[Nursing diagnosis: a good deed or a misdeed?].
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Biomedical subjects
Publications and source records attributed to C Lambert.
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The aims of this study were to investigate the influence of heart failure and dietary sodium content on the natriuretic effect of furosemide. Ten healthy Golden Syrian hamsters (HH) and 10 hamsters with a cardiomyopathy (CMH) were maintained on a normal sodium diet (NSD) and an equal number of animals on sodium deficient diet (SDD) for a minimum of 40 days. Three experiments were conducted on days 1, 20 and 40. Each experiment started with a 24-hour urine collection (control), followed by the administration of 5 mg/kg of furosemide i.p. and a second 24-hour urine collection and finally, the administration of 2 mg/kg of indomethacin i.p. followed 30 minutes later by 5 mg/kg of furosemide and a 24-hour urine collection as well as blood sampling. Sodium, creatinine, furosemide and arginine vasopressin (AVP) were measured in the urine and sodium, creatinine and AVP in plasma. After 134 days on a SDD, four HH resumed a NSD and the response to furosemide was again assessed after 12 days. Our results indicate that the natriuretic response to furosemide is higher in CMH than in HH. The SDD tended to increase the response to furosemide in HH as well as in CMH. Indomethacin did not influence the response to furosemide under any experimental condition. In four HH the increment in the fractional excretion of sodium in response to furosemide was 0.88 +/- 0.21% after 134 days on SDD and decreased to 0.35 +/- 0.12 (p less than 0.05) after 12 days on NSD. In all cases urinary excretion of furosemide was similar. Plasma AVP was higher in CMH and was not influenced by the SDD. In conclusion, SDD as well as cardiomyopathy with congestive heart failure do not decrease the natriuretic effect of furosemide and may not be a cause in the variability of the natriuretic response to furosemide.
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The Special Procedures Laboratory of the Department of Pathology at M.D. Anderson Hospital was concerned with the nationwide shortage of hematoxylin. The amount of this dye required for various staining solutions was calculated to determine thrifty usage. Some solutions required more hematoxylin than was available and prompted the serious investigation of existing techniques and new methods for routine laboratory use. Evaluation of various techniques resulted in a significantly successful modification of Gomori's aldehyde fuchsin technique, which was subsequently adopted as a routine procedure for elastic tissue staining in the Special Procedures Laboratory.
Purified nuclei isolated from mice challenged with nonlethal levels of mercury chloride (10-(3)M) in drinking water for 4 to 7 weeks (experimental) and from animals given deionized water (control) were fractionated and the subsequent fractions were analyzed for mercury by flameless atomic absorption. Control (active) euchromatin contained 1.75 +/- 0.53 micrograms of mercury per milligram of DNA. There was a 12- to 15-fold enrichment of mercury in the euchromatin fraction of challenged animals. Mercury was not detected in control (inactive) heterochromatin, and only trace levels (parts per billion) appeared in experimental heterochromatin. It seems likely that mercury can be incorporated into chromatin as a metal-protein complex, but the possibility of protein-mercury-DNA or mercury-DNA complexes within euchromatin cannot be excluded.
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Deficiencies of the terminal C fragments of the complement system are known to be associated with a remarkable increase in the frequency of Neisseria infections. The correlation is even closer between deficiency of C5 and recurrent N. meningitidis meningitis. The reasons for this bacterial specificity and the immunopathological mechanisms involved have not been clearly established. However, it is known that only adult subjects with homozygous deficiency are affected and that the deficiency is transmitted as an autosomal recessive trait unrelated to the HLA system.
To investigate the relationship between the effects of lidocaine on excitation patterns and its effects on the incidence of arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine, at a dose of either 2.5, 5.0, or 10.0 mg/kg i.v., in 29 open-chest anesthetized pigs. Sixty-three unipolar electrograms and a surface lead electrocardiogram were continuously recorded during atrial pacing and spontaneous ventricular arrhythmias. Ventricular fibrillation (VF) occurred only in four of a total of 45 control occlusions. VF occurred in two of five pigs following injection of lidocaine 2.5 mg/kg, in 15 or 17 pigs following injection of a 5 mg/kg dose, and in all three preparations following injection of a 10 mg/kg dose. Just prior to VF during occlusions preceded by injections of lidocaine 5 mg/kg, activation time of ischemic myocardium in atrial-paced beats was delayed by only 30 +/- 17 ms beyond preocclusion values, compared with 18 +/- 11 ms at a similar time during control occlusions and 33 +/- 18 ms at the end of control occlusions (mean +/- SD; n = 8). As ventricular tachycardia (VT) developed in the presence of lidocaine, conduction was further slowed or blocked in ischemic areas, and slowed in nonischemic regions; at the transition from VT to VF, excitation patterns displayed circus movement involving nonischemic regions.
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