difference of Aβ40-positive vessels observed in non-treated and AQP4 inhibitor-treated animals, although the difference was still significant (P = 0.001), suggesting that larger injection volumes could overwhelm intramural vascular clearance mechanisms. While both small and large vessels accumulated Aβ40, for the ≤ 0.5-μl volume group, the average diameter of the Aβ40-positive vessels tended to be larger in control animals compared with TGN-020-treated animals, although the difference was non-significant (P = 0.066). Using histopathology and ultrastructural microscopy, no vascular structural change was observed after a single massive dose of TGN-020. These data suggest that AQP4 deficiency is directly involved in impaired Aβ brain clearance via the peri-/para-vascular routes, and AQP4-mediated vascular clearance might counteract blood-brain barrier abnormalities and age-related vascular amyloidopathy.

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Redant, Sebastien, Xavier Beretta-Piccoli, Aude Mugisha, Rachid Attou, Ketiane Kaefer, David De Bels, Ashita Tolwani, and Patrick M. Honoré. "Hyperammonemia, the Last Indication of High-Volume Hemodiafiltration in Adult and Children: A Structured Review." Blood Purification 48, no. 4 (2019): 330–35. http://dx.doi.org/10.1159/000501390.

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Ammonia is a neurotoxic molecule that causes cerebral edema and encephalopathy. Ammonia is either produced in excess or poorly purified during severe hepatic insufficiency, poisoning, infection, and inborn errors of metabolism. During continuous renal replacement therapy, ammonia clearance is determined by the dialysate flow rate and the dialyzer surface area. Extra-renal blood purification for ammonia clearance has been studied in neonates with urea cycle disorders. Prognostic factors affecting patient outcome are thought to be the duration of coma, the patient’s clinical status prior to dialysis, and the ammonia removal rate. In this review, we discuss the various dialytic modalities used for ammonia clearance as well as the thresholds for initiating dialysis and the better strategy ensures rapid patient protection from cerebral edema and herniation induced by hyperammonemia.

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Kitagawa, Kazuo, Masayasu Matsumoto, Keisuke Kuwabara, Toshiho Ohtsuki, and Masatsugu Hori. "Delayed, but Marked, Expression of Apolipoprotein E is Involved in Tissue Clearance after Cerebral Infarction." Journal of Cerebral Blood Flow & Metabolism 21, no. 10 (October 2001): 1199–207. http://dx.doi.org/10.1097/00004647-200110000-00008.

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Clearance of infarct tissue would be an important process for tissue repair after a stroke. Delayed clearance may hamper reconstitution of the blood–brain barrier and glial boundary formation. Recent growing evidence has indicated that apolipoprotein E (APOE), a major apoprotein, plays an important role in lipid transport and homeostasis in the brain. The tissue in the infarction contains abundant lipids must be removed for tissue clearance. In the current study, the authors investigated APOE expression after focal ischemia and the functional role of APOE in tissue clearance using APOE-knockout mice. Expression of APOE was delayed, but marked, in immunohistochemistry and immunoblotting 7 days after permanent focal ischemia. Macrophages were found to express APOE in the infarct center. Infarct size was similar after focal ischemia between wild-type and APOE-knockout mice, although there was no APOE protein expression in knockout mice. However, clearance of infarct tissue 2 weeks after ischemia was significantly delayed in APOE-knockout mice compared with wild-type mice. The current study supports current thinking that APOE is a key molecule for tissue remodeling in the brain. Clearance of damaged tissue may be one of the important functions of APOE in the brain.

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Strong, A. J., G. Gibson, Susan A. Miller, and G. S. Venables. "Changes in Vascular and Metabolic Reactivity as Indices of Ischaemia in the Penumbra." Journal of Cerebral Blood Flow & Metabolism 8, no. 1 (February 1988): 79–88. http://dx.doi.org/10.1038/jcbfm.1988.10.

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The reactivities of cerebral cortical blood flow (hydrogen clearance) and of compensated NADH fluorescence to local cortical electrical stimulation were examined on the marginal gyrus before and after transorbital occlusion of the middle cerebral artery in cats. Prestimulus cerebral blood flow (CBF) was 38.2 ± 12.9 (SD) ml 100 g−1 min−1 and fell to 19.8 ± 11.1 following occlusion (p < 0.02). Peak hydrogen clearance rate (percent increase above prestimulus clearance) was 81.6 ± 53.6 and fell to 19.9 ± 29.8 after middle cerebral artery occlusion (p < 0.01). Steady-state NADH fluorescence rose from 33.5 ± 10.7 to 40.5 ± 17.6% full-scale deflection following MCAO (p < 0.01). Latency from stimulus to maximal fluorescence depression in response to cortical stimulation increased from 12.2 ± 8.2 to 22.1 ± 11.9 s (p < 0.01). Hyperaemic responses at anteromedial sites on the marginal gyrus significantly exceeded those at posterolateral sites. The results are interpreted as indicating early ischaemic metabolic change; however, the presence of residual vasodilator responses to stimulation suggests that flow reduction and early ischaemic change in the territory studied are not simply due to inadequate collateral input, but may also reflect deafferentation or functional suppression. The possible significance of diminished vascular reactivity in the penumbra as a cause of increased vulnerability to extracellular release of excitatory amino acids is discussed.

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Spahn, Donat R., Timothy J. Quill, Wei-Chih Hu, Joseph Lu, L. Richard Smith, J. G. Reves, Robert L. McRae, and Bruce J. Leone. "Validation of 133Xe Clearance as a Cerebral Blood Flow Measurement Technique during Cardiopulmonary Bypass." Journal of Cerebral Blood Flow & Metabolism 12, no. 1 (January 1992): 155–61. http://dx.doi.org/10.1038/jcbfm.1992.19.

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133Xe clearance to measure cerebral blood flow (CBF) was examined in 10 dogs during cardiopulmonary bypass. As a reference method, a continuous Kety–Schmidt technique (CBFKS) with 133Xe as indicator was used. Extracranial tissue was removed to directly place the 133Xe detectors on the skull, and the head was covered with a 3 mm lead shield to minimize contamination of the 133Xe clearance curve with extracranial radiation. 133Xe detectors for the Kety–Schmidt technique were embedded in a shielded brass block to minimize interference with radiation from the animal's body. 133Xe clearance data were analyzed using stochastic (CBF10, CBF15, and CBFINF) and initial slope methods (CBFIS), and the results were compared with CBFKS using linear regression. CBF15 and CBFINF yielded similar CBF values as CBFKS (CBFKS = 0.97 · CBF15 − 2.08, r = 0.92, p < 0.01; CBFKS = 1.13 · CBFINF − 1.21, r = 0.92, p < 0.01). CBF10 slightly overestimated CBFKS but still showed a close correlation to CBFKS (CBFKS = 0.89 · CBF10 − 2.58, r = 0.92, p < 0.01) and CBFIS considerably overestimated CBFKS (CBFKS = 0.60 · CBFIS − 1.27, r = 0.87, p < 0.01). With extracranial contamination of the 133Xe clearance curve minimized, all 133Xe clearance techniques used to measure CBF were consistently related to CBFKS in a constant, significant manner. 133Xe clearance therefore is a valid method to assess CBF during cardiopulmonary bypass.

