Statutory and regulatory recognition for clinical nurse specialists in Oregon.

Clinical nurse specialists (CNSs) in Oregon initiated the process of achieving statutory and regulatory recognition several years ago. Throughout this process, specific phases of activity and events helped CNSs to identify what was required to achieve this goal. The resulting lessons learned are shared in this report. Statutory recognition of CNSs in Oregon occurred in 1999, and the administrative rules for CNS practice were published in 2001. These administrative rules delineate the CNS scope of practice and other aspects of CNS practice consistent with national standards.

Effect of triiodothyronine augmentation on rat lung surfactant phospholipids during sepsis.

Surfactant functional effectiveness is dependent on phospholipid compositional integrity; sepsis decreases this through an undefined mechanism. Sepsis-induced hypothyroidism is commensurate and may be related. This study examines the effect of 3,3',5-triiodo-L-thyronine (T3) supplementation on surfactant composition and function during sepsis. Male Sprague-Dawley rats underwent sham laparotomy (Sham) or cecal ligation and puncture (CLP) with or without T3 supplementation [CLP/T3 (3 ng/h)]. After 6, 12, or 24 h, surfactant was obtained by lavage. Function was assessed by a pulsating bubble surfactometer and in vivo compliance studies. Sepsis produced a decrease in surfactant phosphatidylglycerol and phosphatidic acid, with an increase in lesser surface-active lipids phosphatidylserine and phosphatidylinositol. Phosphatidylcholine content was not significantly changed. Sepsis caused an alteration in the fatty acid composition and an increase in saturation in most phospholipids. Hormonal replacement attenuated these changes. Lung compliance and surfactant adsorption were reduced by sepsis and maintained by T3 treatment. Thyroid hormone may have an active role in lung functional preservation through maintenance of surfactant homeostasis during sepsis.

Effects of deferoxamine on H2O2-induced oxidative stress in isolated rat heart.

During myocardial reperfusion injury, iron has been implicated in the Fenton based generation of hydroxyl radical, .OH, leading to further organ injury. Although previous studies have investigated the protective effect of iron chelators including deferoxamine (DFX) in myocardial reperfusion injury, there is little information regarding the role of iron chelation during oxidative stress produced by H2O2 on the heart. Isolated hearts from male Sprague-Dawley rats were retrograde-perfused with Krebs-Henseleit solution at 5 ml/min. After a 60-min equilibration, oxyradical challenge was instituted by the addition of H2O2 (200-600 microM) to the perfusate for 60 min. A subgroup of animals received DFX (400 microM) in the perfusate prior to challenge with 400 microM H2O2. Contractility was continuously monitored; perfusate samples for glutathione (GSH) and lactate dehydrogenase (LDH) estimations were collected at 30-min intervals. Headspace ethane, an indicator of lipid peroxidation, was estimated at 30-min intervals by gas chromatography. Control hearts maintained contractility during the perfusion period. H2O2 perfusion caused a dose dependent decrease in myocardial contractility; DFX pretreatment was partially protective. Headspace ethane slowly accumulated in control hearts; perfusion with H2O2 caused dose dependent increase in ethane accumulation indicative of enhanced lipid peroxidation. GSH and LDH in the perfusate remained low in control hearts. In contrast, H2O2 treated hearts had a dose dependent increase in the efflux of GSH and LDH which was markedly increased by perfusion with 600 microM H2O2. Pretreatment with DFX did not significantly reduce GSH or LDH efflux from hearts perfused with peroxide. While H2O2 perfusion causes a dose dependent decrease in myocardial contractility with a corresponding increase in headspace ethane release with GSH & LDH efflux indicative of oxidative stress, concurrent treatment with DFX reduces myocardial dysfunction and ethane generation. However, sublethal damage of plasma membrane still continues as reflected by continuous enhancement of LDH efflux, possibly indicating involvement of other reactive species besides hydroxyl radical.

Effect of sepsis and 3,5,3'-triiodothyronine replacement on myocardial integrity during oxidant challenge.

