Disaster Olympics: A Model for Resident Education.

OBJECTIVES: The aim of this study was to describe an educational method teaching Disaster Medicine to American Emergency Medicine (EM) physicians and to evaluate knowledge attainment using this method. METHODS: This was an observational study using a pre-test and a post-test. A full-scale disaster exercise (FSE) was conducted at a large academic center with two hospitals in Brooklyn, New York (USA). Eighty-two EM residents (physicians in training, post medical school) participated in the study. Inclusion criteria for study participation was all EM residents training at the State University of New York (SUNY) Downstate at the time of the study. There were no exclusion criteria. The exercise was a disaster drill designed as "Olympic Games." Participants in the exercise took a pre-test and a post-test. The primary outcome of the study was the mean difference between pre-test and post-test scores of the study participants using independent sample t-tests. Secondary outcomes of the study were percent of critical actions met by the residents and the hospitals as measured by direct observation of trained study personnel during the exercise. RESULTS: Mean resident post-test scores were higher than pre-test scores to a degree that was statistically significant (62% versus 53%; P =.002). The residents' performances ranged from 48% to 63% of objectives met. The hospitals' performances met 50% to 100% of their objectives. CONCLUSION: The use of an Olympic Games format was an effective model for disaster education for physicians. The model allowed for evaluation of performance and protocols of participants and hospital systems, respectively, and may be used objectively to evaluate for areas of improvement. The Disaster Olympics drill was found to improve emergency preparedness knowledge in the population studied and may constitute a novel and efficacious methodology in disaster training. Daniel P , Gist R , Grock A , Kohlhoff S , Roblin P , Arquilla B . Disaster Olympics: a model for resident education. Prehosp Disaster Med. 2016;31(3):237-241.

Use of sodium hetastarch (Hespan) solution for reduction of postoperative adhesion formation in rabbits.

A study was conducted to determine the effect of sodium hydroxy ethyl starch (Hespan) on primary adhesion formation in a rabbit model. Hespan is a readily available volume expander. This was a randomized, double-blinded animal model in which New Zealand white rabbits were subjected to midline celiotomy. Adhesions were created by abrasion in both uterine horns, adjacent bowel, and peritoneum. Necropsies were performed at the 2-week interval and adhesions were graded. Significant decreases in type II and type III adhesions (p = .032 and p = .020, respectively) were demonstrated in Hespan-treated animals. Sodium hetastarch appears to decrease significant adhesion formation in treated animals and may have a role as an adjunct for postsurgical prevention.

Placenta increta occurring in a blighted ovum.

We present a rare case of placenta increta, confirmed postoperatively by pathologic analysis, occurring before 20 weeks' gestation in a blighted ovum. Hysterectomy was necessary for control of hemorrhage.

Occupational stress in contemporary fire service.

Although it is universally accepted that firefighting ranks among the most stressful occupations in the U.S., the quality of information on the matter has often been limited and subject to extreme variation. To help address the situation, the authors provide a thorough review of the literature on psychic trauma resulting from critical occupational events, draw specific applications to fire and rescue enterprises, discuss models of addressing stress disorders, and argue for a reasoned, ethical, and effective approach to the problem.

Certification change versus actual behavior change in teenage suicide rates, 1955-1979.

National data on firearm suicides and accidental firearm deaths for persons aged 15-19 from 1955 to 1979 were examined to test hypotheses of increases in reported suicide rates as resulting from (1) improved accuracy in the determination and certification of suicide in equivocal firearm deaths; (2) actual increases in the rate of firearm suicides among teens; or (3) some combination of these factors. Data presented support the hypothesis of certification changes as the primary factor influencing suicide rates during the first 12-year segment, but suggest a period of actual growth combined with continued certification change from 1967 to 1979.

Alpha 2-adrenoceptor blockade attenuates feeding behavior induced by neuropeptide Y and epinephrine.

Neuropeptide Y (NPY, 0.47 nmol) and epinephrine (28.9 nmol) evoked robust, and quantitatively similar, increments in food intake and local eating rate following administration into the third cerebral ventricle (IIIV). Whereas IIIV pretreatment with phentolamine (71 nmol), a nonselective alpha-adrenoceptor antagonist, or prazosin (9.5 nmol), a selective alpha 1-adrenoceptor antagonist, was without effect on NPY-induced feeding behavior, pretreatment with the alpha 2-adrenoceptor antagonist yohimbine (15 nmol) dramatically attenuated the stimulatory effects of NPY or epinephrine on both food intake (by over 50%) and local eating rate. Additionally, yohimbine administered alone was associated with a stimulatory effect on food intake for the periods of 80-110, and 110-140 minutes posttreatment. These data demonstrate that feeding behavior induced by IIIV administration of NPY or epinephrine is attenuated by prior blockade of alpha 2-adrenoceptors and suggest that, as in other systems innervated by neurons displaying NPY and adrenergic transmitter colocalization, the effects of NPY on feeding behavior may, at least in part, be mediated via alpha 2-adrenoceptors.

