@article {4969,
	title = {Vasodilator effects of organotransition-metal nitrosyl complexes, novel nitric oxide donors},
	journal = {Journal of Cardiovascular Pharmacology},
	volume = {35},
	number = {1},
	year = {2000},
	note = {ISI Document Delivery No.: 270ABTimes Cited: 26Cited Reference Count: 14},
	month = {Jan},
	pages = {73-77},
	type = {Article},
	abstract = {Nitrovasodilators cause endothelium-independent relaxation of blood vessels by generating nitric oxide (NO). We examined the relaxation and depressor effects of two organotransition-metal nitrosyl complexes, CpCr(NO)(2)Cl and CpMo(NO)(2)Cl, relative to those of the prototypal nitrovasodilators, nitroglycerin, and sodium nitroprusside (SNP), in phenylephrine-preconstricted aortic rings and conscious, unrestrained rats. CpCr(NO)(2)Cl, CpMo(NO)(2)Cl, nitroglycerin and SNP caused dose-dependent relaxation of aortic rings at maximal responses (E-max) of -118 +/- 4, -113 +/- 4, -104 +/- 1, and -128 +/- 5\% and EC50 of 0.14 +/- 0.04, 22 +/- 4, 1.23 +/- 0.65, and 0.063 +/- 0.013 mu M, respectively. The dose-response curve of CpCr(NO)(2)Cl was displaced to the right by hemoglobin, as well as methylene blue, showing involvement of the NO/cGMP pathway. Unlike nitroglycerin, preexposure for 1 h to CpCr(NO)(2)Cl did not alter subsequent relaxation response to the compound, Intravenous bolus injections of CpCr(NO)(2)Cl, CpMo(NO)(2)Cl, nitroglycerin, and SNP caused dose-dependent decreases in MAP with E-max of -42 +/- 2, -51 +/- 8, -56 +/- 6, and -58 +/- 2 mm Hg and EC50 of 0.041 +/- 0.010, 13 +/- 4, 1.6 +/- 0.4, and 0.037 +/- 0.004 mu mol/kg, respectively. These results show that CpCr(NO)(2)Cl and CpMo(NO)(2)Cl are efficacious nitrovasodilators in vitro and in vivo.},
	keywords = {BLOOD, cyanide, ISOLATED TAIL ARTERY, metal-nitrosyl complexes, nitric oxide, nitroglycerin, nitrovasodilator, pressure, RAT AORTA, relaxation, RELEASE, sodium nitroprusside (SNP), SODIUM-NITROPRUSSIDE},
	isbn = {0160-2446},
	url = {<Go to ISI>://000084512200009},
	author = {Wang, Y. X. and Legzdins,Peter and Poon, J. S. and Pang, C. C. Y.}
}
@article {4584,
	title = {Immunochemical extraction and detection of LSD in whole blood},
	journal = {Journal of Immunological Methods},
	volume = {224},
	number = {1-2},
	year = {1999},
	note = {ISI Document Delivery No.: 195AQTimes Cited: 10Cited Reference Count: 19},
	month = {Apr},
	pages = {11-18},
	type = {Article},
	abstract = {Polyclonal antibodies raised against the hallucinogenic drug, lysergic acid diethylamide (LSD), were used to detect and extract drug from whole blood samples. An indirect ELISA was used to detect as little as 1 pg of total drug in 25 mu l blood. The limit of detection of the immunoassay, calculated from the mean - 3 SD was 39 pg/ml. The analytical recovery of LSD (2.5-0.2 ng/ml) from whole blood was 102-113\%. Within-run CVs for LSD spiked in blood at 1.25, 0.16 and 0.04 ng/ml were 5.6, 3.1, and 8.9\%, respectively (n = 4). There was an overall decrease in precision when whole blood was used in place of urine, due to the increased complexity of the matrix. However, using this technique LSD was calibrated in blood in the sub-ng/ml region of forensic interest. Immunoaffinity extraction was used to isolate LSD from blood and urine samples. The affinity support was prepared by covalently attaching anti-LSD antibodies to Protein A-coated agarose beads. No pre-treatment of the sample was required other than the addition of neutral buffer. Sub-ng/ml concentrations of LSD were routinely extracted from blood and urine samples with greater than 80\% recovery of drug. This technique, which could be used to extract LSD from blood and urine samples prior to confirmatory drug analysis, could be completed in about 10 min. (C) 1999 Elsevier Science B.V. All rights reserved.},
	keywords = {BLOOD, CHROMATOGRAPHY-MASS-SPECTROMETRY, CONFIRMATION, ELISA, HUMAN URINE, immunoaffinity extraction, IMMUNOASSAY, LSD, LYSERGIC-ACID DIETHYLAMIDE, N-DEMETHYL-LSD, RADIOIMMUNOASSAY, SERUM},
	isbn = {0022-1759},
	url = {<Go to ISI>://000080227300002},
	author = {Kerrigan, S. and Brooks, D. E.}
}
@article {3223,
	title = {EVIDENCE FOR ENERGY-DEPENDENT TRANSPORT OF ALUMINUM OUT OF BRAIN EXTRACELLULAR FLUID},
	journal = {Toxicology},
	volume = {98},
	number = {1-3},
	year = {1995},
	note = {ISI Document Delivery No.: QX943Times Cited: 22Cited Reference Count: 36},
	month = {Apr},
	pages = {31-39},
	type = {Article},
	abstract = {Aluminum (Al) can cause CNS toxicity. The mechanism of its blood-brain barrier (BBB) permeation is poorly understood. In this study, microdialysis was used to determine extracellular fluid (ECF) unbound aluminum distribution between frontal cortex (FC) and blood during steady-state aluminum concentrations. The brain/blood aluminum ratio was determined. Over a 16-fold range of aluminum concentrations (dosed as aluminum citrate), brain/blood aluminum ratios were 0.10-0.15, consistently and significantly <1. Aluminum diffusion cannot account for these results, suggesting the presence of a carrier that moves aluminum out of brain extracellular fluid. These aluminum brain/blood ratios (BBRs) were not significantly different over the range of concentrations studied, suggesting an inability to saturate the carrier. Brain/blood aluminum ratios obtained with four aluminum-hydroxypyridinones were also significantly <1 (0.1-0.3), and were generally significantly different among themselves and from the aluminum citrate BBR. Movement of a BBB permeability marker from blood into brain extracellular fluid suggested partial BBB opening. The aluminum BBRs obtained (all much less than 1), in the presence of a partially opened BBR, suggest an efficient carrier moving aluminum out of brain ECF. Addition of cyanide to the brain microdialysis probe solution significantly increased the Al (citrate) BBR to 1, These results suggest the presence of an efficient, energy-dependent carrier that removes aluminum from brain ECF, either into brain cells or blood.},
	keywords = {aluminum, ANTIPYRINE, BARRIER, BLOOD, BLOOD-BRAIN BARRIER, CHELATORS INVITRO, COMPLEXES, ENERGY-DEPENDENT ACTIVE TRANSPORT, INVIVO MICRODIALYSIS, iron, MICRODIALYSIS, MOBILIZATION, permeability, TRANSFERRIN},
	isbn = {0300-483X},
	url = {<Go to ISI>://A1995QX94300004},
	author = {Allen, D. D. and Orvig, Chris and Yokel, R. A.}
}
