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Articles de revues sur le sujet « Blood-brain barrier Physiology »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 3 février 2022

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1

Dunn, Jeff F., and Albert M. Isaacs. "The impact of hypoxia on blood-brain, blood-CSF, and CSF-brain barriers." Journal of Applied Physiology 131, no. 3 (September 1, 2021): 977–85. http://dx.doi.org/10.1152/japplphysiol.00108.2020.

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The blood-brain barrier (BBB), blood-cerebrospinal fluid (CSF) barrier (BCSFB), and CSF-brain barriers (CSFBB) are highly regulated barriers in the central nervous system comprising complex multicellular structures that separate nerves and glia from blood and CSF, respectively. Barrier damage has been implicated in the pathophysiology of diverse hypoxia-related neurological conditions, including stroke, multiple sclerosis, hydrocephalus, and high-altitude cerebral edema. Much is known about the damage to the BBB in response to hypoxia, but much less is known about the BCSFB and CSFBB. Yet, it

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Koziara, J. M., P. R. Lockman, D. D. Allen, and R. J. Mumper. "The Blood-Brain Barrier and Brain Drug Delivery." Journal of Nanoscience and Nanotechnology 6, no. 9 (September 1, 2006): 2712–35. http://dx.doi.org/10.1166/jnn.2006.441.

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The present report encompasses a thorough review of drug delivery to the brain with a particular focus on using drug carriers such as liposomes and nanoparticles. Challenges in brain drug delivery arise from the presence of one of the strictest barriers in vivo—the blood-brain barrier (BBB). This barrier exists at the level of endothelial cells of brain vasculature and its role is to maintain brain homeostasis. To better understand the principles of brain drug delivery, relevant knowledge of the blood-brain barrier anatomy and physiology is briefly reviewed. Several approaches to overcome the

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McCaffrey, Gwen, and Thomas P. Davis. "Physiology and Pathophysiology of the Blood-Brain Barrier." Journal of Investigative Medicine 60, no. 8 (December 1, 2012): 1131–40. http://dx.doi.org/10.2310/jim.0b013e318276de79.

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Serlin, Yonatan, Ilan Shelef, Boris Knyazer, and Alon Friedman. "Anatomy and physiology of the blood–brain barrier." Seminars in Cell & Developmental Biology 38 (February 2015): 2–6. http://dx.doi.org/10.1016/j.semcdb.2015.01.002.

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Robinson, P. J. "MEASUREMENT OF BLOOD-BRAIN BARRIER PERMEABILITY." Clinical and Experimental Pharmacology and Physiology 17, no. 12 (December 1990): 829–40. http://dx.doi.org/10.1111/j.1440-1681.1990.tb01286.x.

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Tietz, Silvia, and Britta Engelhardt. "Brain barriers: Crosstalk between complex tight junctions and adherens junctions." Journal of Cell Biology 209, no. 4 (May 25, 2015): 493–506. http://dx.doi.org/10.1083/jcb.201412147.

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Unique intercellular junctional complexes between the central nervous system (CNS) microvascular endothelial cells and the choroid plexus epithelial cells form the endothelial blood–brain barrier (BBB) and the epithelial blood–cerebrospinal fluid barrier (BCSFB), respectively. These barriers inhibit paracellular diffusion, thereby protecting the CNS from fluctuations in the blood. Studies of brain barrier integrity during development, normal physiology, and disease have focused on BBB and BCSFB tight junctions but not the corresponding endothelial and epithelial adherens junctions. The crossta

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Grant, Gerald A., N. Joan Abbott, and Damir Janigro. "Understanding the Physiology of the Blood-Brain Barrier: In Vitro Models." Physiology 13, no. 6 (December 1998): 287–93. http://dx.doi.org/10.1152/physiologyonline.1998.13.6.287.

