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Sodium azide (NaN3) is known as an inhibitor of catalase, and a nitric oxide (NO) donor in the presence of catalase and H2O2. We showed here that catalase-catalyzed oxidation of NaN3 can generate reactive nitrogen species which contribute to tyrosine nitration in the presence of H2O2. The formation of free-tyrosine nitration and protein-bound tyrosine nitration by the NaN3/catalase/H2O2 system showed a maximum level at pH 6.0. Free-tyrosine nitration induced by peroxynitrite was inhibited by ethanol and dimethyl-sulfoxide (DMSO), and augmented by superoxide dismutase (SOD). However, free-tyrosine nitration induced by the NaN3/catalase/H2O2 system was not affected by ethanol, DMSO and SOD. NO-2 and NO donating agents did not affect free-tyrosine nitration by the NaN3/catalase/H2O2 system. The reaction of NaN3 with hydroxyl radical generating system showed free-tyrosine nitration, but no formation of nitrite and nitrate. The generation of nitrite (NO-2) and nitrate (NO-3) by the NaN3/catalase/H2O2 system was maximal at pH 5.0. These results suggested that the oxidation of NaN3 by the catalase/H2O2 system generates unknown peroxynitrite-like reactive nitrogen intermediates, which contribute to tyrosine nitration.

Nitric oxide (NO) is known as a vasodilatory molecule synthesized by vascular endothelium. The NO-dependent vasodilatory response of coronary artery is impaired after ischemia and reperfusion. In the present study, the release of NO from coronary vasculature was evaluated before and during cardioplegic arrest and after reperfusion. Nine patients undergoing heart surgery were studied. Multidose crystalloid cardioplegics were used for myocardial protection. The coronary affluent and effluent were obtained simultaneously before cardioplegic arrest, at each cardioplegic administration, and after reperfusion; and the levels of nitrite and nitrate, the stable end-products of NO, were measured. The NO release from the coronary vasculature was determined as the difference in the levels of nitrite and nitrate between the coronary effluent and affluent. The level of nitrite/nitrate release from coronary vasculature was 6.8 ± 3.7 μM before cardioplegic arrest. During cardioplegic arrest the nitrite/nitrate release decreased, reaching 1.3 ± 1.3 μM (p< 0.05, vs. before cardioplegic arrest) at the fourth administration of the cardioplegic. At 3 to 5 minutes after reperfusion, nitrite/nitrate release further decreased to 0.36 ± 0.34 μM (p< 0.05, vs. before cardioplegic arrest). During cardioplegic arrest the NO release decreased and reached significance at approximately 70 minutes of cardioplegic arrest compared to that before cardioplegic arrest. After reperfusion, NO release was further reduced, with statistical significance compared to that before cardioplegic arrest. Our data may indicate that cardioplegic arrest and reperfusion cause endothelial dysfunction.

Nitric oxide (NO) is known as a vasodilatory molecule synthesized by vascular endothelium. The NO-dependent vasodilatory response of coronary artery is impaired after ischemia and reperfusion. In the present study, the release of NO from coronary vasculature was evaluated before and during cardioplegic arrest and after reperfusion. Nine patients undergoing heart surgery were studied. Multidose crystalloid cardioplegics were used for myocardial protection. The coronary affluent and effluent were obtained simultaneously before cardioplegic arrest, at each cardioplegic administration, and after reperfusion; and the levels of nitrite and nitrate, the stable end-products of NO, were measured. The NO release from the coronary vasculature was determined as the difference in the levels of nitrite and nitrate between the coronary effluent and affluent. The level of nitrite/nitrate release from coronary vasculature was 6.8 ± 3.7 µM before cardioplegic arrest. During cardioplegic arrest the nitrite/nitrate release decreased, reaching 1.3 ± 1.3 µM (p< 0.05, vs. before cardioplegic arrest) at the fourth administration of the cardioplegic. At 3 to 5 minutes after reperfusion, nitrite/nitrate release further decreased to 0.36 ± 0.34 µM (p< 0.05, vs. before cardioplegic arrest). During cardioplegic arrest the NO release decreased and reached significance at approximately 70 minutes of cardioplegic arrest compared to that before cardioplegic arrest. After reperfusion, NO release was further reduced, with statistical significance compared to that before cardioplegic arrest. Our data may indicate that cardioplegic arrest and reperfusion cause endothelial dysfunction.

Long-term heart rate fluctuations in postoperative and brain-dead patients were investigated. Heart rates were monitored continuously, and the data were stored, edited, and interpolated to allow for data lost during calibration and disconnection of the sensors for various treatments. Heart rate power spectra were calculated using the fast Fourier transform method. The power spectra of the patients who recovered showed that the heart rate fluctuated and produced a 1/f relationship, termed 1/f fluctuations, whereas those of patients who died in the intensive care unit (ICU) consisted of white-noise-like signals. The power spectra in brain-dead patients showed a 1/f relationship under steady-state conditions, while the power density and variation of the frequency distribution were lower than those in a normal subject. Therefore, 1/f fluctuations appear to be universal and occur independent of the central nervous system. (Chronobiology International, 15(6), 633-646, 1998)

A case of late-onset manifestation of organophosphorous insecticide poisoning is described. The patient was a 70-year-old female who ingested 40ml Sumithion emulsion (50% fenitrothion). At first, no toxic symptoms were apparent. However, 48 h after ingestion certain signs became apparent. An impediment in consciousness was observed. Fasciculation and muscular weakness were noted, while plasma and urinary 4-nitro-3-methylphenol (NMC), the degradation product of Sumithion, reached a maximum. Neither atropine sulfate nor PAM (pyridine 2-aldoxime methiodine) were effective. For 3 weeks the patient required ventilatory support, and consequently her muscle strength and neurological status gradually recovered with falling NMC levels.

The patient in this case report was an 88-year-old male. Acute upper airway obstruction by food led to transient cardiac arrest, and negative pressure pulmonary hemorrhage (NPPH) occurred 1 hour after the foreign body obstruction. Using venovenous extracorporeal membrane oxygenation (ECMO) for severe acute respiratory distress syndrome resulting from NPPH, his respiratory state was recovered and hemoptysis stopped. NPPH is a life-threatening disease, the rapid recognition of which is required to initiate appropriate therapy. Although active hemorrhage might be a contraindication for ECMO, our experience showed this to be an effective treatment option. Moreover, our experience suggests that the application of ECMO to elderly patients should be considered on a case-by-case basis.