The aim of this study was to assess the role of nitric oxide (NO) in cardiac anaphylaxis regarding changes in coronary reactivity and oxidative status of the mice heart. The animals were divided into two groups: experimental group (CBA, iNOS(-/-) mice) and control group: wild-type mice (CBA/H). The hearts of male mice (n = 24; 6-8 weeks old, body mass 20-25 g, 12 in each experimental group) were excised and retrogradely perfused according to the Langendorff technique at a constant perfusion pressure (70 cm H2O). Cardiac anaphylaxis was elicited by injection of solution (1 mg/1 ml) of ovalbumin into the aortic cannula. For the next 10 min, in intervals of 2 min (0-2, 2-4, 4-6, 6-8, 8-10 min) coronary flow (CF) rates were measured and samples of coronary effluent were collected. Markers of oxidative stress including index of lipid peroxidation measured as thiobarbituric acid-reactive substances (TBARS), NO measured in the form of nitrites (NO2(-)), superoxide anion radical (O2(-)), and hydrogen peroxide (H2O2) in the coronary venous effluent were assessed spectrophotometrically. After the ovalbumin challenge, CF was significantly lower in the wild mice group. NO and H2O2 release were significantly higher in iNOS(-/-) mice group. TBARS and O2(-) values did not vary significantly between wild and iNOS(-/-) mice groups. Our results indicate that coronary vasoconstriction during cardiac anaphylaxis does not necessarily depend on inducible nitric oxide synthase (iNOS)/NO activity and that iNOS/NO pathway may not be an only influential mediator of redox changes in this model of cardiac anaphylaxis.
Keywords: Cardiac anaphylaxis; Coronary flow; Isolated mice heart; Nitric oxide; Oxidative stress.