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Endothelial cells exposed to inductive central nervous system factors differentiate into a blood-brain barrier phenotype. The blood-brain barrier frequently obstructs the passage of chemotherapeutics into the brain. Tissue culture systems have been developed to reproduce key properties of the intact blood-brain barrier and to allow for testing of mechanisms of transendothelial drug permeation.

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Ermisch, A., P. Brust, R. Kretzschmar, and H. J. Ruhle. "Peptides and blood-brain barrier transport." Physiological Reviews 73, no. 3 (July 1, 1993): 489–527. http://dx.doi.org/10.1152/physrev.1993.73.3.489.

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Sweeney, Melanie D., Zhen Zhao, Axel Montagne, Amy R. Nelson, and Berislav V. Zlokovic. "Blood-Brain Barrier: From Physiology to Disease and Back." Physiological Reviews 99, no. 1 (January 1, 2019): 21–78. http://dx.doi.org/10.1152/physrev.00050.2017.

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The blood-brain barrier (BBB) prevents neurotoxic plasma components, blood cells, and pathogens from entering the brain. At the same time, the BBB regulates transport of molecules into and out of the central nervous system (CNS), which maintains tightly controlled chemical composition of the neuronal milieu that is required for proper neuronal functioning. In this review, we first examine molecular and cellular mechanisms underlying the establishment of the BBB. Then, we focus on BBB transport physiology, endothelial and pericyte transporters, and perivascular and paravascular transport. Next,

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Gray, Sarah M., and Eugene J. Barrett. "Insulin transport into the brain." American Journal of Physiology-Cell Physiology 315, no. 2 (August 1, 2018): C125—C136. http://dx.doi.org/10.1152/ajpcell.00240.2017.

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While there is a growing consensus that insulin has diverse and important regulatory actions on the brain, seemingly important aspects of brain insulin physiology are poorly understood. Examples include: what is the insulin concentration within brain interstitial fluid under normal physiologic conditions; whether insulin is made in the brain and acts locally; does insulin from the circulation cross the blood-brain barrier or the blood-CSF barrier in a fashion that facilitates its signaling in brain; is insulin degraded within the brain; do privileged areas with a “leaky” blood-brain barrier se

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MAYHAN, WILLIAM G. "Regulation of Blood-Brain Barrier Permeability." Microcirculation 8, no. 2 (April 2001): 89–104. http://dx.doi.org/10.1111/j.1549-8719.2001.tb00160.x.

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Chabrier, P. E., P. Roubert, P. Plas, and P. Braquet. "Blood–brain barrier and atrial natriuretic factor." Canadian Journal of Physiology and Pharmacology 66, no. 3 (March 1, 1988): 276–79. http://dx.doi.org/10.1139/y88-047.

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In brain, binding sites for atrial natriuretic factor (ANF) have been characterized in areas such as circumventricular organs that lack the tight capillary endothelial junctions of the blood–brain barrier and therefore are exposed to circulating peptides. Since atrial natriuretic factor acts directly on vascular endothelium and has been proposed to be actively involved in blood pressure regulation and fluid homeostasis, it is interesting to know whether ANF receptors exist on brain capillaries that constitute the blood–brain barrier and participate in the constant fluid exchange between blood

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Patel, Bhuvic, Peter H. Yang, and Albert H. Kim. "The effect of thermal therapy on the blood-brain barrier and blood-tumor barrier." International Journal of Hyperthermia 37, no. 2 (July 16, 2020): 35–43. http://dx.doi.org/10.1080/02656736.2020.1783461.

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Schulze, Dr C. "Understanding the Blood-Brain-Barrier." Neuropathology and Applied Neurobiology 23, no. 2 (April 1997): 150–51. http://dx.doi.org/10.1111/j.1365-2990.1997.tb01197.x.

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Schulze, C. "Understanding the Blood-Brain-Barrier." Neuropathology and Applied Neurobiology 23, no. 3 (June 1997): 150–51. http://dx.doi.org/10.1046/j.1365-2990.1997.t01-1-90098900.x.