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Salehpour, Farzad, Mahsa Khademi, Denis E. Bragin, and Joseph O. DiDuro. "Photobiomodulation Therapy and the Glymphatic System: Promising Applications for Augmenting the Brain Lymphatic Drainage System." International Journal of Molecular Sciences 23, no. 6 (March 10, 2022): 2975. http://dx.doi.org/10.3390/ijms23062975.

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The glymphatic system is a glial-dependent waste clearance pathway in the central nervous system, devoted to drain away waste metabolic products and soluble proteins such as amyloid-beta. An impaired brain glymphatic system can increase the incidence of neurovascular, neuroinflammatory, and neurodegenerative diseases. Photobiomodulation (PBM) therapy can serve as a non-invasive neuroprotective strategy for maintaining and optimizing effective brain waste clearance. In this review, we discuss the crucial role of the glymphatic drainage system in removing toxins and waste metabolites from the brain. We review recent animal research on the neurotherapeutic benefits of PBM therapy on glymphatic drainage and clearance. We also highlight cellular mechanisms of PBM on the cerebral glymphatic system. Animal research has shed light on the beneficial effects of PBM on the cerebral drainage system through the clearance of amyloid-beta via meningeal lymphatic vessels. Finally, PBM-mediated increase in the blood–brain barrier permeability with a subsequent rise in Aβ clearance from PBM-induced relaxation of lymphatic vessels via a vasodilation process will be discussed. We conclude that PBM promotion of cranial and extracranial lymphatic system function might be a promising strategy for the treatment of brain diseases associated with cerebrospinal fluid outflow abnormality.

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Kuwayama, Naoya, Akira Takaku, Jun Harada, Osamu Fukuda, Shunro Endo, and Tateo Saito. "Modified Thermal Diffusion Flow Probe for the Continuous Monitoring of Cortical Blood Flow." Neurosurgery 29, no. 4 (October 1, 1991): 583–89. http://dx.doi.org/10.1227/00006123-199110000-00017.

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Abstract A small thermal diffusion flow probe has been developed to monitor the dynamic changes in cerebral blood flow in small animals. Constantan wire was used as a heat source to make a miniature probe. The pair of thermocouples used to detect the heat gradient between two gold plates was elongated to avoid heat conduction between them, and this improvement allowed us to make quantitative measurements. After several basic experiments, local cerebral blood flow was measured simultaneously, using both the modified thermal probe and the hydrogen clearance method in four rabbits. A close relationship was obtained between the local cerebral blood flow values measured by hydrogen clearance (F, ml/100g/min) and the reciprocal of the thermocouple voltage (1/V;1/mV). The regression line was F = 29111(1/V- 1/226), (r = 0.92, P<0.001). We suggest that the modified thermal probe is a reliable and quantitative means of measuring flow. In addition, another probe modified for clinical use was evaluated. Continuous monitoring of local cerebral blood flow in postoperative patients was performed, and some illustrative cases are described.

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Zhang, Wenhua, Ying Zhou, Jianan Wang, Xiaoxian Gong, Zhicai Chen, Xuting Zhang, Jinsong Cai, et al. "Glymphatic clearance function in patients with cerebral small vessel disease." NeuroImage 238 (September 2021): 118257. http://dx.doi.org/10.1016/j.neuroimage.2021.118257.

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Rogers, A. T., D. A. Stump, D. S. Prough, L. Hinshelwood, and G. P. Gravlee. "CEREBRAL BLOOD FLOW DURING HYPOTHERMIC CARDIOPULMONARY BYPASS BY 133Xe CLEARANCE." Anesthesiology 69, no. 3A (September 1, 1988): A136. http://dx.doi.org/10.1097/00000542-198809010-00136.

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Todd, Nicholas V., Piero Picozzi, and H. Alan Crockard. "Quantitative Measurement of Cerebral Blood Flow and Cerebral Blood Volume after Cerebral Ischaemia." Journal of Cerebral Blood Flow & Metabolism 6, no. 3 (June 1986): 338–41. http://dx.doi.org/10.1038/jcbfm.1986.57.

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CBF obtained by the hydrogen clearance technique and cerebral blood volume (CBV) calculated from the [14C]dextran space were measured in three groups of rats subjected to temporary four-vessel occlusion to produce 15 min of ischaemia, followed by 60 min of reperfusion. In the control animals, mean CBF was 93 ± 6 ml 100 g−1 min−1, which fell to 5.5 ± 0.5 ml 100 g−1 min−1 during ischaemia. There was a marked early postischaemic hyperaemia (262 ± 18 ml 100g−1 min−1), but 1 h after the onset of ischaemia, there was a significant hypoperfusion (51 ± 3 ml 100 g−1 min−1). Mean cortical dextran space was 1.58 ± 0.09 ml 100 g−1 prior to ischaemia. Early in reperfusion there was a significant increase in CBV (1.85 ± 0.24 ml 100 g−1) with a decrease during the period of hypoperfusion (1.33 ± 0.03 ml 100 g−1). Therefore, following a period of temporary ischaemia, there are commensurate changes in CBF and CBV, and alterations in the permeability–surface area product at this time may be due to variations in surface area and not necessarily permeability.

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Roelz, Roland, Christian Scheiwe, Horst Urbach, Volker A. Coenen, and Peter Reinacher. "Stereotactic Catheter Ventriculocisternostomy for Clearance of Subarachnoid Hemorrhage in Patients with Coiled Aneurysms." Operative Neurosurgery 14, no. 3 (June 3, 2017): 231–35. http://dx.doi.org/10.1093/ons/opx129.

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Abstract BACKGROUND Cerebral vasospasm leading to delayed cerebral infarction (DCI) is a central source of poor outcome in patients with aneurysmal subarachnoid hemorrhage (aSAH). Current treatments of cerebral vasospasm are insufficient. Cisternal blood clearance is a promising treatment option. However, a generally applicable, safe, and effective method to access the cisterns of the brain is lacking. OBJECTIVE To report on stereotactic catheter ventriculocisternostomy (STX-VCS) as a method to access the cisterns of the brain for clearance of subarachnoid hemorrhage in patients with aSAH and coiled aneurysms. METHODS In 9 aSAH patients at high risk for DCI (Hunt and Hess grade ≥3, modified Fisher grade ≥3), access to the basal cisterns of the brain was created by STX-VCS. Fibrinolytic and/or spasmolytic lavage therapy was administered. RESULTS STX-VCS was feasible and safe in all patients. Subarachnoid blood was rapidly cleared by irrigation with urokinase. Vasospasm occurred in 2 patients and was interrupted by irrigation with nimodipine. There was 1 fatality due to pneumogenic sepsis. Minor DCI occurred in 1 patient. Eight survived without DCI and are independent (modified Rankin score [mRS] ≤ 3) at 6 mo after aSAH. CONCLUSION STX-VCS allows for rapid clearance of subarachnoid hemorrhage in patients with coiled aneurysms.

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Itakura, Toru, Hideyoshi Yokote, Hiroshi Kimura, Ichiro Kamei, Kazuo Nakakita, Yutaka Naka, Kunio Nakai, Harumichi Imai, and Norihiko Komai. "5-Hydroxytryptamine innervation of vessels in the rat cerebral cortex." Journal of Neurosurgery 62, no. 1 (January 1985): 42–47. http://dx.doi.org/10.3171/jns.1985.62.1.0042.

