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Biomedical subjects

E L Nelson

Publications and source records attributed to E L Nelson.

31 records · Page 2Linked to original sources

Incidence of skull fractures in Olmsted County, Minnesota.

Between 1935 and 1974, 3598 episodes of head trauma among Olmsted County, Minnesota, residents resulted in 1097 skull fractures. Of these, 53% were simple, 16% were depressed, 12% were compound, and 19% were basilar. The age-and sex-adjusted incidence of skull fractures was 44.3 per 100,000 person-years overall, was somewhat greater in the urban than in the rural areas of Olmsted County, and was relatively stable for the final 30 years of the study. Age-specific incidence rates were highest for the very young, and simple linear fractures were the predominant type of skull fracture in this age group and among the elderly. The male:female ratio of incidence rates varied from 2.1:1 to 4.5:1 depending on fracture type. Motor vehicle accidents accounted for 38% of the skull fractures and were a particularly important cause among young males. Falls accounted for 37% of the skull fractures and were the major cause of fractures in the elderly and pediatric age groups. The results of this population-based study may be helpful in formulating recommendations for the evaluation and management of head-injured patients.

Adolescent↗

Effect of chronic exposure to cold on some responses to catecholamines.

An objective of these studies was to test the responsiveness of cold-adapted (8 wk, 5 degrees C) rats to a specific beta-adrenergic agonist. Twenty-four hours after removal from cold, increases in tail skin temperature (Tsk) and colonic temperature (Tco) were measured for 2 h in air at 25 degrees C following subcutaneous (sc) administration of 28, 70 or 136 mug d,l-isoproterenol sulfate dihydrate/kg body wt to restrained male rats. Cold-adapted rats responded to each dose of isoproterenol with greater increases in Tsk than controls. Tco of both groups increased at the two highest doses, but cold-adapted rats showed a greater rise. Thus, cold-adapted rats showed greater metabolic (Tco) and vascular (Tsk) responsiveness to the beta-adrenergic agonist, isoproterenol, than nonadapted controls. No effect of the alpha-adrenergic agonist, phenylephrine (50 or 100 mug/kg body weight, sc), was observed on Tco or Tsk. A second objective was to study the tension developed by aortic smooth muscle rings of cold-adapted and control rats both during stimulation of alpha-adrenergic receptors by norepinephrine and membrane depolarization by KCl. Adaptation to cold air appeared to suppress alpha-adrenergic responsiveness in aortic segments but did not alter responsiveness to KCl. This suggests an unchanged contractile mechanism in aortic rings of cold-adapted rats and a reduced responsiveness either at the level of the alpha-receptor or at a site immediately beyond.

Adaptation, Physiological↗

Effect of hypothyroidism on responsiveness to beta-adrenergic stimulation.

Chronic administration of aminotriazole (0.5 g/kg food) to rats was accompanied by a reduced responsiveness to acute administration of the beta-adrenergic agonist, l-isoproterenol (50-100 mug/kg, sc). The responses tested included water intake, change in heart rate in the anesthetized and unanesthetized rat, change in mean blood pressure, and change in blood glucose concentration. In addition, the increase in tail skin temperature accompanying administration of epinephrine (1 mg/kg, sc) was significantly reduced in the hypothyroid group. Administration of l-thyroxine (25 mug/kg per day, ip) to aminotriazole-treated rats prevented the reduction in responsiveness to beta-adrenergic stimulation. Thus, an interaction appears to exist between the level of thyroid activity and responsiveness to beta-adrenergic agonists in rats.

Adrenergic beta-Agonists↗

Effect of water temperature during cold exposure on thermogenic drinking in rats.

Availability of water at temperatures higher than ambient (15, 25, 35 degrees C) failed both to affect the ratio of water to food intake during exposure to cold air (5 degrees C) and to influence the thermogenic (postcold exposure) drinking response of rats which characteristically occurs immediately after removal from cold air. Thus, availability of warm water during exposure to cold appeared to have no influence on cold-induced dehydration in rats. A specially constructed drinking apparatus was used in this study. It was designed to maintain water at temperatures greater than ambient during exposure to cold. Details for construction of the apparatus are provided.

Animals↗

Prostaglandins and inflammation in the eye.