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Cosolo, W. C., P. Martinello, W. J. Louis, and N. Christophidis. "Blood-brain barrier disruption using mannitol: time course and electron microscopy studies." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 2 (February 1, 1989): R443—R447. http://dx.doi.org/10.1152/ajpregu.1989.256.2.r443.

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Blood-brain barrier disruption with a hyperosmolar agent, mannitol, has previously been demonstrated to increase intracerebral methotrexate levels in rats. To determine the optimum conditions for blood-brain barrier disruption without producing neurological sequelae, adult Sprague-Dawley rats were infused with mannitol via the internal carotid artery at rates varying from 0.25 to 0.5 ml.s-1.kg-1. Methotrexate and Evans blue were used as markers of blood-brain barrier disruption. The optimum rate of mannitol that produced blood-brain barrier disruption without neurological sequelae was 0.25 ml.

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17

Robinson, P. J., and S. I. Rapoport. "Size selectivity of blood-brain barrier permeability at various times after osmotic opening." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 3 (September 1, 1987): R459—R466. http://dx.doi.org/10.1152/ajpregu.1987.253.3.r459.

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Recent experiments have shown that after osmotic opening the blood-brain barrier recloses more rapidly to larger than to smaller molecules. Quantitative theoretical analysis of blood-brain barrier permeability to different-sized molecules at different times after osmotic opening supports the concept of pore creation as a result of opening of tight junctions between endothelial cells. Experiments also suggest significant bulk water flow from capillaries into brain within 10 min after opening at an average rate of approximately 1.6 X 10(-4) cm3 X s-1 X g brain-1. A mathematical model of blood-br

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18

Scherrmann, J. M. "Drug delivery to brain via the blood–brain barrier." Vascular Pharmacology 38, no. 6 (June 2002): 349–54. http://dx.doi.org/10.1016/s1537-1891(02)00202-1.

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Dziegielewska, Katarzyna. "The Blood-Brain Barrier: Biology and Research Protocols." Clinical and Experimental Pharmacology and Physiology 31, no. 3 (March 2004): 195. http://dx.doi.org/10.1111/j.1440-1681.2004.03971.x.

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Pardridge, William M. "S1-01-01: Blood-brain barrier from physiology to therapeutics." Alzheimer's & Dementia 11, no. 7S_Part_2 (July 2015): P114. http://dx.doi.org/10.1016/j.jalz.2015.07.002.

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Pandit, Rucha, Liyu Chen, and Jürgen Götz. "The blood-brain barrier: Physiology and strategies for drug delivery." Advanced Drug Delivery Reviews 165-166 (2020): 1–14. http://dx.doi.org/10.1016/j.addr.2019.11.009.

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Wolburg, Hartwig, and Andrea Lippoldt. "Tight junctions of the blood–brain barrier." Vascular Pharmacology 38, no. 6 (June 2002): 323–37. http://dx.doi.org/10.1016/s1537-1891(02)00200-8.

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Hawkins, Brian T., Richard D. Egleton, and Thomas P. Davis. "Modulation of cerebral microvascular permeability by endothelial nicotinic acetylcholine receptors." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H212—H219. http://dx.doi.org/10.1152/ajpheart.01210.2004.

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Nicotine increases the permeability of the blood-brain barrier in vivo. This implies a possible role for nicotinic acetylcholine receptors in the regulation of cerebral microvascular permeability. Expression of nicotinic acetylcholine receptor subunits in cerebral microvessels was investigated with immunofluorescence microscopy. Positive immunoreactivity was found for receptor subunits α3, α5, α7, and β2, but not subunits α4, β3, or β4. Blood-brain barrier permeability was assessed via in situ brain perfusion with [14C]sucrose. Nicotine increased the rate of sucrose entry into the brain from 0

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24

Hendricks, Benjamin K., Aaron A. Cohen-Gadol, and James C. Miller. "Novel delivery methods bypassing the blood-brain and blood-tumor barriers." Neurosurgical Focus 38, no. 3 (March 2015): E10. http://dx.doi.org/10.3171/2015.1.focus14767.

