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Etoposide-induced blood-brain barrier disruption

Effect of drug compared with that of solvents

Melvin K. Spigelman, Rosario A. Zappulla, James Johnson, Stanley J. Goldsmith, Leonard I. Malis and James F. Holland

T he role of the blood-brain barrier (BBB) in response of malignant brain tumors to chemotherapy remains controversial. 2, 19, 23 There is evidence, however, that the BBB is completely intact in small central nervous system (CNS) neoplasms and at least partially intact in many larger tumors. 9, 11 This evidence forms a basis for the hypothesis that the relative impermeability of the BBB to most chemotherapeutic drugs is an important factor in the treatment of these malignancies. One experimental approach currently under investigation is the search for

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The blood-brain barrier following experimental subarachnoid hemorrhage

Part 1: Response to insult caused by arterial hypertension

Eric W. Peterson and Erico R. Cardoso

T he integrity of the blood-brain barrier (BBB) is essential for maintaining a constant environment for the nervous tissue. Numerous conditions have been found to alter the BBB in the course of disease of the nervous system, including hypertension, infarct, seizures, trauma, and sudden increase in intracranial pressure (ICP). 12, 23, 31, 37, 42–44, 51, 54, 58, 59, 63, 64, 73 It is logical to inquire whether changes in the properties of the BBB may follow bleeding in the subarachnoid space. It is well recognized that elevation of blood pressure may follow

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The blood-brain barrier following experimental subarachnoid hemorrhage

Part 2: Response to mercuric chloride infusion

Eric W. Peterson and Erico R. Cardoso

P revious studies of the blood-brain barrier (BBB) and acute subarachnoid hemorrhage (SAH) showed that SAH did not of itself lead to BBB breakdown, and that it could inhibit the BBB damage that followed induced arterial hypertension. 11, 53 Because we suspected that this might be due to a protective effect of vasospasm sparing the cerebral capillaries from the hypertensive insult, we decided to study the influence of SAH on the effects of a vasotoxic agent on the BBB. Mercuric chloride (HgCl 2 ) in low concentrations is thought to damage the BBB by membrane

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Bernhard Zünkeler, Richard E. Carson, Jeff Olson, Ronald G. Blasberg, Hetty Devroom, Robert J. Lutz, Stephen C. Saris, Donald C. Wright, William Kammerer, Nicholas J. Patronas, Robert L. Dedrick, Peter Herscovitch and Edward H. Oldfield

T he blood-brain barrier (BBB) restricts movement of water-soluble substances between blood and brain parenchyma. 22 Although this cellular barrier protects the brain from rapid fluctuations in blood concentration of hydrophilic solutes in normal individuals, its function can be significantly altered in malignant brain tumors. 27 The endothelial cells of tumor capillaries in high-grade gliomas lose their intercellular tight junctions and ability to prevent or retard the entry of water-soluble substances into tumor parenchyma. This “leakiness” of the blood

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Michiyasu Suzuki, Yuzo Iwasaki, Teiji Yamamoto, Hidehiko Konno and Hiroko Kudo

M odification of the blood-brain barrier (BBB) has recently been introduced to facilitate drug delivery to central nervous system (CNS) tissue as a new strategy for the treatment of brain tumors and inborn enzyme defects. 1, 7, 8, 13–15, 22 Following the pioneer work by Rapoport and his colleagues, 17, 19 arterial infusion of hyperosmotic solutions has been most commonly used as a measure to increase the vascular permeability in both experimental and clinical trials, and a number of studies have been devoted to the elucidation of the mechanism and kinetics

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Dennis E. Bullard and Darell D. Bigner

chemotherapeutic agents, including intra-arterial delivery with or without prior blood-brain barrier (BBB) disruption. Initial work, however, has not clearly defined the role played by the route of delivery in either achieving optimal drug levels in tumor or in therapeutic efficacy. 1, 11, 13, 15 Thus, further work is required in animal models before human studies can be conducted. Several of the most commonly used and best defined animal models employ Fischer 344 rats, * including the 9L gliosarcoma model, 2 the avian sarcoma virus (ASV)-induced glioma model, 7, 25, 26

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Stanley A. Baldwin, Isabella Fugaccia, David R. Brown, Laura V. Brown and Stephen W. Scheff

E ndothelial cells of the brain vasculature form a continuous wall joined by tight junctions, with a high reflective coefficient and electrical resistance that prevent virtually all water-soluble substances from entering the central nervous system (CNS). The unique vascular characteristic of the CNS, known as the blood-brain barrier (BBB), provides protection for the brain and spinal cord from potential neurotoxins circulating in the blood as well as maintaining disparate ion concentrations in the extracellular space of the brain and vascular plasma. 5, 6, 50

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Edward A. Neuwelt, Mark Glasberg, Jan Diehl, Eugene P. Frenkel and Peggy Barnett

T he blood-brain barrier limits the access of most drugs to the central nervous system. This barrier is the result of tight junctions (zonulae occludentes) between the cerebral capillary endothelial cells. It has been clearly demonstrated in experimental models 6, 7, 10 that the blood-brain barrier can be reversibly modified (that is, opened) by the osmotic effect of hypertonic solutions such as mannitol. In order to achieve an effective osmolality at the capillary endothelial cell, the hypertonic solutions must be infused intra-arterially. In our previous

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Joseph H. Goodman, W. George Bingham Jr. and William E. Hunt

external membrane leaflets to form pentalaminar structures at several points along its course. This demonstrates an anatomic substrate of the blood-brain barrier system. L = lumen, P = pericyte, BL = basal lamina. H & E, × 60,000. Fig. 2. Control vessel in white matter showing a prominent collagen (C) containing perivascular space, endothelial junction (arrow) , and fibrous glia. H & E, × 4600. Traumatized Tissue In traumatized tissue, alterations in the endothelial tight junctions in gray matter were seen as early as 1 ½ minutes following injury

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Tej D. Azad, James Pan, Ian D. Connolly, Austin Remington, Christy M. Wilson and Gerald A. Grant

M anagement of most primary brain tumors includes maximal safe resection or biopsy followed by radiation and chemotherapy to target the remaining and potentially invasive tumor cells. However, delivering effective adjuvant treatment to these residual cell populations without damaging physiological brain tissue is a major challenge. One critical obstacle to effective treatments is the blood-brain barrier (BBB). This dynamic structure protects the CNS from environmental toxins and mediates physiological responses, effectively isolating the brain from the