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✓ The role of the central 5-hydroxytryptamine (5-HT) neuron system in cerebral microcirculation of the rat was examined by immunohistochemical and hydrogen clearance methods. Immunohistochemical studies demonstrated 5-HT-immunoreactive nerve fibers along intraparenchymal blood vessels (arterioles, capillaries, and venules). Ultrastructural observation revealed that 5-HT-immunoreactive terminal boutons (0.3 to 1.0 µm in diameter) made contact with the basement membrane of the capillaries. After an intracerebral injection of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin to the 5-HT neuron system, no 5-HT-immunoreactive nerve fibers were found around the injection site with immunohistochemical techniques. With the hydrogen clearance method, the 5,7-DHT-injected cortex showed no significant change in regional cerebral blood flow (rCBF) in the presence of normocapnia, but a significant increase in rCBF with hypercapnia, compared with the untreated cortex. These facts strongly suggest that the central 5-HT neuron system has an important role in carbon dioxide reactivity of the cerebral blood vessels.

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Liao, Rongfang, Longmao Liu, Bo Song, Xinhong Wan, Shuo Wang, and Jianhong Xu. "3D-Slicer Software-Assisted Neuroendoscopic Surgery in the Treatment of Hypertensive Cerebral Hemorrhage." Computational and Mathematical Methods in Medicine 2022 (February 18, 2022): 1–7. http://dx.doi.org/10.1155/2022/7156598.

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Objective. To explore the 3D-slicer software-assisted endoscopic treatment for patients with hypertensive cerebral hemorrhage. Methods. A total of 120 patients with hypertensive cerebral hemorrhage were selected and randomly divided into control group and 3D-slicer group with 60 cases each. Patients in the control group underwent traditional imaging positioning craniotomy, and patients in the 3D-slicer group underwent 3D-slicer followed by precision puncture treatment. In this paper, we evaluate the hematoma clearance rate, nerve function, ability of daily living, complication rate, and prognosis. Results. The 3D-slicer group is better than the control group in various indicators. Compared with the control group, the 3D-slicer group has lower complications, slightly higher hematoma clearance rate, and better recovery of nerve function and daily living ability before and after surgery. The incidence of poor prognosis is low. Conclusion. The 3D-slicer software-assisted endoscopic treatment for patients with hypertensive intracerebral hemorrhage has a better hematoma clearance effect, which is beneficial to the patient’s early recovery and reduces the damage to the brain nerve of the patient.

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Kobayashi, S., A. Satoh, Y. Koguchi, M. Wada, H. Tokunaga, A. Miyata, H. Nakamura, Y. Watanabe, and T. Yagishita. "Clearance of Subarachnoid Clots after GDC Embolization for Acutely Ruptured Cerebral Aneurysm." Interventional Neuroradiology 7, no. 1_suppl (December 2001): 57–60. http://dx.doi.org/10.1177/15910199010070s108.

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It is apparent that subarachnoid clots play an important role in the development of delayed vasospasm that is one of the major causes of mortality and morbidity in patients with acutely ruptured cerebral aneurysm. The purpose of this study is to compare the clearance of subarachnoid clots in the acute stage after the treatment with Guglielmi detachable coils (GDC) and after treatment with direct surgery. Forty-nine patients were treated by GDC embolization within four days of the ictus. After GDC embolization, adjunctive therapies, such as ventricular and/or spinal drainage (67%), intrathecal administration of urokinase (41%), continuous cisternal irrigation (16%), and external decompression (16%), were performed. Seventy-four surgically treated patients were subsequently treated by continuous cisternal irrigation with mock-CSF containing ascorbic acid for ten days. The clearance of subarachnoid clots was assessed by the Hounsfield number serial changes on the CT scans taken on days 0, 4, 7, 10 after subarachnoid hemorrhage. The incidence of symptomatic vasospasm was lower in the GDC group (6%) than in the surgery group (12%). The clearance of subarachnoid clots from both the basal cistern and the Sylvian fissure was more rapid in the GDC cases than in the surgery cases in the first four days. Intrathecal administration of urokinase accelerated the clearance significantly. GDC embolization followed by intrathecal administration of thrombolytic agents accelerates the reduction of subarachnoid clots and favorably acts to prevent delayed vasospasm.

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Paulson, Olaf B., and Ida Vigdis. "Cigarette smoking and cerebral blood flow in a cohort of middle-aged adults." Journal of Cerebral Blood Flow & Metabolism 40, no. 4 (February 12, 2020): 904–5. http://dx.doi.org/10.1177/0271678x20905609.

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Cigarette smoking increases cerebral blood flow. Both nicotine and carbon monoxide contribute to the flow increase. Due to carbon monoxide’s high affinity to hemoglobin and slow clearance from the blood, the effect lasts for hours. Nicotine also stays in the organism for some hours. This immediate effect of smoking may explain a recently observed higher cerebral blood flow in current-smokers as compared to former-smokers.

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von Kummer, Rüdiger, and Sigrid Herold. "Hydrogen Clearance Method for Determining Local Cerebral Blood Flow. I. Spatial Resolution." Journal of Cerebral Blood Flow & Metabolism 6, no. 4 (August 1986): 486–91. http://dx.doi.org/10.1038/jcbfm.1986.83.

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To define the effective spatial resolution of the hydrogen clearance method, serial local CBF (LCBF) measurements were performed at different distances from the cortico–white matter junction of the cat brain. Twenty-five platinum-wire microelectrodes with a sensitive surface of 0.07 mm2 were inserted into the cerebral cortex of three cats through burr holes in the skull and advanced toward the ear-to-ear level in 1- or 0.1-mm steps. Most electrodes passed from high-perfusion regions into low-perfusion areas, indicating that the cortico–white matter junction had been traversed. Whereas within the gray and white matter the LCBF values were fairly constant, a striking decrease of CBF was registered at the cortico–white matter junction. Here the mean LCBF from 12 electrodes showed significant differences in flow between two locations 1 mm apart. On two occasions, a significant difference in CBF was found for locations only 0.1 mm apart. Despite this high spatial resolution, monoexponential clearance curves were detected only in the vicinity of the cortico–white matter junction. It is therefore assumed that factors other than flow might influence H2 clearance.

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Fieschi, C., L. Bozzao, and A. Agnoli. "REGIONAL CLEARANCE OF HYDROGEN AS A MEASURE OF CEREBRAL BLOOD FLOW." Acta Neurologica Scandinavica 41, S14 (January 29, 2009): 46–52. http://dx.doi.org/10.1111/j.1600-0404.1965.tb01952.x.

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Wan, Xiaoming, Tsu-Ching Fu, Alex Funk, and Robert E. London. "Differential clearance of nitroxide MRI contrast agents from rat cerebral ventricles." Brain Research Bulletin 36, no. 1 (January 1995): 91–96. http://dx.doi.org/10.1016/0361-9230(94)00170-6.