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Glioblastoma (GBM) is the most common primary brain tumor and carries a grave prognosis. Despite years of research investigating potentially new therapies for GBM, the median survival rate of individuals with this disease has remained fairly stagnant. Delivery of drugs to the tumor site is hampered by various barriers posed by the GBM pathological process and by the complex physiology of the blood-brain and blood–cerebrospinal fluid barriers. These anatomical and physiological barriers serve as a natural protection for the brain and preserve brain homeostasis, but they also have significantly

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Ezan, Pascal, Pascal André, Salvatore Cisternino, Bruno Saubaméa, Anne-Cécile Boulay, Suzette Doutremer, Marie-Annick Thomas, Nicole Quenech'du, Christian Giaume, and Martine Cohen-Salmon. "Deletion of Astroglial Connexins Weakens the Blood–Brain Barrier." Journal of Cerebral Blood Flow & Metabolism 32, no. 8 (April 4, 2012): 1457–67. http://dx.doi.org/10.1038/jcbfm.2012.45.

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Astrocytes, the most prominent glial cell type in the brain, send specialized processes named endfeet, which enwrap blood vessels and express a large molecular repertoire dedicated to the physiology of the vascular system. One of the most striking properties of astrocyte endfeet is their enrichment in gap junction protein connexins 43 and 30 (Cx43 and Cx30) allowing for direct intercellular trafficking of ions and small signaling molecules through perivascular astroglial networks. The contribution of astroglial connexins to the physiology of the brain vascular system has never been addressed.

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Seo, Suyeong, Hwieun Kim, Jong Hwan Sung, Nakwon Choi, Kangwon Lee, and Hong Nam Kim. "Microphysiological systems for recapitulating physiology and function of blood-brain barrier." Biomaterials 232 (February 2020): 119732. http://dx.doi.org/10.1016/j.biomaterials.2019.119732.

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Mayhan, W. G., F. M. Faraci, and D. D. Heistad. "Disruption of the blood-brain barrier in cerebrum and brain stem during acute hypertension." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 6 (December 1, 1986): H1171—H1175. http://dx.doi.org/10.1152/ajpheart.1986.251.6.h1171.

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The purpose of this study was to examine hemodynamic mechanisms of protection of the blood-brain barrier in the brain stem during acute hypertension. We used a new method to examine the microcirculation of the brain stem. Intravital fluorescent microscopy and fluorescein-labeled dextran were used to evaluate disruption of the blood-brain barrier during acute hypertension in rats. During control conditions, pressure (servo null) in arterioles (60 microns in diameter) was 50 +/- 2% (mean +/- SE) of systemic arterial pressure in the cerebrum and 67 +/- 1% of systemic arterial pressure in the brai

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Harik, S. I., R. A. Behmand, and J. C. LaManna. "Hypoxia increases glucose transport at blood-brain barrier in rats." Journal of Applied Physiology 77, no. 2 (August 1, 1994): 896–901. http://dx.doi.org/10.1152/jappl.1994.77.2.896.

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Prolonged hypoxia causes several adaptive changes in systemic physiology and tissue metabolism. We studied the effects of hypobaric hypoxia on glucose transport at the blood-brain barrier (BBB) in the rat. We found that hypoxia increased the density of brain microvessels seen on immunocytochemical stains using an antibody to the glucose transporting protein GLUT. In addition, we found that hypoxia increased the density of GLUT in isolated cerebral microvessels as determined by specific cytochalasin B binding. The higher GLUT density in isolated cerebral microvessels was evident after 1 wk of h

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Nag, Sukriti, and Stephen C. Pang. "Effect of atrial natriuretic factor on blood–brain barrier permeability." Canadian Journal of Physiology and Pharmacology 67, no. 6 (June 1, 1989): 637–40. http://dx.doi.org/10.1139/y89-101.

