[Changes and reactions produced by lytic substances (acetic acid, nitric acid) in normal tissues. I. Effects on vasculo-nervous fasciae].
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Titanium was polished using several chemical polishing baths containing different ratios of hydrofluoric acid and nitric acid. The meltage, surface roughness, and surface texture of titanium samples after chemical polishing were affected by the ratio of hydrofluoric acid and nitric acid. Generally the meltage increased and surface roughness decreased when the mole concentration of hydrofluoric acid was high and that of nitric acid was low. For example the chemical polishing bath containing 5 mole hydrofluoric acid and 5 mole nitric acid improved the surface texture in one minute, but SEM observation revealed a partially rough surface caused by the excessive solution. The chemical polishing bath containing 1 mole hydrofluoric acid and 5 mole nitric acid did not improve the surface texture in a short time because of low solubility, but improved the surface texture gradually with the extension of the immersion time and a good surface texture was observed by SEM. The chemical polishing using the chemical polishing bath with low solubility and immersion of the prosthetics for a rather long time were considered useful procedures to obtain a smooth surface of titanium prosthetics while maintaining their accuracy.
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Sonochemical nitrous acid formation was investigated in 0.1-4.0 mol dm(-3) aqueous nitric acid solutions under the effect of power ultrasound with 20 kHz frequency. HNO2 steady-state concentration was obtained under long-time sonication; the excess HNO2 formed is decomposed and evoluted from the solution as NO and NO2 gases. The HNO2 steady-state concentration and the HNO2 initial formation rate depend linearly on the HNO3 concentration and acoustic intensity (1.8-3.5 W cm(-2)) and decrease with rising temperature in the range 21-50 degrees C. The HNO2 formation rate depends on the type of saturating gas as follows: Ar > N2 > He > air. NO and O2 are the major gaseous products of HNO3 sonication. The NO2 accumulation of in the gas phase is observed only when the decomposition of HNO2 formed becomes noticeable. The gaseous products formation rates depend on the HNO3 concentration, acoustic intensity and the type of saturating gas. The mechanism of HNO2 sonochemical formation is assumed to be the thermal decomposition of HNO3 in the gaseous vicinity of collapsing bubbles or in the overheated liquid reaction zone surrounding the cavitational bubbles.
The destruction of small lesions by tissue denaturation (fixation) rather than erosion (acid hydrolysis) is accomplished by nitric acid of moderate strength in which nitric acid reduction products are generated by nitric acid oxidation of added organic acids. Such solutions show a temperature-dependent increase or loss of nitrite during storage, with loss of therapeutic activity when nitrite levels decrease after storage at cooler temperatures. Use of a preparation technique that completely consumes all the oxidizable organic components added to generate nitrite results in a stable preparation that is effective, well tolerated, and convenient in the treatment of anogenital warts (condylomata acuminata). Of 50 patients monitored after treatment with a 6.6 mol/L nitric acid preparation with no residual oxidizable organic agents, results were good in 39 patients, satisfactory in four patients, and unsatisfactory in seven patients. These observations lead to a simplified stable preparation of modest nitric acid concentration with adequate nitrate reduction products for efficacy in the topical ablation of small skin lesions such as condylomata acuminata.
We report a case of acute inhalation injury of nitric acid in a 56-year old white male. The patient presented conscious and dyspnoic at the emergency department after cleaning a copper chandelier with nitric acid. He had to be intubated 2 h after admission and mechanically ventilated because of fulminant respiratory insufficiency. As all sources of mechanical ventilation failed, extracorporeal membrane oxygenation had to be established 7 h after admission. With the additional use of surfactant and low dose inhalation therapy with nitric oxide (NO), the patient could be stabilised for 3 days and lung function improved temporarily. Despite all efforts the patient died at the fourth day from refactory respiratory failure. Pathologic examination revealed massive pulmonary edema without signs of inflammation. Thus, nitric acid inhalation induced pulmonary edema appears to be a most severe situation in which even most modern therapeutic interventions fail. As, in respect of recent literature and our case no promising therapy for nitric acid inhalation pulmonary edema is available, our efforts have to be directed towards prevention of nitric acid exposure.