Spontaneously hypertensive rats exhibit reduced hypothalamic noradrenergic input after NaCl loading.

Spontaneously hypertensive rats (SHR) of the Okamoto strain exhibit a significant exacerbation in severity of hypertension when fed diets high in NaCl. To examine the hypothesis that abnormalities in the monoaminergic innervation of the hypothalamus and brainstem contribute to the NaCl-induced exacerbation of hypertension, the monoamine and monoamine metabolite contents of specific hypothalamic and brainstem regions thought to be involved in the pathogenesis of hypertension were determined in SHR fed a diet containing 8% or 1% NaCl for either 2 or 6 weeks beginning at age 8 weeks. SHR maintained on the 8% NaCl diet for 2 weeks displayed significant decreases in norepinephrine in both the anterior and posterior hypothalamic regions but not in other brainstem or hypothalamic regions, as compared with animals consuming 1% NaCl. In addition, stores of the principal terminal norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol were reduced in the anterior hypothalamic region of SHR fed an 8% NaCl diet for 2 weeks. After 6 weeks on the diets, SHR fed 8% NaCl showed small but statistically nonsignificant reductions in norepinephrine stores of the anterior hypothalamic region as compared with SHR fed a basal diet, while WKY fed 8% NaCl had significantly elevated norepinephrine stores in the anterior hypothalamic region as compared with WKY fed a basal diet. There was a significant group X diet interaction (p less than 0.05). After 6 weeks on the 8% NaCl diet, SHR (but not WKY) displayed a significant reduction in norepinephrine content of the posterior hypothalamic region. No NaCl-induced differences in norepinephrine stores were found in the pons or medulla of either strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Exacerbation of hypertension by high chloride, moderate sodium diet in the salt-sensitive spontaneously hypertensive rat.

In salt-sensitive spontaneously hypertensive rats (SHR-S) of the Okamoto strain, dietary salt loading causes an exacerbation of hypertension that is associated with a decrease in noradrenergic input to the depressor neurons in the anterior hypothalamus. In the present study, the contribution of chloride to the salt-induced hypertensive response was examined in the SHR-S, in order to test the hypothesis that diets high in chloride but moderate in sodium elevate blood pressure in genetically predisposed subjects. SHR-S were fed diets high in NaCl (1.97% Na+, 2.93% Cl-; 5% NaCl), high in chloride (2.93%) but moderate in sodium (0.39%) or moderate in NaCl (0.39% Na+, 0.61% Cl-; 1% NaCl). After 2 weeks, rats on the high (5%) NaCl diet exhibited a significant elevation in blood pressure compared to rats on the moderate (1%) NaCl diet, and this elevation was maintained throughout the next 3 weeks. SHR-S on the high chloride diet were not significantly more hypertensive than 1% NaCl-fed SHR-S during the first 3 weeks, but during the fourth and fifth weeks, SHR-S on the high chloride diet displayed a significant exacerbation of hypertension. The diet-induced elevation in blood pressure in groups fed either the 5% NaCl or high chloride (compared to 1% NaCl) diets was associated with significant decreases in norepinephrine stores in the anterior hypothalamic region, but no other changes in monoamines or monoamine metabolites in this region or in the posterior hypothalamic region. The high chloride diet did not increase blood pressure in normotensive Wistar-Kyoto rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Altered responsiveness of regional brain dopamine and DOPAC levels to systemic administration of quinpirole, a dopamine D2 agonist, in DOCA/NaCl-hypertensive rats.

