Cardiopulmonary Reflex Responses during Nitric Oxide inhalation

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Inhaled of mechanical stimulation to the respiratory tracts could elicit several cardiopulmonary responses, includidng changes in blood pressure and heart rate as well as bronchoconstriction and so on. Since there are many receptors such as irritant receptors, stretch receptors and J-receptors in the respiratory tracts of humans, inhaled gases such as nitric oxide, inhalation of which recently inroduced in clinically for patients with pulmonary hypertension or acute respiratory distress syndrome, and nicotine smoke, which is very a popular problem, could elicit cariovascular changes. However there has been no study available as to these points. In the present studies, we aimed to examine how inhalation of gas as well as airway anesthesia affect the reflex responses and had the following results.1)In anesthetized dogs, nitric oxide (NO), 5ppm and 50ppm, did not cause any significant influence on arterial barorefex sensitivity, but significantly suppressed pulmonary arterial responses to hypoxemia.2)Cigarette smoking (nicotine of 0.1mg and 1mg with tar of 13mg) caused to constrict pial arterioles and venules observed using the cranial window in anesthetized rats. The effets seem to be in a concentration-dependent fashione, perhaps to be via nicotinic receptors, at least partly, and sympathetic activation by cigarette smoking.3)Airwayanesthesia using lidocaine's spray attenuated the changes in arterial blood pressure and heart rate associated with airway stimulation which usually causes cardiopulmonary reflex responses in humans.Intravenous administration of bupivacaine and ropivacaine, a new local anesthetic, caused arterial baroreflex responses to suppress in their toxic dose in rats. The supression was not augumented in the presence of mild respiratory acidosis, but atttenuated in the presence of respiratory alkalosis.