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Recent studies have demonstrated receptors for atrial natriuretic factor on endothelium of intracerebral vessels. The physiological role of these receptors is not known. The present study was undertaken to determine whether atrial natriuretic factor has an effect on blood–brain barrier permeability to protein and ions using horseradish peroxidase and lanthanum as markers of permeability alterations. This study does not demonstrate a significant effect of atrial natriuretic factor on blood–brain barrier permeability mechanisms in steady states.Key words: blood–brain barrier, atrial natriuretic

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Hathaway, Christopher A., Caroline B. Appleyard, William H. Percy, and John L. Williams. "Experimental colitis increases blood-brain barrier permeability in rabbits." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 5 (May 1, 1999): G1174—G1180. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1174.

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Extraintestinal manifestations of inflammatory bowel disease are numerous. This study examined the effects of two models of acute colitis on cerebral blood flow (CBF) and permeability of the blood-brain barrier in rabbits. CBF (measured with radiolabeled microspheres), or the extraction ratio or permeability-surface area (PS) product of the blood-brain barrier to fluorescein and FITC-dextran, was measured 48 h after colitis induction with acetic acid (HAc) or trinitrobenzene sulfonic acid (TNBS). PS product for fluorescein increased ( P < 0.05) in TNBS colitis (1.33 × 10−5 ± 0.52 × 10−5 ml/

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Urakawa, M., K. Yamaguchi, E. Tsuchida, S. Kashiwagi, H. Ito, and T. Matsuda. "Blood-brain barrier disturbance following localized hyperthermia in rats." International Journal of Hyperthermia 11, no. 5 (January 1995): 709–18. http://dx.doi.org/10.3109/02656739509022502.

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Stonestreet, B. S., C. S. Patlak, K. D. Pettigrew, C. B. Reilly, and H. F. Cserr. "Ontogeny of blood-brain barrier function in ovine fetuses, lambs, and adults." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 6 (December 1, 1996): R1594—R1601. http://dx.doi.org/10.1152/ajpregu.1996.271.6.r1594.

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The ontogeny of regional blood-brain barrier function was quantified with the rate constant for influx (Ki) across the blood-brain barrier with the small molecular weight synthetic, inert hydrophilic amino acid alpha-aminoisobutyric acid (AIB) in chronically instrumented early (87 days of gestation, 60% of gestation) and late (137 days of gestation, 90% of gestation) gestation fetal, newborn (3 days of age), older (24 days of age), and adult (3 years of age) sheep. The Ki was significantly (P < 0.05) lower in the brain regions of the adult sheep and in most brain regions of newborn and olde

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Tennant, M., and L. D. Beazley. "A breakdown of the blood-brain barrier is associated with optic nerve regeneration in the frog." Visual Neuroscience 9, no. 2 (August 1992): 149–55. http://dx.doi.org/10.1017/s0952523800009615.

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AbstractWe have examined the integrity of the blood-brain barrier during optic nerve regeneration in the frog Liloria (Hyla) moorei using rhodamine B-labeled bovine serum albumin (RBA). A transient localized breakdown of the blood-brain barrier was observed between 1 and 5 weeks after extracranial optic nerve crush. The zone of breakdown progressed along the experimental optic nerve, ascended the opposite optic tract, and swept rostro-caudally across the tectum contralateral to the crushed nerve. By 7 weeks, the blood-brain barrier was once again intact along the length of the optic pathway. I

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Reidelberger, Roger D., Dean Heimann, Linda Kelsey, and Martin Hulce. "Effects of peripheral CCK receptor blockade on feeding responses to duodenal nutrient infusions in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 2 (February 1, 2003): R389—R398. http://dx.doi.org/10.1152/ajpregu.00529.2002.