Traumatic injury of the eye promotes the release of prostaglandins E2 and F2alpha from the iris and other tissues. These induce vasodilation, increased capillary permeability and an increase in protein content of the aqueous. They are leukotactic. With an influx of leukocytes PGE1 appears in the aqueous having been synthesized by these cells. Infectious agents also attract leukocytes and sensitized lymphocytes characterize inflammation of both allergic and infectious origin. The cascade of molecular and cellular events seen in ocular inflammation of various origin seem ultimately to result in a reaction largely mediated by prostaglandins. Effective therapy should be directed at preventing their synthesis (synthetase inhibitors), interferring with their action once synthesized (receptor blockers), and inhibiting the migration of leukocytes into the eye.

Animals↗

Water exchange in rats exposed to cold, hypoxia, and both combined.

Male rats were exposed chronically to cold (5 degrees C air), hypoxia (12% oxygen in nitrogen), and both combined. Intake of water and food, as well as urinary excretion, were measured during both a 5-d pretreatment control period and throughout the first 3 weeks of the treatment period. Regression analysis of water intake on urine output revealed that, at a given water intake, all three treated groups excreted significantly more urine than controls. No significant differences occurred among treated groups. Serum osmolalities of all three treated groups, measured at the end of the 48-d treatment period, were elevated significantly above the level of the control group. All treated groups also manifested a thirst immediately following return to control environment (26 degrees C, 20.9% oxygen). Water intakes of all three treated groups were significantly greater than that of the control group during the first 2 h after return to control environment. Thus, the three treated groups appeared to be dehydrated relative to the control group. The results further suggest that the effect of combined cold (5 degrees C) and hypoxia (12% oxygen) on water exchange is not a summation of that occurring separately during cold and hypoxia. The factors inducing dehydration in cold and hypoxia are apparently related to increased evaporative water loss and to alterations in thirst and renal mechanisms.

Animals↗

Factors affecting thermogenic drinking in rats.

After as little as 6 h of exposure to cold air, drinking was induced in rats following transfer from air at 5 degreesC to air at 26 degreesC. Drinking began within 15 min after transfer from the cold enviroment and lasted approximately 1 h. The stimulus for initiation of drinking was most likely the temperature change resulting from the transfer, since an ambient temperature difference of 10 centigrade degrees or more was required to initiate a drinking response after transfer from air at 5 degreesC. Thermogenic drinking was not thwarted by preventing access to water for either 1 or 2h following transfer to warm air, but either intragastric or intraperitoneal administration of a water load equal to 3% of body weight inhibited water intake following transfer.The characteristics of the drinking response following transfer than 5 to 26 degrees C were similiar to those observed following 24 h of dehydration at 26 degrees C. Thus, the cold-exposed rat is relatively dehydrated compared with controls.

Animals↗

Reduced beta-adrenergic responsiveness in hypothyroid rats.

The beta-adrenergic agonist isoproterenol (100-200 mug/kg body wt sc) induces vasodilation and an increase in skin temperature of the tail of the euthyroid but not the hypothyroid rat. Administration of thyroxine (25 mug/kg body wt per day) to rats made hypothyroid by means of the antithyroid drug aminotriazole (0.5 g/kg of foof) returned responsiveness to control level. Reduced responsiveness to isoproterenol occurred between 1 and 5 wk of treatment with aminotriazole. Increase in tail skin temperature induced in euthyroid rats by isoproterenol was blocked by administration of propranolol (7.5 mg/kg ip). Other beta-adrenergic-induced responses, including increased water intake and increased plasma glucose concentration, also were reduced in hypothyroid rats and returned to control level by administration of thyroxine. Thus, hypothyroidism appears to be accompanied by a reduced beta-adrenergic responsiveness as assessed by changes in tail skin temperature, water intake, and plasma glucose concentration after injection of isoproterenol. Since administration of thyroxine returned the responses of hypothyroid rats to control levels, it appears that thyroxine is important in maintaining beta-adrenergic responsiveness under these conditions.

Animals↗

Peripheral body temperature and thermogenic drinking in cold-treated rats.

Transfer of rats abruptly from air at 5 degrees C to air at 26 degrees C was accompanied by a significant increase in water intake (thermogenic drinking) during the first hour after transfer. A possibility existed that the increased water intake observed under these conditions was attributable to the rapid change in skin temperature. Thus, the objective of this study was to determine the effect on thermogenic drinking of a slow, as opposed to an abrupt, change in ambient temperature. The results indicated that warming room air rates of either 0.5 or 1.0 centigrade deg/min had no effect on thermogenic drinking when compared with the water intake of rats removed abruptly from cold. Thermogenic drinking does not appear to be initiated by a specific pattern of changes in peripheral temperature relative to colonic temperature.

Acclimatization↗