Electrocardiographic abnormalities in rats by acute exposure to nitrogen dioxide.

  title={Electrocardiographic abnormalities in rats by acute exposure to nitrogen dioxide.},
  author={H. Tsubone and H. Oda and A. Suzuki and K. Kubota},
  journal={Toxicology letters},
  volume={12 2-3},
Changes in cardiac function of rats acutely exposed to nitrogen dioxide (NO2) were examined by electrocardiographic (ECG) records. Bradycardia and arrhythmia which were observed by exposure to 20 ppm NO2 or more for 3 h were abolished by injection of atropine sulfate. ECGs were recorded following experimental formation of nitrite (NO-2) and nitrate (NO-3) in blood of normal rats by administration of NaNO2 solution, but no remarkable changes were observed on ECG. These results suggest that… Expand
7 Citations
Effects of acute exposure to ozone on heart rate and blood pressure of the conscious rat.
In general, heart rate and mean arterial blood pressure of rats significantly decreased during exposure to O3, whereas these functional parameters remained almost stable during Exposure to filtered air. Expand
Altered atrial responses to drugs after acute exposure to nitrogen dioxide and/or ethanol.
The data indicates that acute exposure to NO2, ET and/or the interaction between these agents can alter cardiac activity. Expand
Ozone-induced bradycardia and arrhythmia and their relation to sleep-wakefulness in rats
Compared with control rats, heart rates of the O3-exposed rats decreased and the number of bradyarrhythmic episodes increased with an increase in O3 levels, and parasympathetic mechanisms were suggested on those cardiac abnormalities. Expand
Changes of cardiac and respiratory rhythm in non- and tracheostomized rats exposed to nitrogen dioxide.
It was suggested that the cardiac and respiratory abnormalities could be induced without the irritation to upper respiratory tracts, and that the vagal efferent pathway had an important role in the appearance of the abnormalities during exposure. Expand
Reflex cardiopulmonary responses by stimulation to type J receptors in rats exposed to NO2.
The results suggest that the augmentation of the reflex cardiopulmonary responses due to stimulation to the type J receptors was produced by exposures with a higher concentration of NO2. Expand
Acute effects of ozone on EEG activity, sleep-wakefulness and heart rate in rats.
It is suggested that the O3-induced bradycardia results from enhanced activity of cardiac parasympathetic nerves and that the changes in W and SWS result secondarily from some circulatory factor including the bradycardsia. Expand
The Role of the Autonomic Nervous System in Cardiovascular Toxicity
The neural, molecular, and physical foundations by which the ANS may confer toxicity to cardiovascular tissue are detailed, emphasizing how ANS imbalance may evoke electrophysiological cardiac defects, vascular pathologies, pathogenic myocardial cell signaling, oxidative stress, inflammation, and neural defects throughout the cardiovascular tissue. Expand


Altered Function in Animals Inhaling Low Concentrations of Ozone and Nitrogen Dioxide
Abstract Quantitative measurements of respiratory function of guinea pigs were made before, during, and after exposure to low concentrations of ozone, and nitrogen dioxide. The earliest effectsExpand
Alterations of nitrite and nitrate concentrations in the blood of mice exposed to nitrogen dioxide.
Blood nitrite and nitrate of mice were determined using naphthylethylenediamine and a Cu-Cd reduction column and indicated a rapid conversion of nitrite to nitrate with an increase of methemoglobin, whereas addition to sodium nitrate did not cause any changes. Expand
Fate and distribution of inhaled nitrogen dioxide in rhesus monkeys.
The results demonstrated that 50 to 60% of the inspired pollutant was retained by the primate during quiet respiration; the gas was distributed throughout the lungs. Expand
Parasympathetic control of the heart.
Investigations have clearly indicated that stimulation of the vagosympathetic trunk produces a negative inotropic effect in the canine ventricle, and cholinergic and adrenergic influences interact synergistically and antagonistically in their actions upon the heart. Expand
Airborne chemical irritants. Role of the trigeminal nerve.
Electrical reccrding from the sensory trigeminal nerves provided direct evidence that relates chemical irritation of the nasal mucosa to afferent impulses on the trigeminals narve, resulting in inhibition of respiratory rate. Expand
Sensory irritation by airborne chemicals.
  • Y. Alarie
  • Medicine
  • CRC critical reviews in toxicology
  • 1973