| Abstrakt: |
Cardiac contractility in rats was decreased after 24-h immobilization-painful stressing, as indicated by lower growth rate of myocardium contraction and relaxation, LVP, heart rate, and maximum functioning intensity (MIF) in comparison to intact group during functional tests on adrenoreactivity and maximum isometric workload. Stressed animals pretreated with the GABA-A receptors blocker bicuculline (2 mg/kg, i.p.) exhibited more pronounced reduction in inotropic my- ocardial function in comparison to that in rats of the control group, as evidenced by a smaller increase in +dP/dtmax, -dP/dtmax, LVP, and MIF during functional tests. Under conditions of NO-synthase inhibition (L-NAME 10 mg/kg, i.p.), the resistance to stress and inotropic cardiac functio reserves in stressed animals decrease to a much greater degree (on average, by 50%; p < 0.05) than under conditions of GABA-A receptors blockade, which can be seen from weak growth rates of myocardium contraction and relaxation, LVP, and MIFS, as well as from high percentage of animal deaths during stressing, anesthesia, necropsy thorax, and after functional tests. Thus, NO deficiency leads to more pronounced myocardial contractility disorders in stressed animals than under conditions of inhibition of GABA-A receptors. |