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Chambers, I. R., M. S. Choksey, A. Clark, A. Green, A. Jenkins, and A. D. Mendelow. "A thermal clearance probe for continuous monitoring of cerebral blood flow." Clinical Physics and Physiological Measurement 13, no. 4 (November 1992): 311–21. http://dx.doi.org/10.1088/0143-0815/13/4/002.

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Zhu, Pengxiang, Ryuji Hata, Masahito Ogasawara, Fang Cao, Kenji Kameda, Kohei Yamauchi, Alfred H. Schinkel, Kazutaka Maeyama, and Masahiro Sakanaka. "Targeted Disruption of Organic Cation Transporter 3 (Oct3) Ameliorates Ischemic Brain Damage through Modulating Histamine and Regulatory T Cells." Journal of Cerebral Blood Flow & Metabolism 32, no. 10 (June 27, 2012): 1897–908. http://dx.doi.org/10.1038/jcbfm.2012.92.

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The organic cation transporters OCT1, 2, and 3 (SLC22A1-3) have been implicated in the elimination of biogenic amines such as histamine. Among them, OCT3 was identified as an uptake-2 transporter, responsible for clearance of histamine. Because increasing evidence suggests the involvement of histamine in cerebral ischemia, we investigated the effects of targeted disruption of organic cation transporter-3 (Oct3) on the severity of ischemic brain damage. Transient focal ischemia for 1 hour was induced by occlusion of the middle cerebral artery (MCA) of homozygous Oct3-deficient mice and their wild-type (Wt) littermates. Although targeted disruption of Oct3 did not affect physiological parameters after MCA occlusion, this disruption significantly increased histamine content in the ischemic cortex and significantly reduced the infarct volume after cerebral ischemia. Furthermore, targeted disruption of Oct3 prevented the reduction of regulatory T-cell proportion after cerebral ischemia while this disruption did not affect Th1 and Th2 cells proportions after ischemia. Since repeated administration of L-histidine (a precursor of histamine) to Wt mice also showed the same effects, our observations suggested that OCT3 is the molecule responsible for clearance of ischemia-induced histamine in the brain and targeted disruption of Oct3 ameliorated ischemic brain damage through an increase in regulatory T cells.

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Iida, Hidehiro, Satoshi Iguchi, Noboru Teramoto, Kazuhiro Koshino, Tsutomu Zeniya, Akihide Yamamoto, Nobuyuki Kudomi, et al. "Adequacy of a Compartment Model for CMRO2 Quantitation Using 15O-Labeled Oxygen and PET: A Clearance Measurement of 15O-Radioactivity Following Intracarotid Bolus Injection of 15O-Labeled Oxyhemoglobin on Macaca Fascicularis." Journal of Cerebral Blood Flow & Metabolism 34, no. 9 (July 9, 2014): 1434–39. http://dx.doi.org/10.1038/jcbfm.2014.118.

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We aimed at evaluating the adequacy of the commonly employed compartmental model for quantitation of cerebral metabolic rate of oxygen (CMRO2) using 15O-labeled oxygen (15O2) and positron emission tomography (PET). Sequential PET imaging was carried out on monkeys following slow bolus injection of blood samples containing 15O2–oxyhemoglobin (15O2–Hb), 15O-labeled water (H215O), and C15O-labeled hemoglobin (C15O–Hb) into the internal carotid artery (ICA). Clearance slopes were assessed in the middle cerebral artery territory of the injected hemisphere. The time–activity curves were bi-exponential for both 15O2–Hb and H215O. Single exponential fitting to the early (5 to 40 seconds) and late (80 to 240 seconds) periods after the peak was performed and the 15O2–Hb and H215O results were compared. It was found that a significant difference between the clearance rates of the 15O2–Hb and H215O injections is unlikely, which supports the mathematical model that is widely used to describe the kinetics of 15O2–Hb and H215O in cerebral tissues and is the basis of recent approaches to simultaneously assess CMRO2 and cerebral blood flow in a single PET session. However, it should be noted that more data are necessary to unequivocally confirm the result.

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Ghanghoriya, Pawan, Purusharth Srivastava, and Praveen K. Bharti. "Study clinical response and parasite clearance response to Artemisinins in severe malaria in children." International Journal of Contemporary Pediatrics 5, no. 3 (April 20, 2018): 905. http://dx.doi.org/10.18203/2349-3291.ijcp20181511.

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Background: The research was conducted to study the clinical response and parasite clearance response to Artesunate therapy, in children admitted with severe malaria at a tertiary care centre in Central India.Methods: It is a prospective analytical study. 18 microscopy positive children diagnosed with severe malaria were included. Baseline blood samples collected for microscopy and biochemical tests. All patients were administered standard intravenous Artesunate therapy and were watched every 12 hourly for: 1. Resolution of clinical signs and symptoms. Clinical parameters included level of consciousness in form of GCS, vital signs like pulse rate, respiration, signs of bleeding, development of icterus, pallor, urine output and laboratory parameters included blood sugar levels, renal and liver function tests. 2. Time taken for conversion of microscopic Smear positive to Smear negative.Results: The mean age was 8.34±4.35 years. Males and females were equally affected. 61% of severe malaria patients were infected by P. falciparum and remaining were infected by P. vivax. The most common clinical features were Pallor: 100%, Respiratory distress: 66.7%, Cerebral malaria: 55.6%. After giving Artesunate therapy, Mean GCS in Cerebral malaria patients showed improvement (on admission: 9±1.15, at 72 hours: 12.5±3.7). Effect was marginally better in P. vivax cases. Respiratory distress and tachycardia improved in majority of patients (75% and 80% respectively). The number of patients with icterus progressively increased. Improvement in liver function and renal function was minimal. 100% parasite clearance was achieved. The mean parasite clearance time is 46±9.43 hours. 72.2% were successfully discharged, 22.2% took Leave Against Medical Advice (LAMA) and 5.6% certified dead.Conclusions: Artesunate is an effective drug in severe malaria patients in terms of rapid improvement of cerebral function, improvement and stabilization of vitals, parasite clearance with favorable long-term outcome. There is no evidence of plasmodium resistance to Artesunate currently as per the present study.

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Younkin, D. P., M. Reivich, J. L. Jaggi, W. D. Obrist, and M. Delivoria-Papadopoulos. "The Effect of Hematocrit and Systolic Blood Pressure on Cerebral Blood Flow in Newborn Infants." Journal of Cerebral Blood Flow & Metabolism 7, no. 3 (June 1987): 295–99. http://dx.doi.org/10.1038/jcbfm.1987.66.

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The effects of hematocrit and systolic blood pressure on cerebral blood flow were measured in 15 stable, low birth weight babies. CBF was measured with a modification of the xenon-133 (133Xe) clearance technique, which uses an intravenous bolus of 133Xe, an external chest detector to estimate arterial 133Xe concentration, eight external cranial detectors to measure cephalic 133Xe clearance curves, and a two-compartmental analysis of the cephalic 133Xe clearance curves to estimate CBF. There was a significant inverse correlation between hematocrit and CBF, presumably due to alterations in arterial oxygen content and blood viscosity. Newborn CBF varied independently of systolic blood pressure between 60 and 84 mm Hg, suggesting an intact cerebrovascular autoregulatory mechanism. These results indicate that at least two of the factors that affect newborn animal CBF are operational in human newborns and may have important clinical implications.

