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Keizo Kaba, Eiichi Tani, Tatsuo Morimura, and Tsuyoshi Matsumoto

Recently, calcium channel blockers and calmodulin inhibitors have been found to enhance vincristine cytotoxicity, particularly in vincristine-resistant murine and human tumor cells. 19–25 Since vincristine has been widely used as a chemotherapeutic drug together with cell-cycle nonspecific agents for the treatment of human glioma, 4, 7, 10, 11, 15 the present study examines the effect of calcium channel blockers and calmodulin inhibitors on vincristine cytotoxicity for human and murine glioma cells. Materials and Methods Glioma Cells Five glioma cell lines

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Ab Guha, Charles H. Tator, and Ian Piper

T he vascular physiology of the spinal cord and brain are similar in that autoregulation, the blood-central nervous system (CNS) barrier phenomenon, and CO 2 -reactivity exist in both. 14–16, 29 Furthermore, insults such as hemorrhage or trauma produce similar pathophysiological reactions in both tissues. 8, 40, 42 Calcium channel blockers have been studied extensively in the brain and have shown promise in promoting dilation of cerebral vessels and an increase in cerebral blood flow in normal and pathological states. 1, 30, 31, 44, 48 The current study was

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Abhijit Guha, Charles H. Tator, and Ian Piper

blood flow (SCBF) as well as microangiographic studies after spinal cord injury have shown ischemia at the injury site and extending considerable distances. 8, 9, 18, 19, 22, 30, 34–38 The understanding and treatment of posttraumatic ischemia are therefore of great interest. Calcium channel blockers, especially nimodipine with its selective vasodilatation of cerebral vessels, are being investigated for the treatment of cerebral ischemic states such as post-subarachnoid hemorrhage vasospasm. 1, 2, 20, 28, 29, 31, 40, 46 Previously, it was shown in our laboratory

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Koichi Okiyama, Douglas H. Smith, Mark J. Thomas, and Tracy K. McIntosh

channel blockers have been shown to exert protective effects following cerebral ischemia 22, 27 and subarachnoid hemorrhage. 43, 60 In addition, clinical studies have investigated the effect of calcium channel blockers on outcome after head injury. 2, 11, 26 However, few experimental studies have addressed the effect of calcium channel blockers on traumatic brain injury. A novel phenylalkylamine calcium antagonist, (S)-emopamil ((2s)-2-isopropyl-5-methylphenethylamino-2-phenylvaleronitrile hydrochloride), was developed especially for CNS penetration. This compound

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Robert F. Berman, Bon H. Verweij, and J. Paul Muizelaar

, 37 As a result, there has been a major focus on the role of calcium in brain-injury mechanisms, as well as interest in the development of calcium channel blocking agents as potential neuroprotective agents after brain injury. 13, 19, 32, 33, 35 Entry of calcium into neurons is regulated in part by VSCCs. At least six types of VSCCs have been described including L, N, P, Q, R, and T. 15, 19, 20 The L-, N-, and P-type VSCCs play major roles in the release of various neurotransmitters, including glutamate. 34 Specific antagonists to the VSCCs have been developed

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Bon H. Verweij, J. Paul Muizelaar, Federico C. Vinas, Patti L. Peterson, Ye Xiong, and Chuan P. Lee

efficiency of ATP synthesis accompanying the oxygen consumption of a respiring substrate. The higher the P/O ratio, the better the phosphorylating efficiency of the mitochondria. Mitochondrial Calcium Content We have shown elsewhere that one of the hallmarks of mitochondrial dysfunction after experimental TBI is near-doubling of the mitochondrial calcium content. Because Ziconotide is a calcium channel blocker, we believe that it would be interesting to investigate the drug's effect on calcium content. A number of other parameters, such as State 4 respiratory rate, the

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Tadayoshi Nakagomi, Neal F. Kassell, Tomio Sasaki, Shigeru Fujiwara, R. Michael Lehman, Hiroo Johshita, and James C. Torner

ethyleneglycol-bis ( β -aminoethylether)-N, N′-tetra-acetic acid (EGTA) for 15 minutes. Then 10 −6 M PGF 2 α was added, and hypoxia was induced when the preparations showed stable contraction. Ten minutes after the induction of hypoxia, 2.5 mM Ca ++ was added. Finally, the effect of nicardipine, a calcium channel blocking agent, on the hypoxic potentiation was investigated. Preparations were exposed to nicardipine (10 −9 to 10 −7 M) for 15 minutes before the addition of 25 mM KCl, 3 × 10 −7 M PGF 2 α , or 10 −6 M hemoglobin. In this experiment, the effect of nicardipine

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Mark W. Roy, Robert J. Dempsey, Kathleen L. Meyer, David L. Donaldson, Phillip A. Tibbs, and A. Byron Young

observe changes in blood pressure or CBF with verapamil infusion prior to MCA occlusion. However, the inappropriately elevated blood flow in the nonischemic hemisphere following MCA occlusion certainly suggests that verapamil's vasodilating effects interfere with mechanisms normally restricting blood flow in the nonischemic zones. Although it is also classified as a calcium channel blocker, diltiazem is structurally dissimilar to verapamil. 8 Diltiazem is also a vasodilator, but produces virtually no tachycardia in normal individuals. 9 Judging from the differing

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Seiji Kondo, Dali Yin, Tatsuo Morimura, and Juji Takeuchi

resistance to the cytotoxic effects of cisplatin is not yet clear. In this study, we first found that multidrug-resistant (MDR) human glioblastoma GB-1 cells demonstrated significantly more resistance to cisplatin than did nondrug-resistant human glioblastoma U87-MG cells. Therefore, we attempted to determine whether calcium channel blockers, as chemosensitizers, enhance the cytotoxicity of cisplatin against GB-1 cells. In addition, in our study of the mechanism responsible for the synergism between cisplatin and calcium channel blockers, we have attempted to determine

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The effect of nimodipine on intracranial pressure

Volume-pressure studies in a primate model

Mark N. Hadley, Robert F. Spetzler, Mary S. Fifield, William D. Bichard, and John A. Hodak

N imodipine , a calcium channel blocker, has been shown to increase cerebral blood flow (CBF), particularly in areas of the brain where the blood-brain barrier has been disrupted. Increased CBF in these regions could potentially lead to deleterious increases of intracranial pressure (ICP), particularly in a patient with extensive swelling from stroke or a mass lesion. For this reason, investigators have cautioned against using calcium antagonists in acute stroke patients. 1, 3, 5 This laboratory investigation was undertaken to define the effects of nimodipine