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Type A cholecystokinin receptor (CCKAR) antagonists differing in blood-brain barrier permeability were used to test the hypothesis that duodenal delivery of protein, carbohydrate, and fat produces satiety in part by an essential CCK action at CCKARs located peripheral to the blood-brain barrier. Fasted rats with open gastric fistulas received devazepide (1 mg/kg iv) or A-70104 (700 nmol · kg−1· h−1iv) and either a 30-min intravenous infusion of CCK-8 (10 nmol · kg−1· h−1) or duodenal infusion of peptone, maltose, or Intralipid beginning 10 min before 30-min access to 15% sucrose. Devazepide pe

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Saint-Pol, Julien, Fabien Gosselet, Sophie Duban-Deweer, Gwënaël Pottiez, and Yannis Karamanos. "Targeting and Crossing the Blood-Brain Barrier with Extracellular Vesicles." Cells 9, no. 4 (April 1, 2020): 851. http://dx.doi.org/10.3390/cells9040851.

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The blood–brain barrier (BBB) is one of the most complex and selective barriers in the human organism. Its role is to protect the brain and preserve the homeostasis of the central nervous system (CNS). The central elements of this physical and physiological barrier are the endothelial cells that form a monolayer of tightly joined cells covering the brain capillaries. However, as endothelial cells regulate nutrient delivery and waste product elimination, they are very sensitive to signals sent by surrounding cells and their environment. Indeed, the neuro-vascular unit (NVU) that corresponds to

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Thrippleton, Michael Jonathan. "MRI measurement of blood–brain barrier leakage: minding the gaps." Journal of Physiology 597, no. 3 (December 25, 2018): 667–68. http://dx.doi.org/10.1113/jp277425.

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HARDEBO, J. E., and J. KÅHRSTRÖM. "Endothelial negative surface charge areas and blood-brain barrier function." Acta Physiologica Scandinavica 125, no. 3 (November 1985): 495–99. http://dx.doi.org/10.1111/j.1748-1716.1985.tb07746.x.

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Osipova, Elena D., Oxana V. Semyachkina-Glushkovskaya, Andrey V. Morgun, Natalia V. Pisareva, Natalia A. Malinovskaya, Elizaveta B. Boitsova, Elena A. Pozhilenkova, et al. "Gliotransmitters and cytokines in the control of blood-brain barrier permeability." Reviews in the Neurosciences 29, no. 5 (July 26, 2018): 567–91. http://dx.doi.org/10.1515/revneuro-2017-0092.

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AbstractThe contribution of astrocytes and microglia to the regulation of neuroplasticity or neurovascular unit (NVU) is based on the coordinated secretion of gliotransmitters and cytokines and the release and uptake of metabolites. Blood-brain barrier (BBB) integrity and angiogenesis are influenced by perivascular cells contacting with the abluminal side of brain microvessel endothelial cells (pericytes, astrocytes) or by immune cells existing (microglia) or invading the NVU (macrophages) under pathologic conditions. The release of gliotransmitters or cytokines by activated astroglial and mic

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Jezova, D. "Neuroendocrine responses and blood-brain barrier during stress." Pathophysiology 1 (November 1994): 129. http://dx.doi.org/10.1016/0928-4680(94)90280-1.

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Huber, Jason D., Richard D. Egleton, and Thomas P. Davis. "Molecular physiology and pathophysiology of tight junctions in the blood–brain barrier." Trends in Neurosciences 24, no. 12 (December 2001): 719–25. http://dx.doi.org/10.1016/s0166-2236(00)02004-x.

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Harik, Sami I. "Changes in the glucose transporter of brain capillaries." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 1992): S113—S117. http://dx.doi.org/10.1139/y92-252.

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Brain capillary endothelium has a high density of the GLUT-1 facilitative glucose transporter protein. This is reasonable in view of the brain's high metabolic rate for glucose and its isolation behind unique capillaries with blood – brain barrier properties. Thus, the brain endothelium, which constitutes less than 0.1% of the brain weight, has to transport glucose for the much larger mass of surrounding neurons and glia. I describe here the changes that occur in the density of glucose transporters in brain capillaries of subjects with Alzheimer disease, where there is a decreased cerebral met

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ÖztaşL, B., and M. Küçük. "Reversible blood-brain barrier dysfunction after intracarotid hyperthermic saline infusion." International Journal of Hyperthermia 14, no. 4 (January 1998): 395–401. http://dx.doi.org/10.3109/02656739809018241.