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Lyu, Zhongkuan, Yuanjin Chan, Qiyue Li, Qiang Zhang, Kaili Liu, Jun Xiang, Xiangting Li, et al. "Destructive Effects of Pyroptosis on Homeostasis of Neuron Survival Associated with the Dysfunctional BBB-Glymphatic System and Amyloid-Beta Accumulation after Cerebral Ischemia/Reperfusion in Rats." Neural Plasticity 2021 (August 14, 2021): 1–11. http://dx.doi.org/10.1155/2021/4504363.

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Neuroinflammation-related amyloid-beta peptide (Aβ) accumulation after cerebral ischemia/reperfusion (I/R) accounts for cerebral I/R injuries and poststroke dementia. Recently, pyroptosis, a proinflammatory cell death, has been identified as a crucial pathological link of cerebral I/R injuries. However, whether pyroptosis acts as a trigger of Aβ accumulation after cerebral I/R has not yet been demonstrated. Blood-brain barrier (BBB) and glymphatic system mediated by aquaporin-4 (AQP-4) on astrocytic endfeet are important pathways for the clearance of Aβ in the brain, and pyroptosis especially occurring in astrocytes after cerebral I/R potentially damages BBB integrity and glymphatic function and thus influences Aβ clearance and brain homeostasis. In present study, the method of middle cerebral artery occlusion/reperfusion (MCAO/R) was used for building models of focal cerebral I/R injuries in rats. Then, we used lipopolysaccharide and glycine as the agonist and inhibitor of pyroptosis, respectively, Western blotting for detections of pyroptosis, AQP-4, and Aβ1-42 oligomers, laser confocal microscopy for observations of pyroptosis and Aβ locations, and immunohistochemical stainings of SMI 71 (a specific marker for BBB integrity)/AQP-4 and Nissl staining for evaluating, respectively, BBB-glymphatic system and neuronal damage. The results showed that pyroptosis obviously promoted the loss of BBB integrity and AQP-4 polarization, brain edema, Aβ accumulation, and the formation of Aβ1-42 oligomers and thus increased neuronal damage after cerebral I/R. However, glycine could inhibit cerebral I/R-induced pyroptosis by alleviating cytomembrane damage and downregulating expression levels of cleaved caspase-11/1, N-terminal gasdermin D, NLRP3 (nucleotide-binding domain, leucine-rich repeat containing protein 3), interleukin-6 (IL-6) and IL-1β and markedly abate above pathological changes. Our study revealed that pyroptosis is a considerable factor causing toxic Aβ accumulation, dysfunctional BBB-glymphatic system, and neurological deficits after cerebral I/R, suggesting that targeting pyroptosis is a potential strategy for the prevention of ischemic stroke sequelae including dementia.

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Rogers, H. B., T. Schroeder, N. H. Secher, and J. H. Mitchell. "Cerebral blood flow during static exercise in humans." Journal of Applied Physiology 68, no. 6 (June 1, 1990): 2358–61. http://dx.doi.org/10.1152/jappl.1990.68.6.2358.

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Cerebral blood flow (CBF) was determined in humans at rest and during four consecutive unilateral static contractions of the knee extensors. Each contraction was maintained for 3 min 15 s with the subjects in a semisupine position. The contractions corresponded to 8, 16, 24, and 32% of the maximal voluntary contraction (MVC) and utilized alternate legs. CBF (measured by the 133Xe clearance technique) was expressed by a noncompartmental flow index (ISI). Heart rate and mean arterial pressure increased from resting values of 73 (55-80) beats/min and 88 (74-104) mmHg to 106 (86-138) beats/min and 124 (102-146) mmHg, respectively (P less than 0.0005), during the contraction at 32% MVC. Arterial PCO2 and central venous pressure did not change. Corrected to the average resting PCO2, CBF during control was 55 (35-73) ml.100 g-1.min-1 and remained constant during contractions. Cerebral vascular resistance increased from 1.5 (1.0-2.2) to 2.4 (1.4-3.0) mmHg. 100 g.min.ml-1 (P less than 0.025) at 32% of MVC. There was no difference in CBF between the two hemispheres at rest or during exercise. In contrast to dynamic leg exercise, static leg exercise is not associated with an increase in global CBF when measured by the 133Xe clearance technique.

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von Kummer, Rüdiger, Friedrich von Kries, and Sigrid Herold. "Hydrogen Clearance Method for Determining Local Cerebral Blood Flow. II. Effect of Heterogeneity in Cerebral Blood Flow." Journal of Cerebral Blood Flow & Metabolism 6, no. 4 (August 1986): 492–98. http://dx.doi.org/10.1038/jcbfm.1986.84.

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The time course of hydrogen uptake and washout was followed simultaneously in extracranial arterial blood, cortex, subcortical white matter, and caudate nucleus of the cat brain to study intercompartmental hydrogen concentration differences. A clear delay of 1–2 min was seen between the onsets of concentration increase in arterial blood and low-flow brain tissues. Equilibration time was dependent on local CBF and varied between 3 and 34 min. Hydrogen was not cleared simultaneously from the regions under detection. This led to considerable concentration differences within the cerebral tissue during washin and washout phases. Analysis of the clearance curves revealed that secondary equilibration occurs during washout. Hydrogen concentration in the external carotid artery was not a reliable reflection of tracer input in the brain tissues. The consequences of these observations for other techniques of CBF measurement using less diffusive gases and external detection are discussed.

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Hetherington, Hoby P., Min-Jie Tan, Kang-Li Luo, Gerald M. Pohost, James H. Halsey, and Karl A. Conger. "Evaluation of Lactate Production and Clearance Kinetics by 1H NMR in a Model of Brief Repetitive Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 14, no. 4 (July 1994): 591–96. http://dx.doi.org/10.1038/jcbfm.1994.73.

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Pilots of high-performance aircraft are subject to repeated transient cerebral ischemia during high-gravitational stress maneuvers. Previously we have demonstrated that repeated episodes of transient cerebral ischemia and reflow are cumulative and lactate accumulations appear to be exponential. To evaluate the metabolic events determining the kinetics of lactate accumulation, and therefore the rates of substrate utilization, we have used in vivo 1H nuclear magnetic resonance with a 5-s time resolution to measure lactate production and clearance. The individual rates for each animal were then used to predict the accumulation of lactate in the same animal during 30 episodes of ischemia and reflow. Lactate accumulation was modeled as the balance between a zero-order production process during the ischemic period and a first-order clearance process. The predicted lactate accumulation showed excellent agreement with the observed time course, validating the predictive power of the simple model used. The highly reproducible nature of this model and its accuracy in predicting lactate accumulation should enable more accurate studies of the deleterious effects of lactate accumulation in cerebral ischemia by providing a highly reproducible means for generating a specific level of lactate accumulation.

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Davies, J. Graham, Elizabeth F. Greenwood, J. Christopher Kingswood, Paul Sharpstone, and Martin K. Street. "Quinine Clearance in Continuous Venovenous Hemofiltration." Annals of Pharmacotherapy 30, no. 5 (May 1996): 487–90. http://dx.doi.org/10.1177/106002809603000511.

