[Cardiovascular manifestations of acute nitrite intoxication in laboratory rats]

The systemic and peripheral hemodynamics was studied in male white rats under conditions of acute nitrite hypoxia (subcutaneous administration of sodium nitrite at doses of 1, 3, and 5 mg/100 g body mass). By the electrocardiographic, rheographic, and other methods there were recorded the heart rate (HR), minute circulation volume (MCV), cardiac output (CO), skeletal muscle circulation (SMC), brain circulation (BC), and systemic arterial pressure (AP). Nitrite was shown to produce a fast, dose-dependent AP decrease accompanied by a decrease of MCV due to development of bradycardia and a fall of CO. At the phase of the steady hypotension, CO increased due to a significant rise of CO on the background of the continuing bradycardia. The systemic circulatory effects of NaNO2 were found to be accompanied by a redistribution of peripheral circulation in the form of a dose-dependent increase of BC and a sharp fall of MCV. It was shown that 1-1.5 h after the nitrite injection the parameters of systemic and peripheral hemodynamics approached the initial levels. Possible triggering mechanisms of the initial stage of the rat cardiovascular adaptation to conditions of acute nitrite hypoxia are discussed.