sodium-nitrite and Acute-Disease

Topics: Acute Disease; Adult; Aftercare; Amyl Nitrite; Antidotes; Cyanides; Decontamination; Emergency Medical Services; Emergency Nursing; Emergency Treatment; Humans; Hydroxocobalamin; Life Support Care; Male; Nurse's Role; Parkinsonian Disorders; Poisoning; Sodium Nitrite; Suicide, Attempted; Thiosulfates; Triage

The mechanical obstruction and pulmonary vasoconstriction are major determinants of the sudden right ventricular (RV) afterload increases observed during acute pulmonary thromboembolism (APT). Vasodilators and antioxidants agents have been shown to mitigate pulmonary hypertension. We examined whether sodium nitrite and the antioxidant tempol combination could be advantageous in an APT sheep model.. APT was induced in anesthetized sheep by autologous blood clots (250 mg/kg) into the right atrium. Thirty minutes after APT induction, the animals received a continuous infusion of tempol (1.0 mg/kg/min), increasing sodium nitrite infusion (5, 15, and 50 μmol/kg), or a simultaneous combination of both drugs. Saline was used as a control treatment. Hemodynamic measurements were carried out every 15 min. Also, whole blood nitrite and serum 8-isoprostanes levels were measured.. APT induced sustained pulmonary hypertension, increased dp/dt. Nitrite and tempol combination protects against APT-induced RV wall stress. The association of both drugs may offer an advantage to treat RV failure during severe APT.

Topics: Acute Disease; Animals; Antioxidants; Cyclic N-Oxides; Heart Ventricles; Hypertension, Pulmonary; Male; Sheep; Sodium Nitrite; Spin Labels

Sodium nitrite (NaNO. At the first hour after treatment, a decrease in Fe and Ca levels was observed. One day following NaNO. The results of the present study demonstrate that acute NaNO

Topics: Acute Disease; Animals; Calcium; Iron; Male; Metals; Mice, Inbred ICR; Sodium Nitrite; Spectrophotometry, Atomic; Spleen; Zinc

Generalized hypoxic pulmonary vasoconstriction (HPV) occurring during exposure to hypoxia is a detrimental process resulting in an increase in lung vascular resistance. Nebulization of sodium nitrite has been shown to inhibit HPV. The aim of this project was to investigate and compare the effects of nebulization of nitrite and different formulations of acidified sodium nitrite on acute HPV.. Ex vivo isolated rabbit lungs perfused with erythrocytes in Krebs-Henseleit buffer (adjusted to 10% hematocrit) and in vivo anesthetized catheterized rabbits were challenged with periods of hypoxic ventilation alternating with periods of normoxic ventilation. After baseline hypoxic challenges, vehicle, sodium nitrite or acidified sodium nitrite was delivered via nebulization. In the ex vivo model, pulmonary arterial pressure and nitric oxide concentrations in exhaled gas were monitored. Nitrite and nitrite/nitrate were measured in samples of perfusion buffer. Pulmonary arterial pressure, systemic arterial pressure, cardiac output and blood gases were monitored in the in vivo model.. In the ex vivo model, nitrite nebulization attenuated HPV and increased nitric oxide concentrations in exhaled gas and nitrite concentrations in the perfusate. The acidified forms of sodium nitrite induced higher levels of nitric oxide in exhaled gas and had longer vasodilating effects compared to nitrite alone. All nitrite formulations increased concentrations of circulating nitrite to the same degree. In the in vivo model, inhaled nitrite inhibited HPV, while pulmonary arterial pressure, cardiac output and blood gases were not affected. All nitrite formulations had similar potency to inhibit HPV. The tested concentration of appeared tolerable.. Nitrite alone and in acidified forms effectively and similarly attenuates HPV. However, acidified nitrite formulations induce a more pronounced increase in nitric oxide exhalation.

Topics: Acute Disease; Administration, Inhalation; Animals; Blood Pressure; Cardiac Output; Chemistry, Pharmaceutical; Disease Models, Animal; Dose-Response Relationship, Drug; Exhalation; Hydrogen-Ion Concentration; Hypoxia; Male; Nebulizers and Vaporizers; Nitrates; Nitric Oxide; Perfusion; Pulmonary Artery; Rabbits; Sodium Nitrite; Time Factors; Vasoconstriction; Vasodilator Agents