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OBJECTIVE: TO describe a case involving the removal of quinine by continuous venovenous hemofiltration (CVVH) in a patient with malaria and acute renal failure and to present recommendations on the dosing of quinine in such patients. CASE SUMMARY: A 50-year-old white man developed Plasmodium falciparum malaria following a visit to Nigeria. Although he received intravenous quinine, his condition deteriorated and he required intensive care management, including CWH for the management of his acute renal failure. Quinine plasma concentrations were measured to determine both total body and extracorporeal clearance of the drug. DISCUSSION: TO our knowledge this is the first report quantifying the removal of quinine by CVVH. The drug is not significantly removed by this extracorporeal process. The filter clearance accounted for less than 1.5% of the total body clearance. CONCLUSIONS: Initially the dosage of quinine administered to patients presenting with P. falciparum infection should not be reduced because of renal failure. This is particularly important when cerebral involvement is suspected. Subsequent dosage modification should reflect the severity of the patient's clinical condition and the plasma quinine concentration achieved, and should not be limited by the degree of renal impairment present.

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Ito, Shingo, Sumio Ohtsuki, Yuki Katsukura, Miho Funaki, Yusuke Koitabashi, Akihiko Sugino, Sho Murata, and Tetsuya Terasaki. "Atrial Natriuretic Peptide is Eliminated from the Brain by Natriuretic Peptide Receptor-C-Mediated Brain-to-Blood Efflux Transport at the Blood—Brain Barrier." Journal of Cerebral Blood Flow & Metabolism 31, no. 2 (July 14, 2010): 457–66. http://dx.doi.org/10.1038/jcbfm.2010.108.

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Cerebral atrial natriuretic peptide (ANP), which is generated in the brain, has functions in the regulation of brain water and electrolyte balance, blood pressure and local cerebral blood flow, as well as in neuroendocrine functions. However, cerebral ANP clearance is still poorly understood. The purpose of this study was to clarify the mechanism of blood–brain (BBB) efflux transport of ANP in mouse. Western blot analysis showed expression of natriuretic peptide receptor (Npr)-A and Npr-C in mouse brain capillaries. The brain efflux index (BEI) method confirmed elimination of [125I]human ANP (hANP) from mouse brain across the BBB. Inhibition studies suggested the involvement of Npr-C in vivo. Furthermore, rapid internalization of [125I]hANP by TM-BBB4 cells (an in vitro BBB model) was significantly inhibited by Npr-C inhibitors and by two different Npr-C-targeted short interfering RNAs (siRNAs). Finally, treatment with 1α,25-dihydroxyvitamin D3(1,25(OH)2D3) significantly increased Npr-C expression in TM-BBB4 cells, as determined by liquid chromatography–tandem mass spectrometry (LC-MS/MS)-based targeted absolute proteomics. Our results indicate that Npr-C mediates brain-to-blood efflux transport of ANP at the mouse BBB as a pathway of cerebral ANP clearance. It seems likely that levels of natriuretic peptides in the brain are modulated by 1,25(OH)2D3 through upregulation of Npr-C expression at the BBB.

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van de Lagemaat, Monique, Laura A. van de Pol, Inge A. Zonnenberg, Bregje C. M. Witjes, and Petra J. W. Pouwels. "MR Spectroscopy Shows Long Propylene Glycol Half-Life in Neonatal Brain." Neonatology 118, no. 6 (2021): 693–701. http://dx.doi.org/10.1159/000519282.

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Introduction: Neonatal propylene glycol (PG) clearance is low with long plasma half-life. We hypothesized that neonatal brain PG clearance is diminished and may be related to perinatal asphyxia, infection, or stroke, via different blood-brain barrier permeability. This study aimed to estimate cerebral PG half-life with a clearance model including PG measured with MR spectroscopy (MRS) in neonates that received phenobarbital as the only PG source and to evaluate whether PG clearance was related to intracerebral pathology, for example, perinatal asphyxia, infection, or stroke. Methods: In this retrospective cohort study, 45 neonates receiving any dose of phenobarbital underwent MRS (short echo time single-voxel MRS at 1.5 T). Cumulative phenobarbital/PG doses were calculated. MRS indications were perinatal asphyxia (n = 22), infection (n = 4), stroke (n = 10), metabolic disease (n = 4), and others (n = 5). Results: Medians (interquartile range) included gestational age 39.4 (3.1) weeks, birth weight 3,146 (1,340) g, and cumulative PG dose 700 (1,120) mg/kg. First-order kinetics with mono-exponential decay showed cerebral PG half-life of 40.7 h and volume of distribution of 1.6 L/kg. Zero-order kinetics showed a rate constant of 0.048 mM/h and a volume of distribution of 2.3 L/kg, but the fit had larger residuals than the first-order model. There were no differences in ΔPG (i.e., PG estimated with clearance model minus PG observed with MRS) in infants with perinatal asphyxia, infection, or stroke. Discussion/Conclusion: This study showed a long cerebral PG half-life of 40.7 h in neonates, unrelated to perinatal asphyxia, infection, or stroke. These findings should increase awareness of possible toxic PG concentrations in neonatal brain due to intravenous PG-containing drugs.

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Findlay, J. M., B. K. A. Weir, K. Kanamaru, M. Grace, P. Gordon, R. Baughman, and A. Howarth. "Intrathecal Fibrinolytic Therapy after Subarachnoid Hemorrhage: Dosage Study in a Primate Model and Review of the Literature." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 16, no. 1 (February 1989): 28–40. http://dx.doi.org/10.1017/s0317167100028481.

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ABSTRACT:Because of the naturally low fibrinolytic activity of CSF many erythrocytes entrapped in subarachnoid blood clot undergo hemolysis in situ, releasing vasogenic oxyhemoglobin (OxyHb) in high concentrations around the basal cerebral arteries. In order to promote more rapid clearance of erythrocytes from the basal subarachnoid cisterns we are currently investigating intrathecal thrombolytic therapy with human, recombinant, tissue plasminogen activator (rt-PA) in a primate model of subarachnoid hemorrhage (SAH) and cerebral vasospasm (VSP). In the present study 16 monkeys were divided into 4 groups of 4, and each group received a different dose of sustained-release gel rt-PA at the time of experimental SAH. Cerebral angiography seven days later showed that whereas no VSP occurred in the groups receiving 0.5 or 0.75 mg of rt-PA, mild to moderate VSP occurred in the groups receiving 0.125 or 0.25 mg of rt-PA. Analysis of the combined 2 smaller dosage groups revealed significant (P<0.05) reduction of lumen caliber in the clotside internal carotid (C3 and C4), proximal anterior cerebral (A1) and middle cerebral (MCA) arteries. Gross subarachnoid clot remained in all of the animals in the 0.125 and 0.25 mg dose groups, in 2 of the animals in the 0.5 mg dose group, and none of the animals in the 0.75 mg dose group. It was concluded that 0.75 mg of gel rt-PA is sufficient to completely lyse a 4.25 ml SAH and prevent VSP in our primate model. The literature on fibrinolysis and erythrocyte clearance in cerebrospinal fluid (CSF) is reviewed.

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Pennington, G. L., and M. J. McKinley. "Reduction of cerebral NaCl concentration can abolish mineralocorticoid escape." American Journal of Physiology-Renal Physiology 259, no. 5 (November 1, 1990): F839—F846. http://dx.doi.org/10.1152/ajprenal.1990.259.5.f839.

