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Toxicity continued

After the initial IV dose, some clinicians administer 1 to 2 g/hr by constant IV infusion. Subsequent IM doses of 4 to 5 g magnesium sulfate may be injected into alternate buttocks every 4 hours, depending on the presence of the patellar reflex, adequate respiratory function, and absence of signs of magnesium toxicity. Continue therapy until paroxysms cease. [Pg.1271]

Table 3 Examples of Recently Reported Excipient Toxicity (Continued)... [Pg.28]

Table 2-5. Ongoing Studies for Aluminum Toxicity (continued)... Table 2-5. Ongoing Studies for Aluminum Toxicity (continued)...
In severe cases of exposure to toxicants, a population may go to zero and stay there so long as exposure continues or, if the toxicant is removed, until immigration from outside the ecosystem restores the population. In other cases, the population is reduced and remains at a lower level so long as exposure to the toxicant continues. Another possibility is for a population to decline, and then rise again as the population develops resistance to the effects of the toxic substance. This effect has been observed in the case of exposure to insecticides of insects whose short reproductive times enable natural selection to build populations resistant to the insecticides. [Pg.129]

Monitor valproic acid toxicity over time—if toxicity continues, consider decreasing dose... [Pg.1914]

Sulfacetamide is the IV-acetyl derivative of sulfanilamide. The sodium salt of sulfacetamide, because of its effectiveness and low toxicity, continues to be the most widely prescribed sulfonamide in the form of eye-drops and ointment for ophthalmic infections. It was introduced in Europe as "Albucid" in 1938 for various eye and other topical infections. Since its use in the treatment of corneal ulcers (1), sulfacetamide is still popular in ophthalmology. The sodium salt is highly soluble at the physiologic pH of 7.4, and is especially suited, as a 10-30% solution, for repeated topical application in the local management of ophthalmic infections (2-4). It is used mainly in the treatment of acute conjunctivitis and in the prophylaxis of ocular infections after injuries or burns (5). Several reviews on various aspects of sulfacetamide have been published (6-10). [Pg.473]

Anthracyclines - Adriamycin (ADR 20) has continued to be the dominant force in the expanding use of chemotherapeutic agents. Its wide spectrum of activity coupled with its dose-limiting cardiac toxicity continue to stimulate the search for structurally modified agents with improved biological profiles. Recent reviews on daunomycin (DNR 21),ADR and related antibiotics have appeared that discuss their chemistry and pharmacology. N-Trifluoroacetyladriamycin-14-valerate (AD-32 22), unlike the basic anthracyc lines, ADR and DNR, has been shown not to... [Pg.135]

Levin AA, Bosakowski T, Earle LL, et al. 1988. The reversibility of nitrobenzene-induced testicular toxicity Continuous monitoring of sperm output from vasocystotomized rats. Toxicology 53 219-230. [Pg.86]

TABLE IM. COMMON ANTIBACTERIAL AGENTS AND THEIR TOXICITIES (CONTINUED) ... [Pg.84]

TABLE 44.2 The Spilled Substances and Their Toxicity Continued)... [Pg.968]

It has long been known that copper salts given in excess to animals are toxic. Continuous ingestion of copper in excess of nutritional requirements leads to an accumulation of the element in the body tissues, especially in the liver. Copper can be regarded as a cumulative poison, so that considerable care is required in administering copper salts to animals. The tolerance to copper varies considerably between species. Pigs are highly tolerant (see Box 6.3) and cattle relatively so. On the other... [Pg.124]

One non-anticholinesterase effect of OPs has been discussed in section 10.3.1.3, namely OPIDP. The degree to which non-acetylcholinesterase inhibition effects contribute to acute OP toxicity continues to be a matter of interest and has been reviewed. Thus, Chambers " noted a poor correlation between rat oral LD50 values of various phosphorothionate insecticides and inhibition potency of corresponding oxons for brain acetylcholinesterase. However, there are a number of possible explanations for this, other than differences in target molecule notably, differences in site and magnitude of desulfuration of the thionate to the active oxon may be important. Studies by Duysen and colleagues with acetylcholinesterase knockout mice suggested that non-acetylcholinesterase inhibitory effects must contribute to the acute toxicity of VX. Maxwell et... [Pg.60]


See other pages where Toxicity continued is mentioned: [Pg.250]    [Pg.233]    [Pg.130]    [Pg.26]    [Pg.355]    [Pg.756]    [Pg.227]    [Pg.433]    [Pg.145]    [Pg.934]    [Pg.876]    [Pg.183]    [Pg.52]    [Pg.32]    [Pg.273]    [Pg.966]    [Pg.320]    [Pg.127]    [Pg.387]    [Pg.194]   


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