The nature of and response to poisonings in the school setting has not been characterized. To define these problems a retrospective review of calls to a Regional Poison Information Center (RPIC) involving school exposures was done for the 1988-89 academic year. 362 cases were reported; 74% were reported by school nurses, 10% by other school employees, 10% by parents, 5% by health care facilities, and 1% by students themselves. Ingestions accounted for 45% of exposures, dermal 24%, ocular 19%, inhalation 7%, with the remainder being combinations of routes. Correct treatment prior to RPIC consultation occurred in only 40% of the cases. None developed major symptoms, 23% had minor and 10% had moderate symptoms. High school students accounted for the greatest number (20) of suicide gestures, while middle schools reported more cases of substance abuse. School nurses often were unaware of situations until several hours later. 61% of suicide gestures were referred to an HCF; 7 of these developed moderate symptoms. Exposures to chemicals in science or vo-tech classes accounted for 102 cases; 28% were referred to a HCF and 15% had moderate symptoms. There was often a delay in evaluation by the school nurse and initial decontamination was inadequate or absent. Parents were often instructed by school personnel to contact the RPIC for information and then relay it to the school. These delays could have resulted in greater toxicity. School nurses should be targeted for educational programs by poison centers, but teachers and other school employees must also be included since often they are the first at the scene. Students should be instructed to report exposures to a teacher immediately.

Accidents↗

PubMed1991

Agonist-sensitive calcium stores in arteries from steroid hypertensive rats.

The present study characterizes cellular calcium stores that are sensitive to norepinephrine and caffeine in arteries from deoxycorticosterone acetate hypertensive rats. Mesenteric arteries from normotensive and hypertensive rats were excised and cut into helical strips for isometric force recording. In calcium-free solution, phasic contractile responses to norepinephrine (5.9 x 10(-9) to 5.9 x 10(-6) M), but not caffeine (0.3-30 mM), were greater in hypertensive arteries. D-600, a calcium channel blocker, or removal of the endothelium did not alter phasic contractions to norepinephrine or caffeine. In contrast, contractions to both norepinephrine and caffeine were inhibited by ryanodine, a drug that depletes calcium from intracellular stores. An inhibitor of phospholipase C (2-nitro-4-carboxyphenyl N,N-diphenylcarbamate) attenuated contractions to norepinephrine but not those to caffeine. The augmented response to norepinephrine in hypertensive rats did not occur early after implantation of the mineralocorticoid, suggesting that this vascular change may not play a role in the development of high blood pressure in this experimental model. The augmented response to norepinephrine was reduced in mineralocorticoid-treated rats maintained on a low sodium diet, and these rats had blood pressures in the normotensive range. Because contractile responses to caffeine were not enhanced in arteries from hypertensive rats, we conclude that the cellular store for calcium is not enlarged compared with that in normotensive arteries. In contrast, the mobilization of calcium from cellular stores by norepinephrine is augmented in mineralocorticoid hypertension. This augmented response may be linked to altered phospholipase C activity and thus to an augmented action of inositol trisphosphate that releases calcium from intracellular sites.

Animals↗

PubMed1991