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The effect of lowering cerebrospinal fluid (CSF) Na concentration on renal Na excretion (UNaV) was investigated in conscious sheep undergoing mineralocorticoid escape induced by intravenous infusion of aldosterone (20 micrograms.ml-1.h-1) for 3 days. On the 3rd day of aldosterone administration, when plasma and CSF Na concentration and mean arterial blood pressure (MABP) were increased as a result of the mineralocorticoid treatment, a reduction in the CSF Na concentration was induced by infusing a Na-free solution of 300 mmol/l mannitol (1 ml/h) into a lateral cerebral ventricle. This caused significant reductions in UNaV and MABP and a significant increase in renal free water clearance (CH2O). There was no significant change in glomerular filtration rate or plasma atrial natriuretic peptide concentration, but renal lithium clearance decreased. Simultaneous intravenous infusion of vasopressin (0.03 microgram/h) and lowering of CSF Na concentration also caused significant reductions in UNaV and MABP, but CH2O did not increase. We propose that increased Na concentration of brain fluid may initiate natriuretic and pressor mechanisms contributing to the process of mineralocorticoid escape. Reduced UNaV may have been due to reduced MABP, but it is unlikely to have been due to reduced plasma vasopressin levels.

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Fei, Yu-xing, Tian-hong Zhang, Jing Zhao, He Ren, Ya-nan Du, Chun-ling Yu, Qiang Wang, et al. "In vitro and in vivo evaluation of hypothermia on pharmacokinetics and pharmacodynamics of nimodipine in rabbits." Journal of International Medical Research 46, no. 1 (August 29, 2017): 335–47. http://dx.doi.org/10.1177/0300060517720056.

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Objective To investigate the effect of hypothermia on the pharmacokinetics and pharmacodynamics of nimodipine in rabbits using in vivo and in vitro methods. Methods Five healthy New Zealand rabbits received a single dose of nimodipine (0.5 mg/kg) intravenously under normothermic and hypothermic conditions. Doppler ultrasound was used to monitor cerebral blood flow, vascular resistance, and heart rate. In vitro evaluations of protein binding, hepatocyte uptake and intrinsic clearance of liver microsomes at different temperatures were also conducted. Results Plasma concentrations of nimodipine were significantly higher in hypothermia than in normothermia. Nimodipine improved cerebral blood flow under both conditions, but had a longer effective duration during the hypothermic period. Low temperature decreased the intrinsic clearance of liver microsomes, with no change in protein binding or hepatocyte uptake of nimodipine. Conclusion Nimodipine is eliminated at a slower rate during hypothermia than during normothermia, mainly due to the decreased activity of cytochrome P450 enzymes. This results in elevated system exposure with little enhancement in pharmacological effect.

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Lei, Hao, and James Peeling. "Effect of temperature on the kinetics of lactate production and clearance in a rat model of forebrain ischemia." Biochemistry and Cell Biology 76, no. 2-3 (May 1, 1998): 503–9. http://dx.doi.org/10.1139/o98-039.

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To investigate the effect of brain temperature on metabolic perturbations during and following forebrain ischemia, localized 1H magnetic resonance spectroscopy was used to measure the kinetics of lactate production and clearance in a rat model of 12- or 20-min forebrain ischemia (two-vessel occlusion with hypotension) at a brain temperature of either 34.5 ± 0.5°C or 37.5 ± 0.5°C. During ischemia, lactate production was modeled with apparent first order kinetics. Hypothermia did not affect the rate or the extent of lactate production during ischemia. Upon reperfusion, a delay in the decrease of the cerebral lactate level was found in the normothermia groups. Such a delay was absent in hypothermia groups, which may reflect faster resumption of cerebral oxidative metabolism upon reperfusion in the hypothermic animals. The rate constant for lactate clearance postischemia was larger for normothermic animals and for the 20-min ischemia groups, perhaps because of increased blood-brain barrier permeability following more severe ischemia.Key words: forebrain ischemia, temperature, hypothermia, lactate, magnetic resonance spectroscopy.

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Salcman, Michael, Eiji Moriyama, Henry J. Elsner, Herman Rossman, Robert A. Gettleman, Gordon Neuberth, and Gregory Corradino. "Cerebral blood flow and the thermal properties of the brain: a preliminary analysis." Journal of Neurosurgery 70, no. 4 (April 1989): 592–98. http://dx.doi.org/10.3171/jns.1989.70.4.0592.

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✓ Safe and effective use of hyperthermia for the treatment of brain tumors requires precise control of the distribution of temperatures (that is, the thermal field) within the tumor and within the adjacent brain. Major influences upon the distribution of temperatures include the passive thermal properties of the brain, such as its specific heat (Cb), and the contribution of cerebral blood flow (CBF). Recently, an electrical-mechanical analog model of heat flow within the brain has been developed from which an expression for CBF has been derived: CBF = Cb/(τρc) where τ is the thermal decay constant, ρ is the density of blood, and c is its specific heat. To test this model a series of experiments was carried out in adult dogs in which stereotaxically implanted microwave antennas operating at 2450 MHz, fluoro-optical thermometry probes, and platinum electrodes were used to simultaneously measure CBF by thermal washout and hydrogen clearance techniques. The correlation coefficient for estimates of CBF derived by the two methods in 52 paired observations was 0.89. Measurements of CBF were more reliable at increased distances from the microwave antenna, since CBF is sensitive to the degree of temperature elevation (ΔT). The ratio of post-heating CBF to pre-heating CBF varies linearly with ΔT and has a correlation coefficient of 0.86. When values of CBF determined by the hydrogen clearance method were employed in the above equation, it was possible to derive Cb as 0.70 ± 0.08 cal/gm-°C. Use of this value for Cb in this equation produces estimates of CBF by thermal clearance that are within 10% of the values for CBF as measured by the hydrogen clearance method. It is concluded that this model of thermal flow within the brain may have heuristic value for treatment planning and that microwave antennas and fluoro-optical probes may represent a new methodology for the clinical estimation of CBF. These methods have recently been employed in patients undergoing combined hyperthermia and chemotherapy.

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Janigro, Damir. "Cerebral Waste Accumulation and Glymphatic Clearance as Mechanisms of Human Neurological Diseases." Journal of Neurology and Neuromedicine 1, no. 7 (October 1, 2016): 15–19. http://dx.doi.org/10.29245/2572.942x/2016/7.1082.

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Zhang, Xiangnan, Haijing Yan, Yang Yuan, Jieqiong Gao, Zhe Shen, Yun Cheng, Yao Shen, et al. "Cerebral ischemia-reperfusion-induced autophagy protects against neuronal injury by mitochondrial clearance." Autophagy 9, no. 9 (September 29, 2013): 1321–33. http://dx.doi.org/10.4161/auto.25132.

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46

Huang, Jianpan, Peter C. M. van Zijl, Xiongqi Han, Celia M. Dong, Gerald W. Y. Cheng, Kai-Hei Tse, Linda Knutsson, et al. "Altered d-glucose in brain parenchyma and cerebrospinal fluid of early Alzheimer’s disease detected by dynamic glucose-enhanced MRI." Science Advances 6, no. 20 (May 2020): eaba3884. http://dx.doi.org/10.1126/sciadv.aba3884.

