IQUIMEFA   05518
INSTITUTO QUIMICA Y METABOLISMO DEL FARMACO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Thyroid status modifies cardiac nitric oxide synthases during hemorrhagic shock
Autor/es:
SARATI, C. MARTINEZ, N. ARTÉS, N. ARRECHE, A.M. BALASZCZUK, A. FELLET.
Lugar:
Oslo
Reunión:
Congreso; 20 th European Meeting on Hypertension,; 2010
Resumen:
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 XES, n¼9/ 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.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 XES, n¼9/ 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.ES, n¼9/ 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.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 ofNOand 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.
animals.The production ofNOand 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.
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 ofNOand 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.
animals.The production ofNOand 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.