OBJECTIVE: To determine whether sepsis, with or without thyroid hormonal augmentation, induces myocardial tolerance to an oxidant challenge. DESIGN: A prospective, randomized, controlled animal trial. SETTING: University research laboratory. SUBJECTS: Twenty male Sprague-Dawley rats. INTERVENTIONS: After anesthesia, animals underwent cecal ligation and puncture, with or without 3,5,3'-triiodothyronine replacement (3 ng/hr), or sham surgery. Twenty-four hours later, the heart was rapidly excised for retrograde Langendorff perfusion. Oxyradical challenge consisted of the addition of 200 microM of hydrogen peroxide to the perfusate for 60 mins. MEASUREMENTS AND MAIN RESULTS: Myocardial contractility and relaxation were continuously recorded. Perfusate glutathione and lactate dehydrogenase concentrations were determined enzymatically at 30-min intervals for 90 mins. Oxyradical perfusion alone significantly increased glutathione efflux and decreased myocardial contractility when compared with control animals. Prior cecal ligation and puncture decreased oxidant-mediated glutathione efflux and maintained myocardial contractility. 3,5,3'-triiodothyronine supplementation appeared to increase late cardiac contractility and cellular integrity during oxidant challenge. However, this increase was not statistically significant. CONCLUSIONS: Antecedent septic challenge appears to induce tolerance to further myocardial oxyradical exposure and improves myocardial functional and biochemical integrity. Thyroid hormonal supplementation may provide a modest additional benefit in septic animals.

Retrograde gastroesophageal intussusception complicating chronic achalasia.

We treated a patient with retrograde gastroesophageal intussusception complicating chronic achalasia. Operation consisted of diaphragmatic division in the median plane to facilitate reduction, followed by Heller myotomy and fundoplication for the achalasia. The patient was able to eat normally after recovery.

Challenges in integrating biological data sources.

Scientific data of importance to biologists reside in a number of different data sources, such as GenBank, GSDB, SWISS-PROT, EMBL, and OMIM, among many others. Some of these data sources are conventional databases implemented using database management systems (DBMSs) and others are structured files maintained in a number of different formats (e.g., ASN.1 and ACE). In addition, software packages such as sequence analysis packages (e.g., BLAST and FASTA) produce data and can therefore be viewed as data sources. To counter the increasing dispersion and heterogeneity of data, different approaches to integrating these data sources are appearing throughout the bioinformatics community. This paper surveys the technical challenges to integration, classifies the approaches, and critiques the available tools and methodologies.

The effects of carbon monoxide on persistent changes in young rat heart: cardiomegaly, tachycardia and altered DNA content.

Newborn rat pups that inhale 500 ppm carbon monoxide (CO) for 32 days and develop increased heart mass (i.e. cardiomegaly) show persistent cardiomegaly and elevated resting heart rate as adults. Studies were carried out to explore the relationship of these phenomena to CO concentration and initial cardiomegaly using exposures of 350, 500 and 700 ppm CO. Initial cardiomegaly was greater in the right ventricle free wall (RV) than in the left ventricle plus interventricular septum (LV + S) at all three CO concentrations, and RV mass excess increased with CO concentration. Initial RV cardiomegaly was greater at 350 and 700 ppm CO in females than in males. Persistent cardiomegaly in the RV also increased with CO concentration, and was significantly greater in the females. Persistent cardiomegaly in the RV increased with initial cardiomegaly but at a decreasing rate at the higher CO concentrations, and when expressed as a percentage of initial cardiomegaly (i.e. 'efficiency'), the relative response was greatest at 500 ppm CO. For LV + S, efficiency of development of persistent cardiomegaly was greatest at 350 ppm CO. Persistent tachycardia increased with CO concentration in males but failed to do so in females, and was only weakly correlated with degree of persistent cardiomegaly. Thus, persistent cardiomegaly and persistent tachycardia (in males) are related to CO concentration. Myocardial DNA content of 32-day-old juveniles was significantly increased at 350 and 700 ppm CO. Adult DNA content of the RV was significantly elevated at 350 ppm CO (females) and continued to rise with CO concentration. DNA concentrations of the RV and LV were increased at 700 ppm CO.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart and lung hypertrophy, changes in blood volume, hematocrit and plasma renin activity in rats chronically exposed to increasing carbon monoxide concentrations.

Changes in blood volume, heart and lung mass and composition and plasma renin activity were examined in two strains of male albino rats inhaling incrementally-increasing concentrations of CO: 250 ppm for 17 days, 500 ppm for 13-14 days, 750 ppm for 10 days, and 1300 ppm for 10 days. Blood volume increased 86% and erythrocyte mass increased 212% at 1300 ppm, while plasma volume was unchanged or decreased slightly. 'Real' hematocrit (hematocrit corrected for plasma trapping) increased from 50% in controls to a peak of 75% at 1300 ppm CO. Wet weight of right ventricle (RV) and combined right and left atria (2A) increased linearly with CO concentration, paralleling changes in blood volume; while real hematocrit increased non-linearly. Left ventricle + interventricular septum (LV + S) wet weight increased less than RV, but more in Sprague-Dawley than in Wistar rats. Plots of RV, LV + S and 2A weight vs real hematocrit showed sharp upward inflections at real hematocrit 65%, suggesting a possible role of increased viscosity in CO cardiomegaly at the higher hematocrit. Assymetric septal hypertrophy was not present. Lung weight increased with CO concentration, but was not due to increased lung blood volume or edema. Hydroxyproline measurements on heart and lung failed to show increased collagen content. Plasma renin activity measured by radioimmunoassay was depressed at 500 ppm, but was normal at 750 and 1300 ppm CO. Neither heart, lung, liver nor plasma renin measurements suggest congestive heart failure, supporting previous studies in the rat with chronic carboxyhemoglobinemia, in spite of enormously increased blood volume, hematocrit and heart weight.

