Biomedical subjects
K P Kelly
Publications and source records attributed to K P Kelly.
Randomised comparison of partial liquid ventilation, nebulised perfluorocarbon, porcine surfactant, artificial surfactant, and combined treatments on oxygenation, lung mechanics, and survival in rabbits after saline lung lavage.
OBJECTIVE: To compare gas exchange, lung mechanics, and survival to 12 h in surfactant-depleted lung-injured rabbits, treated with partial liquid ventilation (PLV) with perfluorocarbon, nebulised perfluorocarbon, and porcine or artificial surfactant. DESIGN: Prospective randomised controlled study. SETTING: Animal laboratory, University of Edinburgh, UK. SUBJECTS: Eighty-two adult female New Zealand white rabbits with surfactant deficiency and acute lung injury induced by repeated saline lavage. INTERVENTIONS: Animals were randomised to one of seven treatments: (a) control (n = 20); (b) PLV with perfluorocarbon PF 5080 (n = 12); (c) nebulised PF 5080 (n = 10); (d) artificial surfactant (n = 10); (e) porcine surfactant (n = 10); (f) artificial surfactant+PLV (n = 10); (g) porcine surfactant+PLV (n = 10). MEASUREMENTS AND MAIN RESULTS: Arterial blood gases and dynamic compliance (Cdyn) were measured hourly until 12 h. Oxygenation was improved by PLV, porcine surfactant, porcine surfactant+PLV and artificial surfactant+PLV. Cdyn improved after treatment with PLV, porcine surfactant and PLV+porcine surfactant. Survival was greater with PLV and artificial surfactant+PLV. Neither nebulised PF 5080 nor artificial surfactant had a detectable effect. CONCLUSIONS: PLV, porcine surfactant and combinations of surfactant with PLV improved oxygenation, Cdyn and survival, but none was clearly superior to the others.
Pediatric oncology nursing in cooperative group clinical trials comes of age.
OBJECTIVES: To provide a review of the nursing committees in both the Children's Cancer Group and the Pediatric Oncology Group and discuss intergroup nursing research collaboration in preparation for the merger of these cooperative clinical trials groups. DATA SOURCES: Review articles, reports, and newsletters from cooperative clinical trials groups. CONCLUSIONS: Nurses have established a vital presence in the pediatric cancer cooperative groups over the past 20 years through education, clinical practice, and collaborative research. IMPLICATIONS FOR NURSING PRACTICE: With the unification of the pediatric cooperative groups into the single Children's Oncology Group, the time is uniquely right to build a program of nursing research allied with pediatric oncology cooperative group clinical trials.
Cocaine and exercise: alpha-1 receptor blockade does not alter muscle glycogenolysis or blood lactacidosis.
In our previous work, we routinely observed that a combined cocaine-exercise challenge results in an abnormally rapid muscle glycogen depletion and excessive blood lactacidosis. These phenomena occur simultaneously with a rapid rise in norepinephrine and in the absence of any rise in epinephrine. We postulated that norepinephrine may cause vasoconstriction of the muscle vasculature through activation of alpha-1 receptors during cocaine-exercise, thus inducing hypoxia and a concomitant rise in glycogenolysis and lactate accumulation. To test this hypothesis, rats were pretreated with the selective alpha-1-receptor antagonist prazosin (P) (0.1 mg/kg iv) or saline (S). Ten minutes later, the animals were treated with cocaine (-C) (5 mg/kg iv) or saline (-S) and run for 4 or 15 min at 22 m/min at 10% grade. In the S-S group, glycogen content of the white vastus lateralis muscle was unaffected by exercise at both time intervals, whereas in S-C rats glycogen was reduced by 47%. This effect of cocaine-exercise challenge was not attenuated by P. Similarly, blood lactate concentration in S-C rats was threefold higher than that of S-S after exercise, a response also not altered by pretreatment with P. On the basis of these observations, we conclude that the excessive glycogenolysis and lactacidosis observed during cocaine-exercise challenge is not the result of vasoconstriction secondary to norepinephrine activation of alpha-1 receptors.
Acute lymphocytic leukemia in children. A medical success story.
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Radiation therapy in childhood cancer.
