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At least 19 recordsLinked to original sources
PubMed2000

Drug storage temperatures in rescue vehicles.

This study was conducted to determine storage temperatures of drugs carried on rescue vehicles. Recording thermometers were placed inside drug boxes carried on rescue vehicles. Those temperatures were compared with ambient air temperatures, temperatures inside mechanically cooled compartments of the rescue vehicles, and USP-recommended drug storage temperatures. The results indicate that drug storage temperatures in some prehospital rescue vehicles exceed USP guidelines. Mechanical cooling of the storage compartment results in drug storage temperatures within the USP guidelines. Mechanical cooling of drug storage compartments on vehicles is technologically and financially possible.

Ambulances↗
PubMedDate not supplied

In-home drug storage and utilization habits: a Sudanese study.

Community drug-use habits were studied in 469 household units in different areas of Sudan. About 97.7% of the investigated families had at least one drug product stored at home. The study revealed a high rate of self-medication (46.9%), repeated use of unfinished stored drugs (55.0%), a high rate of drug exchange among families (59.3%) and poor compliance (71.2%). In Sudan there is still a great need to educate and to motivate the general public regarding the principles of rational drug use in order to safeguard health and avoid economic losses.

Drug Prescriptions↗
PubMed1991

Changes in saccharide and phospholipid content associated with drug storage in cultured rabbit aorta muscle cells.

In the investigation of cellular changes associated with intracellular drug storage, we incubated cultured rabbit aorta muscle cells with various amphiphilic agents. Disobutamide, chloroquine, and desipramine each increased cellular content of rhamnose, arabinose, mannose, glucose, and total saccharides; these agents also elevated total and individual phospholipid of all classes. Amiodarone did not alter total saccharide content, but increased total phospholipid. Tilorone, in contrast, decreased total saccharides, but phospholipid content was unchanged. All test agents decreased xylose content. By light microscopy, disobutamide, chloroquine, and tilorone induced clear cytoplasmic vacuoles; desipramine induced dense cytoplasmic granules; and amiodarone induced both cytoplasmic changes. By electron microscopy, the content of the cellular alterations induced by disobutamide was primarily electron lucent; that of the alterations induced by desipramine was primarily concentric lamellar bodies/flocculent electron-dense structures; and that of the alterations induced by amiodarone was a mixture of both. There was no correlation, therefore, between the induced cellular chemical contents and morphologic changes. Despite the physicochemical similarity of the amphiphilic drugs (all have cationic and lipophilic moieties), the chemical responses they induced were different. The results suggest that amphiphilic drugs alter processes involving saccharides as well as those of phospholipid metabolism. The origin of the saccharide moieties associated with the induced changes in monosaccharide contents is not known. Increased content of phosphatidylinositol, mannose, and glycosyl residues is consistent with the suggestion that amphiphilic drugs may cause an increase in membrane anchor synthesis. The inhibition of lysosomal enzyme activities responsible for the degradation of phospholipid and other anchors may also account for the observed increase in monosaccharides and phosphatidylinositol content.

Amines↗
PubMed1989

Disobutamide: a model agent for investigating intracellular drug storage.

Disobutamide, a bis tertiary amine (pKa1 = 8.6; pKa2 = 10.2) cationic amphiphilic compound, and a putative cardiac antiarrhythmic drug induced clear cytoplasmic vacuoles in dogs and rats. Ultrastructurally, the vacuoles were membrane-bound vesicles containing primarily electron-lucent material. Some concentric lamellar bodies indicative of phospholipidosis were also present. Although numerous vacuoles were seen in one-year toxicity studies in dogs and rats, there was no apparent evidence of necrosis, inflammation, atrophy, hypoplasia, hyperplasia, or metaplasia. Clinical signs or laboratory findings indicative of functional impairment were also not apparent. The picture of the vacuolation in vivo was one of storage. In cultured cells vacuoles were shown to be storage sites for disobutamide and specifically in distended vesicles of the cytoplasmic acidic compartments, such as lysosomes, endocytic, and probably transport vesicles. Storage of the drug in acidic vesicles is compatible with the dibasic nature of the cationic moiety of disobutamide. The intrinsic cell chemicals which accumulate in the vacuoles along with disobutamide remain unknown. Disobutamide may be a useful agent for defining experimentally the borderline between physiologic limits (normal function) and toxicity (functional impairment) in the condition of intracellular drug storage abnormalities and for advancing knowledge of storage mechanisms.

Animals↗
PubMed1989

Investigations in intracellular drug storage: localization of disobutamide in lysosomal and nonlysosomal vesicles.

In the investigation of the dynamic nature of intracellular drug-induced storage disorder associated with clear cytoplasmic vacuoles (CCV), rat urinary bladder carcinoma cells (RBT CC-8) were cultured with [14C]disobutamide. Cell monolayers were then harvested and analytical cell fractionation techniques were employed to examine the association of disobutamide with the various subcellular fractions. Disobutamide distributed into two modes: as a free, organelle-independent fraction and as a light membrane-associated fraction that overlapped with markers for the plasma membrane, endoplasmic reticulum, and lysosomes. The similarity in buoyant densities of these organelles derived from RBT CC-8 cells precluded resolution of these structures by isopycnic centrifugation. In additional experiments, disobutamide was incubated in vitro with a suspension of isolated rabbit renal proximal tubules. In these cells, analytic fractionation showed that the drug localized predominantly to lysosomes and to a separate light membrane fraction that was clearly resolved from the markers for the endoplasmic reticulum, brush border, mitochondria, and peroxisomes; this fraction overlapped with the most buoyant aspects of the Golgi apparatus and basolateral plasma membrane. The buoyant density of this disobutamide-associated nonlysosomal fraction was 1.11 g/ml. Electron microscopy of the disobutamide-exposed tubules showed a substantial formation of apical vesicles, especially small, smooth-surfaced vesicles, typical of the endocytic apparatus. From these findings and based on the physicochemical properties of the cationic moiety of disobutamide, we conclude that the drug localizes in lysosomal and nonlysosomal acidic vesicles.

Animals↗