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Phan, Duc TT, R. Hugh F. Bender, Jillian W. Andrejecsk, Agua Sobrino, Stephanie J. Hachey, Steven C. George, and Christopher CW Hughes. "Blood–brain barrier-on-a-chip: Microphysiological systems that capture the complexity of the blood–central nervous system interface." Experimental Biology and Medicine 242, no. 17 (February 14, 2017): 1669–78. http://dx.doi.org/10.1177/1535370217694100.

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The blood–brain barrier is a dynamic and highly organized structure that strictly regulates the molecules allowed to cross the brain vasculature into the central nervous system. The blood–brain barrier pathology has been associated with a number of central nervous system diseases, including vascular malformations, stroke/vascular dementia, Alzheimer’s disease, multiple sclerosis, and various neurological tumors including glioblastoma multiforme. There is a compelling need for representative models of this critical interface. Current research relies heavily on animal models (mostly mice) or on

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Banks, William A. "The blood-brain barrier: Connecting the gut and the brain." Regulatory Peptides 149, no. 1-3 (August 2008): 11–14. http://dx.doi.org/10.1016/j.regpep.2007.08.027.

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Harris, Andrew P., Roderick Robinson, Raymond C. Koehler, Richard J. Traystman, and Christine A. Gleason. "Blood-brain barrier permeability during dopamine-induced hypertension in fetal sheep." Journal of Applied Physiology 91, no. 1 (July 1, 2001): 123–29. http://dx.doi.org/10.1152/jappl.2001.91.1.123.

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Dopamine is often used as a pressor agent in sick newborn infants, but an increase in arterial blood pressure could disrupt the blood-brain barrier (BBB), especially in the preterm newborn. Using time-dated pregnant sheep, we tested the hypothesis that dopamine-induced hypertension increases fetal BBB permeability and cerebral water content. Barrier permeability was assessed in nine brain regions, including cerebral cortex, caudate, thalamus, brain stem, cerebellum, and spinal cord, by intravenous injection of the small tracer molecule [14C]aminoisobutyric acid at 10 min after the start of dop

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Robinson, Peter J. "FACILITATION OF DRUG ENTRY INTO BRAIN BY OSMOTIC OPENING OF THE BLOOD-BRAIN BARRIER." Clinical and Experimental Pharmacology and Physiology 14, no. 11-12 (December 1987): 887–901. http://dx.doi.org/10.1111/j.1440-1681.1987.tb02425.x.

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Banks, William A., and Abba J. Kastin. "Permeability of the blood-brain barrier to melanocortins." Peptides 16, no. 6 (January 1995): 1157–61. http://dx.doi.org/10.1016/0196-9781(95)00043-j.

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Abbott, N. Joan. "Physiology of the blood–brain barrier and its consequences for drug transport to the brain." International Congress Series 1277 (April 2005): 3–18. http://dx.doi.org/10.1016/j.ics.2005.02.008.

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Fischer, H., R. Gottschlich, and A. Seelig. "Blood-Brain Barrier Permeation: Molecular Parameters Governing Passive Diffusion." Journal of Membrane Biology 165, no. 3 (October 1, 1998): 201–11. http://dx.doi.org/10.1007/s002329900434.

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Schlosshauer, Burkhard, and Heiko Steuer. "Comparative Anatomy, Physiology and In Vitro Models of the Blood-Brain and Blood-Retina Barrier." Current Medicinal Chemistry-Central Nervous System Agents 2, no. 3 (September 1, 2002): 175–86. http://dx.doi.org/10.2174/1568015023357978.

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