A digestion procedure involving nitric acid, magnesium nitrate hexahydrate, and hydrochloric acid suffices for selenium determinations in whole blood, serum, and urine by molecular fluorescence spectrometry. To test the accuracy of the method we compared the results with those from hydride-generation atomic absorption spectrometry, and we also analyzed reference materials.
Injury to the triangular fibrocartilage complex (TFCC) is frequently implicated in the etiology of ulnar-sided wrist pain. This study examines the nervous anatomy of the TFCC using a nitric acid maceration technique and attempts to correlate this information with known tear patterns. Ten fresh frozen cadaveric specimens were studied in detail. Gross dissection of each upper-extremity specimen included removal of all flexor and extensor tendons. After identification and labeling with permanent color of the ulnar nerve, dorsal sensory branch of the ulnar nerve, posterior interosseous nerve, anterior interosseous nerve, and median nerve, an en bloc excision of the distal radioulnar region was performed. Digestion of the soft tissue was performed with nitric acid at sequential concentrations of 50% and 33% for 9 of 10 specimens. The digestion was halted by immersing the specimen in a mixture of 10% formaldehyde and 1% glycerine. After removal of bone, the specimens were fixed in paraffin, sectioned, and stained with hematoxylin and eosin. Nine of the 10 specimens were studied microscopically to determine the contribution of the grossly identified nerves to each zone of the triangular fibrocartilage complex as defined by Palmer's classification of acute TFCC tears. The anterior interosseous, median, and superficial radial nerves did not contribute to the innervation of the TFCC. The intraarticular course of the peripheral nerves could not be defined in the one specimen that was not digested with nitric acid. Nitric acid maceration is a rediscovered technique for identifying the nervous anatomy of soft tissues. The study showed that the triangular fibrocartilage complex is innervated by branches of the posterior interosseous, ulnar, and dorsal sensory ulnar nerves in a fairly consistent manner. Improved treatment of TFCC tears may result from an enhanced understanding of the supporting structures' innervation and mechanical function.
The airway effect of a 4-hr exposure (via a Plexiglas hood) to 1.6 ppm nitric acid vapor were evaluated in seven normal and seven allergic sheep, i.e., animals that have a history of reacting with bronchospasm to inhalation challenge with Ascaris suum antigen. The nitric acid vapor was generated by ultrasonic nebulization of a 2% nitric acid solution. Airway effects were assessed by measuring the change in specific pulmonary flow resistance before and after a standard inhalation challenge with 2.5% carbachol aerosol. Nitric acid exposure did not produce bronchoconstriction in either group. Pre-exposure increases in specific pulmonary flow resistance after carbachol inhalation were 68% (SD +/- 13%) and 82% (SD +/- 35%) for the normal and allergic sheep, respectively. Within 24 hr, the largest post exposure increased in specific pulmonary flow resistance for the normal and allergic sheep were 108% [SD +/- 51% (P less than .06)] and 175% [SD +/- 87% (P less than .02)], respectively. We conclude that a short-term exposure to nitric acid vapor at levels below the industrial threshold limit (2 ppm), produces airway hyperreactivity to aerosolized carbachol in allergic sheep.
A laboratory study was performed to evaluate the transmission of nitric acid through different materials. Copper, stainless steel, sodium glass and chromium-plated stainless steel proved to be poor choices for the construction of size classifiers, transfer lines and filter holder plates of air sampling devices, as they adsorb significant amounts of nitric acid. Tubes made of Teflon or pyrex exhibited good HNO3 transmission but, unexpectedly, devices machined from Teflon rods (cyclones, manifolds) showed a noticeable sorption capacity. Moreover, the Teflon of different manufacturers behaved differently. The features of a sampling unit capable of accurate measurements of nitric acid and ammonium nitrate in the atmosphere are discussed.