OBJECTIVES: To review treatment-related issues and acute and late side effects of radiation therapy for the treatment of childhood malignancies. DATA SOURCES: Research and review articles, oncology textbooks, and clinical experience. CONCLUSIONS: Radiation therapy is a key component in the treatment of childhood malignancies. Children receiving radiation have special nursing care needs that are dependent on growth and developmental issues. IMPLICATIONS FOR NURSING PRACTICE: Nurses play an important role in the education of families and children receiving radiation therapy. In addition, nurses are key in the management of acute and late toxicities from childhood radiation therapy.
Septic shock from the administration of a bacterially contaminated platelet transfusion.
We report the case of a 6-year-old boy who began to have fever and hypotension during the administration of a platelet transfusion. Subsequent investigation revealed the etiology to be bacterial contamination of the platelet product. Seratia marcescens was cultured from both the patient's blood and the platelet product. When fever and/or cardiorespiratory problems develop during the administration of blood products, possible bacterial contamination of the product must be considered so that appropriate therapy can be instituted. We discuss the etiology, possible preventive strategies, and the treatment of this problem.
Studying clinical decision making by patients, parents, and health care providers in pediatric oncology.
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Developing intergroup nursing research in pediatric oncology.
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Partial liquid ventilation--turning back a PAGE on evolution.
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Cocaine and exercise: temporal changes in plasma levels of catecholamines, lactate, glucose, and cocaine.
To determine the combined sympathoadrenal effects of cocaine and exercise in awake animals, rats were assigned to one of four treatment groups: saline-rest (SR), saline-exercise (SE), cocaine-rest (CR), and cocaine-exercise (CE). Venous blood samples from jugular catheters were obtained at -40, 0-4, 7, 10, 13, 16, 19, 26, and 36 min after intravenous injection of cocaine (5 mg/kg) or saline and the simultaneous onset of a 16-min treadmill run (26 m/min, 10% grade). CE increased plasma epinephrine (24.2 nM at 16 min), norepinephrine (28.0 nM at 10 min), and lactate (11.2 mM at 4 min) to levels 2-5 times greater than either treatment (SE and CR) alone (P<0.05) and 11-35 times higher that SR. Blood glucose values were significantly depressed in CE (-33% vs. SE) but increased in CR (+26% vs. SR). Plasma cocaine peaked < 2 min after injection in both CR and CE, and the peak was 69% higher in CE (P<0.05); however, the plasma elimination half-life (12-14 min) was not different. These results indicate that the combined effect of the two sympathoadrenal stimulants, exercise and cocaine, amplify the catecholamine responses to levels far greater than when each stimulant is used alone.
Leucopenia associated with lamotrigine.
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Cocaine alters myosin isoform expression in the rat soleus.
The purpose of this study was to determine whether chronic cocaine administration alters the expression of myosin isoforms in the rat soleus. Forty-five adult Sprague-Dawley rats were divided into three groups: chronic cocaine (n = 15), 12.5 mg/kg cocaine-HCl injected intraperitoneally twice daily for 14 days and one injection of cocaine (12.5 mg/kg ip) on day 15; acute cocaine (n = 15), saline injections twice daily for 14 days and one injection of cocaine (12.5 mg/kg ip) on day 15; and chronic saline (n = 15), saline injections twice daily for 14 days and one saline injection on day 15. Myosin isoform content of the soleus (native and heavy chains) was identified by electrophoresis. The solei samples from the chronic saline and acute cocaine animals contained slow myosin only. However, solei samples from the chronic cocaine group contained slow myosin and two to three other myosin isoforms and the associated heavy chains IIa and IIx. Therefore, chronic cocaine administration causes in the rat soleus a shift in myosin expression from slow isoforms to fast isoforms.
Cocaine and exercise: physiological responses of cocaine-conditioned rats.