Crude water-soluble polysaccharides (BRP) were extracted from the root of Brassica rapa L. using boiling-water. The polysaccharides were successively purified by chromatography on DEAE-cellulose and Sephadex G-100 column, giving three major polysaccharide fractions termed BRP1-1, BRP2-1, BRP3-1. The gel permeation chromatography (GPC) analysis showed that the average molecular weight (Mw) of polysaccharides (BRP1-1, BRP2-1, BRP3-1) were approximately 5.53×10(3) Da, 3.35×10(4) Da and 3.37×10(4) Da, respectively. Monosaccharide components analysis indicated that BRP1-1 was composed of arabinose and glucose in a molar ratio of 1.66:98.34. BRP2-1 was composed of arabinose, galactose and glucose in a molar ratio of 9.3:14.63:76.07. BRP3-1 was composed of arabinose, rhamnose, galactose and glucose in a molar ratio of 24.98:24.10:44.09:6.83. The evaluation of anti-hypoxia activity in vivo revealed that BRP is a novel potential anti-hypoxia agent.

Topics: Acute Disease; Animals; Brain Ischemia; Brassica rapa; Chemical Fractionation; Chromatography; Erythrocyte Count; Hemodynamics; Hemoglobins; Hypoxia; Male; Mice; Molecular Weight; Monosaccharides; Polysaccharides; Sodium Nitrite; Spectroscopy, Fourier Transform Infrared; Survival Analysis; Time Factors; Toxicity Tests

Acute pulmonary embolism produces acute pulmonary hypertension, which can be counteracted by activating the nitric oxide-cyclic guanosine 3',5'-monophosphate (cGMP) pathway. While previous studies have shown that sildenafil (an inhibitor of cGMP-specific phosphodiesterase type 5) or nitrite (a storage molecule for nitric oxide) produces beneficial effects during acute pulmonary embolism, no previous study has examined whether the combination of these drugs can produce additive effects. Here, we expand previous findings and examine whether sildenafil enhances the beneficial haemodynamic effects produced by a low-dose infusion of nitrite in a dog model of acute pulmonary embolism. Haemodynamic and arterial blood gas evaluations were performed in non-embolized dogs treated with saline (n = 4), and in embolized dogs (intravenous injections of microspheres) that received nitrite (6.75 micromol/kg intravenously over 15 min. followed by 0.28 micromol/kg/min.) and sildenafil (0.25 mg/kg over 30 min.; n = 8), or nitrite followed by saline (n = 8), or saline followed by sildenafil (n = 7), or only saline (n = 8). Plasma thiobarbituric acid-reactive substances (TBARS) concentrations were determined using a fluorometric method. Acute pulmonary embolism increased pulmonary artery pressure by approximately 24 mmHg. While the infusion of nitrite or sildenafil infusions reversed this increase by approximately 42% (both P < 0.05), the combined infusion of both drugs reversed this increase by approximately 58% (P < 0.05). Similar effects were seen on the pulmonary vascular resistance index. Nitrite or sildenafil alone produced no significant hypotension. However, the combined infusion of both drugs caused transient hypotension (P < 0.05). Both drugs, either alone or combined, blunted the increase in TBARS concentrations caused by acute pulmonary embolism (all P < 0.05). These results suggest that sildenafil improves the beneficial haemodynamic effects of nitrite during acute pulmonary embolism.

Topics: Acute Disease; Animals; Blood Pressure; Disease Models, Animal; Dogs; Drug Synergism; Drug Therapy, Combination; Female; Hemodynamics; Hypertension, Pulmonary; Infusions, Intravenous; Lipid Peroxides; Male; Phosphodiesterase Inhibitors; Piperazines; Pulmonary Artery; Pulmonary Embolism; Purines; Respiration; Sildenafil Citrate; Sodium Nitrite; Sulfones; Vascular Resistance

A case of attempted homicide by cyanide ingestion is reported. The victim, a 19-year-old woman, unknowingly ingested cyanide and presented to the Emergency Department unresponsive, in shock, and in profound metabolic acidosis. The differential diagnosis of this presentation and the patient's successful treatment are reviewed. The important management issues surrounding the treatment of cyanide poisoning are discussed.

Topics: Acidosis; Acute Disease; Adult; Antidotes; Cyanides; Diagnosis, Differential; Electrocardiography; Emergency Treatment; Female; Fluid Therapy; Homicide; Humans; Respiration, Artificial; Shock; Sodium Nitrite; Spouse Abuse; Thiosulfates

A 41-year-old woman ingested apricot kernels purchased at a health food store and became weak and dyspneic within 20 minutes. The patient was comatose and hypothermic on presentation but responded promptly to antidotal therapy for cyanide poisoning. She was later treated with a continuous thiosulfate infusion for persistent metabolic acidosis. This is the first reported case of cyanide toxicity from apricot kernel ingestion in the United States since 1979.