The acute toxicity of nitric acid to fingerling rainbow trout was measured in 7 day bioassays at 11 degrees C. The LC50 was about pH 4.0. Fish which died at low pH (3.0-4.0) exhibited classical symptoms of acid toxicity. Comparison of our results with other toxicity measurements suggests that nitric acid is intermediate in toxicity between H2SO4 and HCl at pH 3.0 and less toxic than either acid at pH 3.3 and above.
Although nitric acid is a component in some new bonding systems, the action of nitric acid as an etchant for the improvement of adhesion of bonding systems for resin composites to dentin and enamel has not been reported. A determination of the extent of etching on both dentin and enamel using 2.5% HNO3 solution at various application time periods was the purpose of this study. Extracted human molars were cleaned and sectioned so that flat samples of dentin and enamel would be produced. Surfaces were abraded with 320-grit aluminum-oxide paper, washed with distilled water for 10 s, and blown with air for 10 s. Duplicate samples of dentin and enamel were treated with a drop of 2.5% HNO3. Application periods varied by 10-second intervals, from 10 s up to 60 s. After being rinsed with distilled water and dried, the sections were routinely processed for observation by SEM. The micrographs of the treated surfaces showed various degrees of etching and erosion proportional to the length of application time. The 30-second application revealed a well-etched surface with minimal erosion.
AIMS: In order to assess the possible participation of nitric oxide (NO) in renal function during compensated hepatic cirrhosis, we studied renal function, the plasma and urinary levels of cGMP and the concentration of nitrates and nitrites, as markers of NO synthesis in blood and urine, in 10 patients with Child A hepatic cirrhosis as compared with 10 control subjects, both under basal conditions and during stimulation (amino acid-induced glomerular hyperfiltration). METHODS: To study renal function, the glomerular filtration rate (GFR), effective renal plasma flow (ERPF), renal functional reserve (RFR), renal venous resistance (RVR) and the filtration fraction (FF) were measured. Renin and aldosterone levels were determined to assess the possible involvement of these compounds in the renin-angiotensin-aldosterone axis. RESULTS: GFR and ERPF were significantly lower in the patients with cirrhosis than in the controls (mean GFR: 82+/-12.3 vs. 105+/-15 ml/min, p = 0. 01; ERPF 452+/-86 vs. 543+/-56 ml/min, p = 0.002). The RFR value was similar in both groups. In the basal situation cGMP levels were higher in plasma and urine in patients with cirrhosis than in the controls (plasma cGMP in cirrhosis 8.4+/-2.4 vs. 4.2+/-3.5 pmol/ml; urine cGMP in cirrhosis 1.2+/-2.1 vs. 0.68+/-0.1 pmol/ml). The NO levels were also higher in plasma and urine in patients with cirrhosis vs. controls (plasma NO in cirrhosis 45.5+/-9.2 vs. 30. 3+/-1.2 micromol/l; urinary NO in cirrhosis 6.2+/-1.3 vs. 3.1+/-2.3 micromol/ml). In both groups the amino acid perfusion increased GFR, ERPF, cGMP and NO levels in plasma and urine. In the patients with cirrhosis the RVR decreased significantly during perfusion and no noteworthy changes in FF were observed. The GFR values observed during amino acid perfusion were similar in patients with cirrhosis and portal hypertension to those observed in the controls (27.2+/-12 vs. 25.3+/-16%). However, the changes induced the ERPF were more marked in patients with cirrhosis (cirrhosis 35.3+/-15 vs. 22. 2+/-13%, p = 0.02). CONCLUSIONS: The present findings point to certain alterations in renal function in patients with hepatic cirrhosis and portal hypertension without ascitis, a clear difference being visible between the ERPF and GFR following amino acid-induced stimulation. The significant elevation in cGMP and NO levels in plasma and urine implies a maintained vasodilatory action that may at least partly compensate the vasoconstrictor effects of angiotensin II.
