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THYROID STATUS MODIFIES CARDIAC NITRIC OXIDE SYNTHASES DURING HEMORRHAGIC SHOCK: PP.22.400

The regulation of cardiac function is a complex process in which nitric oxide (NO) is a mediator and the thyroid status has a role. Objectives: To study the involvement of thyroid status and NO synthases (NOS) on hemodynamic changes induced by acute hemorragic shock. Animals euthyroid (E), hyperthyroid (H) and hypothyroid (h), are divided into two groups, control (C), and hemorrhaged rats (H) (withdrawal of 20 % of blood volume). Right atrium (A) and left ventricule (V) were removed at 120 min of hemorrhage. Histochemical NOS activity (NADPH-diaphorase technique), NOS, caveolin 1 and 3 (cav 1 and 3) protein levels (western blot) were evaluated. The results are expresed as X ± ES, n = 9/ group. Analysis of variance (ANOVA) followed by the ad hoc Bonferroni test was used for multiple comparisons. The 5% probability level was used as a criterion for biological significance. Results: Blood loss did not change neither eNOS and nNOS protein levels in A and V nor cav-3 protein levels in V. Conclusions: Acute blood loss increased NOS activity in A and V of euthyroid rats that correlated with changes in i-NOS protein levels. Hypovolemic state induced by acute hemorrhage induced changes in the cav-1 protein levels in A of hyperthyroid rats and in V of hyper and hypothyroid animals. The production of NO and its involvement in the cardiac adaptation to hemorrhage depend on the thyroid status. The coordinated expressional changes in NOS isoforms and their allosteric regulators, such as caveolin, may be viewed as a compensatory mechanism to maintain the production of bioactive NO. Figure 1. No caption available.