To compare the physiological response to a cocaine-exercise challenge in cocaine-conditioned animals with that of acute-cocaine animals, rats were injected i.p. with either cocaine (20 mg.kg-1) or saline, twice daily for 14 consecutive days. On the 15th day (test day) cocaine-conditioned rats received an i.v. injection of cocaine (5 mg.kg-1) (chronic group). One-half of the chronic saline rats also received the cocaine injection (acute group), while the other half received saline (saline group). Immediately after injection, all rats were either rested or exercised (22 m.min-1, 10% grade) for 30 min. For most parameters there was no difference between the responses of the chronic and acute cocaine groups at rest or to the cocaine-exercise challenge. During exercise, both cocaine groups had similarly higher lactate values than the saline animals (P < 0.05). Both groups had similarly greater reductions in glycogen content of the white and red vastus muscles than occurred in the saline group; and both groups had similar increases in corticosterone. In contrast, cocaine-conditioned animals had a greater rise in norepinephrine (P < 0.059) and epinephrine (P < 0.001) in response to cocaine-exercise than did the acute group. The mechanism responsible for the exaggerated catecholamine response in the chronic cocaine animals is unknown.
Effects of cocaine, exercise, and resting conditions on plasma corticosterone and catecholamine concentrations in the rat.
Cocaine and exercise are both known as stressors, but little is known about the combined effects of these two treatments. In this study, rats under the influence of cocaine (12.5 mg/kg, intraperitoneally [IP]) or saline were exposed to a variety of resting conditions, as well as exercise (running, 26 m/min, 10% grade, for 30 minutes), to evaluate the amount of stress imposed by these conditions as determined by the changes in the plasma concentrations of corticosterone (C) and catecholamines (norepinephrine [NE], epinephrine [E], dopamine [DA]). After injection of saline, resting near the operating treadmill for 30 minutes caused the concentration of C to increase from 0.07 +/- 0.03 to 0.30 +/- 0.05 microgram/mL (P less than .05), compared to the increase to only 0.15 +/- 0.04 micrograms/mL after resting in a cage. This increase due to proximity to the treadmill subsided after 50 minutes. After cocaine, the 30-minute resting values were 0.70 +/- 0.15 (treadmill) and 0.55 +/- 0.13 (cage) (P less than .05), and did not subside after 50 minutes. Cocaine also increased levels of E, NE, and DA above those in saline under all rest conditions. With exercise, the value for C in saline increased to 0.61 +/- 0.18, but, in cocaine, the value went to 0.93 +/- 0.05 (P less than .05). The concentrations of E (946 +/- 74 v 603 +/- 101 pg/mL, cocaine v saline) and NE (1,027 +/- 102 v 440 +/- 153, cocaine v saline) during exercise also were exaggerated by cocaine treatment (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of cocaine on plasma catecholamine and muscle glycogen concentrations during exercise in the rat.
This study was designed to test the hypothesis that cocaine (C) alters the normal physiological responses to exercise. Male rats were injected with saline (S) or C (12.5 mg/kg) either intravenously (iv) or intraperitoneally (ip). After injection the animals were allowed to rest for 30 min or were run on the treadmill (26 m/min, 10% grade). At rest plasma epinephrine values were 245 +/- 24 pg/ml in the S group and 411 +/- 43 (ip) and 612 +/- 41 (iv) pg/ml in the C groups (P less than 0.05 between S and C). During exercise plasma epinephrine levels were 615 +/- 32 pg/ml in S and 1,316 +/- 58 (ip) and 1,208 +/- 37 (iv) pg/ml in the C groups (P less than 0.05 between S and C). Similar results were obtained for norepinephrine. Glycogen content in the white vastus lateralis muscle was reduced to 31 +/- 2 mumol/g in S after exercise, but after C and exercise the values were 12 +/- 4 (ip) and 16 +/- 3 (iv) mumol/g (P less than 0.05 between S and C). There was no effect of the drug on this parameter at rest. Blood lactate rose to 4.8 +/- 1.0 (ip) and 5.8 +/- 1.3 (iv) mM in the C groups but to only 3.0 +/- 0.2 in the S group after exercise (P less than 0.05 between S and C). These results show that C and exercise combined exert a more dramatic effect on plasma catecholamine, muscle glycogen, and blood lactate concentrations than do C and exercise alone. They provide further insight into explaining the adverse effects of C on exercise endurance observed previously (Bracken et al., J. Appl. Physiol. 66: 377-383, 1989).
Effects of cocaine on the physiology of exercise.
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