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Altered cerebral glucose uptake is one of the hallmarks of Alzheimer’s disease (AD). A dynamic glucose-enhanced (DGE) magnetic resonance imaging (MRI) approach was developed to simultaneously monitor d-glucose uptake and clearance in both brain parenchyma and cerebrospinal fluid (CSF). We observed substantially higher uptake in parenchyma of young (6 months) transgenic AD mice compared to age-matched wild-type (WT) mice. Notably lower uptakes were observed in parenchyma and CSF of old (16 months) AD mice. Both young and old AD mice had an obviously slower CSF clearance than age-matched WT mice. This resembles recent reports of the hampered CSF clearance that leads to protein accumulation in the brain. These findings suggest that DGE MRI can identify altered glucose uptake and clearance in young AD mice upon the emergence of amyloid plaques. DGE MRI of brain parenchyma and CSF has potential for early AD stratification, especially at 3T clinical field strength MRI.

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Tomita, Minora, Fumio Gotoh, Norio Tanahashi, Masahiro Kobari, Yasuo Terayama, Ban Mihara, Kouichi Ohta, and Ingo Gerdsen. "Comparison between the Photoelectric Method and H2 Clearance Method for Measuring Cerebrocortical Blood Flow in Cats." Journal of Cerebral Blood Flow & Metabolism 8, no. 5 (October 1988): 727–32. http://dx.doi.org/10.1038/jcbfm.1988.120.

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The photoelectric method using carbon black as a nondiffusible tracer of blood was compared with the hydrogen clearance (H2) method in nine anesthetized cats. A photoelectric apparatus and H2 electrode were applied to a small region of the cerebral cortex (left ectosylvian gyrus) for simultaneous measurement of the regional CBF. The values of CBF(H2) and CBF(photoelectric) were 50.7 ± 19.2 and 52.1 ± 14.5 ml − 100 g−1 · min−1, respectively. CBF(H2) and CBF(photoelectric) were found to correlate well ( r = 0.588, p < 0.01) when changes in CBF were induced by CO2 inhalation, exsanguination, hyperventilation, and occlusion of the middle cerebral artery. The correlation between CBF(H2) and CBF(photoelectric) was much better in the case of intraindividual comparisons ( r = 0.957, p < 0.01). In addition to its merits in common with the H2 clearance method, such as handiness, low cost, and strict regionality, the photoelectric method displayed the following advantages: time-to-time measurements of CBF (<20 s), immediate display of the microcirculatory flow pattern, and simultaneous monitoring of cerebral blood volume. However, measurements from deep structures of the brain are better performed by the H2 method despite the disadvantage of the use of a potentially explosive gas.

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Tranmer, Bruce I., Ted S. Keller, Glenn W. Kindt, and David Archer. "Loss of cerebral regulation during cardiac output variations in focal cerebral ischemia." Journal of Neurosurgery 77, no. 2 (August 1992): 253–59. http://dx.doi.org/10.3171/jns.1992.77.2.0253.

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✓ Focal cerebral ischemia was induced in anesthetized macaque monkeys by unilateral middle cerebral artery occlusion. The effect of blood volume expansion by a colloid agent and subsequent exsanguination to baseline cardiac output (CO) on local cerebral blood flow (CBF) was measured by the hydrogen clearance technique in both ischemic and nonischemic brain regions. Cardiac output was increased to maximum levels (159% ± 92%, mean ± standard error of the mean) by blood volume expansion with the colloid agent hetastarch, and was then reduced a similar amount (166% ± 82%) by exsanguination during the ischemic period. Local CBF in ischemic brain regions varied directly with CO, with a correlation coefficient of 0.89 (% change CBF/% change CO), while CBF in nonischemic brain was not affected by upward or downward manipulations of CO. The difference in these responses between ischemic and nonischemic brain was highly significant (p < 0.001). The results of this study show a profound loss of regulatory control in ischemic brain in response to alterations in CO, thereby suggesting that blood volume variations may cause significant changes in the intensity of ischemia. It is proposed that CO monitoring and manipulation may be vital for optimum care of patients with acute cerebral ischemia.

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Kranich, Jan, Nike Julia Krautler, Jeppe Falsig, Boris Ballmer, Shulei Li, Gregor Hutter, Petra Schwarz, et al. "Engulfment of cerebral apoptotic bodies controls the course of prion disease in a mouse strain–dependent manner." Journal of Experimental Medicine 207, no. 10 (September 13, 2010): 2271–81. http://dx.doi.org/10.1084/jem.20092401.

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Progressive accumulation of PrPSc, a hallmark of prion diseases, occurs when conversion of PrPC into PrPSc is faster than PrPSc clearance. Engulfment of apoptotic bodies by phagocytes is mediated by Mfge8 (milk fat globule epidermal growth factor 8). In this study, we show that brain Mfge8 is primarily produced by astrocytes. Mfge8 ablation induced accelerated prion disease and reduced clearance of cerebellar apoptotic bodies in vivo, as well as excessive PrPSc accumulation and increased prion titers in prion-infected C57BL/6 × 129Sv mice and organotypic cerebellar slices derived therefrom. These phenotypes correlated with the presence of 129Sv genomic markers in hybrid mice and were not observed in inbred C57BL/6 Mfge8−/− mice, suggesting the existence of additional strain-specific genetic modifiers. Because Mfge8 receptors are expressed by microglia and depletion of microglia increases PrPSc accumulation in organotypic cerebellar slices, we conclude that engulfment of apoptotic bodies by microglia may be an important pathway of prion clearance controlled by astrocyte-borne Mfge8.

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Northington, Frances J., G. Paul Matherne, Sharon D. Coleman, and Robert M. Berne. "Sciatic Nerve Stimulation Does Not Increase Endogenous Adenosine Production in Sensory-Motor Cortex." Journal of Cerebral Blood Flow & Metabolism 12, no. 5 (September 1992): 835–43. http://dx.doi.org/10.1038/jcbfm.1992.115.

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Adenosine participates in the coupling of cerebral blood flow to oxygen consumption in the brain during such stimuli as hypoxia, ischemia, and seizures. It has been suggested that it also participates in the regulation of cerebral blood flow during somatosensory stimulation, a condition during which cerebral blood flow and oxygen consumption appear to be uncoupled. Interstitial adenosine was estimated by the microdialysis technique and cerebral blood flow was measured by hydrogen clearance in the hindlimb sensory-motor cortex during sciatic nerve stimulation. Cerebral blood flow increased from 102 to 188 ml min−1 100 g−1 (p < 0.001) in the cortex contralateral to the stimulated leg without an associated increase in interstitial adenosine (baseline 0.624 μ M, stimulation 0.583 μ M). Infusion of the adenosine antagonist 8-sulfophenyltheophylline failed to block an increase in cerebral blood flow during central sciatic nerve stimulation, but decreased basal cerebral blood flow (69 ml min−1 100 g−1). These results suggest that adenosine does not mediate changes in cerebral blood flow during somatosensory stimulation, but may participate in the regulation of cerebral blood flow in the basal state.

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