Our previous studies have demonstrated that administration of quinpirole (LY171555), a potent and highly selective dopamine (DA) D2 receptor agonist, to conscious Sprague-Dawley rats produces increases in arterial pressure through the activation of sympathetic outflow and vasopressinergic activity. To test the hypotheses that quinpirole inhibits in vivo release of DA from central dopaminergic neurons by activation of DA receptors in the central nervous system (CNS) and that this mechanism may be altered in the desoxycorticosterone acetate (DOCA)/NaCl model of hypertension, we examined the effects of quinpirole on stores of DA and its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in brain regions of 4-week DOCA/NaCl-hypertensive rats and their normotensive controls. Levels of DA and DOPAC were measured in brain regions by HPLC 15 min after the i.v. administration of quinpirole (1 mg/kg). Quinpirole resulted in a significant increase in DA stores and decrease in DOPAC stores in most brain regions examined in both DOCA/NaCl-hypertensive rats and normotensive controls, presumably by inhibiting DA release through a presynaptic mechanism. In the vehicle-treated groups, DA stores in the anterior hypothalamus and DOPAC stores in the nucleus accumbens were lower in DOCA/NaCl-hypertensive rats than in H2O controls. Following quinpirole administration, DA stores in the anterior hypothalamus increased significantly in DOCA/NaCl-treated rats but not in H2O controls and DOPAC stores in the nucleus accumbens decreased significantly in H2O control rats but not in DOCA/NaCl-treated rats. These observations provide further evidence for the presence of inhibitory DA D2 receptors which modulate the activity of dopaminergic neurons in the CNS.(ABSTRACT TRUNCATED AT 250 WORDS)

Blunted responsiveness of posterior hypothalamic norepinephrine to quinpirole in DOCA/NaCl hypertensive rats.

Our previous studies have demonstrated that the specific dopamine D2 receptor agonist, quinpirole (LY171555), has a pressor effect in conscious normotensive rats and that this is accompanied by a centrally mediated increase in sympathetic activity and arginine vasopressin release. This pressor response to quinpirole is blunted in the DOCA/NaCl hypertensive rat. To examine the hypothesis that the responsiveness of the central noradrenergic and serotonergic systems to quinpirole treatment is altered in DOCA/NaCl rats, the norepinephrine (NE), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) contents of hypothalamic and brainstem areas were measured in 4-week DOCA/NaCl hypertensive and H2O control rats 15 minutes after the intravenous administration of quinpirole (1 mg/kg). The results demonstrate that quinpirole selectively reduced (26%) posterior hypothalamic NE content in control rats, but not in DOCA/NaCl hypertensive rats. The NE content in the spinal cord and 5-HIAA content in the pons were greater in DOCA/NaCl rats than in normotensive controls in both saline and quinpirole treated groups. Our data suggest that the specific D2 agonist may effect its central pressor response by stimulating NE release from posterior hypothalamic area, a "pressor" region of hypothalamus, and that this D2 agonist induced pressor mechanism may be blunted in DOCA/NaCl hypertension.

Sympathetic innervation alters growth and intrinsic heart rate of fetal rat atria maturing in oculo.

The influence of sympathetic innervation on the growth and intrinsic rate of beating established by fetal rat heart was studied by culturing fetal atrial tissue in sympathetically innervated and denervated anterior eye chambers of adult Sprague-Dawley rats. One anterior eye chamber in each host rat was sympathetically denervated by removing the ipsilateral superior cervical ganglion. In oculo, atrial grafts were vascularized by blood vessels sprouting from the iris and innervated by sympathetic and parasympathetic fibers from the ground plexus of the iris. Innervation was assessed by light-activated efferent nerve stimulation to the grafts that changed their rates of beating. The norepinephrine contents of 16 atria cultured for 2.5 months in sympathetically innervated and denervated eye chambers were 5.7 +/- 1.1 ng/implant vs. 0.2 +/- 0.07 ng/implant (mean +/- SEM), indicating permanent sympathetic denervation of the anterior eye chamber and the implanted atria. By 8 weeks in oculo, atria maturing in sympathetically innervated anterior eye chambers were 86% larger than those in denervated eye chambers (2.22 +/- 0.29 vs. 1.19 +/- 0.13 mm2); the weight of innervated transplants was over 3 times that of noninnervated grafts (2.35 +/- 0.75 vs. 0.76 +/- 0.21 mg). After implanted atria had ceased growing rapidly (2.5 months in oculo), bipolar electrodes were implanted adjacent to the cornea to record impulses from atrial grafts while host rats were unanesthetized. The dark-adapted baseline heart rates of sympathetically innervated and noninnervated atria were virtually identical (289 vs. 290 bpm). Graft intrinsic heart rate was estimated by combined beta-adrenergic and muscarinic receptor blockade with atenolol (1.0 mg/kg) and methylatropine (10 micrograms/kg). Sympathetically innervated transplants had lower intrinsic heart rates than noninnervated atria (134 +/- 25 vs. 213 +/- 12 bpm). These data suggest that sympathetic innervation of the developing heart influences both growth and intrinsic rate of beating.