Topics: Acidosis; Acute Disease; Adult; Antidotes; Emergency Treatment; Female; Food, Organic; Fruit; Humans; Hydrogen Cyanide; Poisoning; Poisons; Seeds; Sodium Nitrite; Thiosulfates

The authors reviewed the clinical manifestations, complications, and the prognosis affected by Lilly Cyanide Antidote in 21 victims of acute cyanide poisoning over a 10-year period. The clinical signs and symptoms in cyanide poisoning are variable. Among 21 cases, loss of consciousness (15), metabolic acidosis (14), and cardiopulmonary failure (9) were the three leading manifestations of cyanide intoxication. Anoxic encephalopathy (6) was not uncommon in the severely intoxicated victims. Diabetes insipidus (1) or clinical signs and symptoms mimicking diabetes insipidus (3) may be an ominous sign to encephalopathy victims. The major cause of fatal cyanide poisoning is the intentional ingestion of cyanide compounds as part of a suicide attempt. Decrease of arteriovenous difference of O2 partial pressure may be a clue for the suspicion of cyanide intoxication. Although the authors cannot show a statistically significant difference (P = .47) for the Lilly cyanide antidote kit in terms of improving the survival rate for victims of cyanide poisoning, the antidote kit was always mandatory in our study in the cases of severely intoxicated victims who survived. Early diagnosis, prompt, intensive therapy with antidote, and supportive care are still the golden rules for the treatment of acute cyanide poisoning, whether in the ED or on the scene.

Topics: Acute Disease; Adult; Amyl Nitrite; Antidotes; Cyanides; Drug Combinations; Emergencies; Female; Humans; Male; Middle Aged; Poison Control Centers; Poisoning; Prognosis; Retrospective Studies; Severity of Illness Index; Sex Factors; Sodium Nitrite; Survival Rate; Taiwan; Thiosulfates

The EPR spectrum was optimally recorded at 20 degrees C in the blood sample. The rotatory ability of the probe, expressing the microviscosity of the blood, was shown to depend on the dose of administered solution of the sodium nitrite and to correlate with the degree of hypoxic state. An analysis of probable causes of the changes in the blood microviscosity in acute hypoxia was carried out.

Topics: Acute Disease; Animals; Blood Viscosity; Dose-Response Relationship, Drug; Electron Spin Resonance Spectroscopy; Hypoxia; Rats; Rats, Wistar; Sodium Nitrite; Temperature

Cyanide poisoning is a life threatening condition. But specific antidotes exist and can be easily prepared from available substances in hospital. Administration of antidotes will produce methemoglobin, which itself causes hypoxia. Nitrite induced methemoglobin can be extremely dangerous and even lethal. Before administering the antidotes, the diagnosis should be confirmed. Nitrite should not be given if the poisoning is mild or diagnosis is uncertain, to avoid excessive methemoglobin, dosage of sodium nitrite must be adjusted according to hemoglobin level (Table 1). Usage of sodium nitrite and sodium thiosulfate in the recommended doses are safe and effective for cyanide poisoning.

Topics: Acute Disease; Adult; Antidotes; Humans; Male; Methemoglobinemia; Poisoning; Potassium Cyanide; Sodium Nitrite; Thiosulfates

Topics: Acute Disease; Adult; Antidotes; Cyanides; Edetic Acid; Humans; Male; Potassium Cyanide; Respiration, Artificial; Sodium Nitrite; Suicide, Attempted

Management of the acutely poisoned patient should start with decontamination of the skin and irrigation of the eyes, if necessary, and assessment of cardiorespiratory status, neurologic status, and pupils and eye movement. If a definable toxic syndrome is present, the specific "antidote" should be given. If no such syndrome is apparent and the patient is comatose, 50 ml of 50% glucose and 0.4 mg of naloxone (Narcan) intravenously should be tried. General measures, applicable in either situation, include induction of emesis or lavage and administration of charcoal and cathartics.

Topics: Acute Disease; Antidotes; Carbon Monoxide Poisoning; Consciousness; Cyanides; Depression, Chemical; Humans; Naloxone; Nitrates; Nitrites; Organophosphate Poisoning; Oxygen; Parasympatholytics; Poisoning; Pupil; Sodium Nitrite; Thiosulfates

Topics: Accidents, Occupational; Acute Disease; Amyl Nitrite; Hospitals, Community; Humans; Hydrogen Sulfide; Male; Middle Aged; Sodium Nitrite