Trace elements in liquid biological samples may be determined by direct electrothermal atomic absorption spectrometry (ETAAS). In our previous work it was found that samples containing proteins or DNA may leak out of the graphite tube before the drying step, despite the addition of various modifiers. In order to keep the sample to the graphite tube, samples were diluted before analysis 1 + 1 with 32% v/v nitric acid, or 5 microl of 32% v/v nitric acid was added to the graphite tube before ETAAS determination. Applying the proposed procedure, the concentrations of lead in eluted fractions after gel chromatographic separation of human cerebellar nucleus dentatus supernatant and platinum in isolated DNA samples were determined. The use of nitric acid in sample pretreatment prevent sample leakage out of the graphite tube, provided for even drying and considerably reduced nonspecific absorption in lead determination. The repeatability of measurements was better than + 6%. The accuracy of the procedure was checked by spiking samples. The recoveries for both elements lay between 93--104%. Nitric acid was found to be a better modifier than TRITON X-100.
Workers engaged in thin nitric acid manufacturing are exhibited to the combined action of both physical and chemical factors (noise, heating microclimate, nitric oxides, ammonia). Within the working hours, ECG changes and arterial blood pressure instability are displayed in operators and technicians. Influenza, acute respiratory disorders and osseo-muscular diseases present the main causes of morbidity with temporary disability. Technicians are characterized by a markedly greater morbidity rate. Ammonia and nitric oxides, as aggressive media, lead to higher rates of oral mucoid, hard dental tissues and periodontium lesions. Health-related labour conditions improvement measures are proposed.
We report two patients who suffered from acid burns while working in chemical factories. Case 1: a 44-year-old man who received burn induced by nitric acid on the face and extremities. Despite his protecting facial mask, he was exposed to nitric acid on his face through a gap between the mask and skin surface. Nitric acid was also sprinkled on his scalp which was not covered by a helmet or a protecting device. In addition, he suffered from acid burn on the right scapular region, the right upper arm, and the lower extremities through the work clothes. Case 2: a 26-year-old man who suffered from sulfuric acid burn on the forearms. Both patients were accidentally exposed to acids while they filled tanks with the acids through a hose. Following the manual of the factories, they washed the exposed skin with water for more than 15 minutes after the exposure. Although they recovered without any serious sequel, there remained partial deep tissue destruction of the skin. We reviewed these two cases from the aspect of industrial medicine, and proposed the following three points for improvement in the workplace to prevent accidental acid burns. 1) re-education or enlightenment activities for the well-experienced workers to avoid negligence to the danger of strong acid. 2) recommendation to take a complete shower to avoid overlooking of unaware acid injury. 3) improvement in the protecting facial mask. In addition, clinicians who examine acid-burn patients should not pass over the presence of deep ulcers lying behind the thick crust on the injured area.
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Passivation of Ti6Al4V and cpTi implants using methods based on the ASTM-F86 nitric acid protocol are used with the intention of reducing their surface reactivity, and consequently the corrosion potential, in the highly corrosive biologic milieu. The ASTM-F86 passivation protocol was originally developed for surgical implants made of stainless steel and chrome cobalt alloy. Using X-ray photoelectron spectroscopy (XPS) to examine the effect of nitric acid passivation on the surface oxide layer of mill-annealed Ti6Al4V and cpTi, we have found that such treatment actually reduced the oxide thickness on the alloy while having no significant effect on the pure metal. These results correlated with observations obtained using graphite furnace atomic absorption spectrophotometry (GFAAS) to detect trace element release from solid, mill-annealed, Ti6Al4V and cpTi into serum-containing culture medium. We detected significantly greater levels of Ti, Al, and V in the presence of passivated compared to nonpassivated Ti6Al4V. In contrast, nitric acid passivation did not influence Ti release from mill-annealed cpTi. These results, derived from two mill-annealed Ti-based metals, would indicate that re-examination of ASTM-F86-based passivation protocols with respect to Ti6Al4V should be considered in view of the widespread use of this alloy for biomedical devices.