Time course of blood volume change with carbon monoxide inhalation and its contribution to the overall cardiovascular response.

Adult male Sprague-Dawley rats inhaled 500 ppm CO continuously for 42 days in order to examine the blood volume response in a time course manner. Plasma volume as measured by Evan's blue dye dilution technique did not change significantly from the control value of 3.96% of body weight (BW). Total blood volume estimated using plasma volume and hematocrit increased steadily from 7.34% of BW to 11.69%, almost entirely as the result of a more than 2-fold increase in erythrocyte mass (3.42% increased to 7.55%). Absolute blood volume increased from 28.51 ml to 58.26 ml; normal growth contributed to this increase, i.e. BW increased from 350.0 g to 499.1 g. "Real hematocrit" determined by dye dilution increased from 46.5% to 64.6%, reaching a near-equilibrium level within 15 days. Hemoglobin concentration increased from 13.68 g/dl to 20.07 g/dl, and erythrocyte count increased from 6,150,000 per cubic mm to 9,140,000 per cubic mm. Minor changes in erythrocyte indices (i.e. mean corpuscular hemoglobin concentration and mean corpuscular volume) occurred during the 42 days. Concurrently, the weight of right ventricle increased more than left ventricle + septum, reflecting somewhat greater right-sided cardiomegaly. Increases in both ventricles were correlated with changes in blood volume and hematocrit. Plasma atrial natriuretic peptide activity increased 2.5 fold after 15 and 30 days of CO exposure, possibly reflecting increasing atrial stretch caused by increased blood volume. Like the polycythemic hypervolemic state of chronic hypoxic hypoxia, blood volume in CO hypoxia increases solely through addition of erythrocytes.

Effects of acute cold exposure on muscle amino acid and protein in rats.

To test the effects of acute cold on muscle amino acid and protein 1) rats were exposed to 4 degrees C for 24 h, functionally hepatectomized (eviscerated) and accumulation in the blood used to indicate changes in amino acid release from the tissues; 2) other rats were left intact, and urinary excretion of 3-methylhistidine (proportional to muscle protein breakdown) determined during cold exposure. In the eviscerated group, cold enhanced loss of total amino acids from the tissues (as alpha-amino nitrogen), but the loss (213 +/- 14.8% of basal in 2 h) was not due to excess alanine (180 +/- 8.5%). By comparison, in fasted rats total amino acid was 182 +/- 12.3, alanine 309 +/- 17.2%. Also, the cold-induced loss resembled the effects of streptozotocin diabetes and depended on a depression by cold of serum insulin (to 35.7 +/- 2.3 muU/ml). Therefore it was prevented when insulin was restored by infusion (40 mU . 100 g-1 . h-1) or by adrenodemedullation before cold exposure. Epinephrine (10 micrograms/100 g sc) depressed insulin in the latter and permitted amino acid release to recur. In intact rats, 3-methylhistidine excretion was unaffected by cold. The results suggest that although cold fails to stimulate alanine synthesis or protein breakdown, it inhibits insulin release sympathetically, thereby diminishing the amount of amino acid incorporated into muscle protein.

Shivering thermogenesis and glucose uptake by muscles of normal or diabetic rats.

Acute cold exposure of normal rats (4 degrees C for 24 h) increased food intake, reduced plasma glucose and liver glycogen, caused a small increase in plasma free fatty acids, and lowered serum insulin concentration by 50%. In fasted rats, cold raised fatty acid levels twice as high as in fed. In mild diabetes (40 mg/kg streptozotocin iv) cold reduced glucose levels in blood and urine, but in severe diabetes (90 mg/kg) cold aggravated hyperglycemia and ketonuria. Changes in muscle glucose utilization were also studied, after evisceration (functional hepatectomy) of rats from each group. Uptake was calculated from the fall in plasma glucose concentration during the 4-h period after a load of 50% glucose iv. Cold normally increased uptake 67%, but it failed to do so in fasted rats. In diabetic rats, cold enhanced uptake, but only if the disease were mild or insulin controlled. Sensitivity of uptake to insulin was unaffected by cold. The results suggest that shivering thermogenesis, like exercise, can promote glucose uptake by skeletal muscle, if enough insulin is present to prevent excess mobilization of lipid substrates.