Cardiac mitochondrial nitric oxide: Hemorrhagic shock in conscious and anesthetized rats.

ANA CANIL, GISSELLA VALLI, TAMARA ZAOBORNYJ, LAURA VALDEZ, ALBERTO BOVERIS, ANA BALASZCZUK, ANDREA FELLET.

Santa Bárbara

Congreso; Oxygen Club of California. Oxidants and Antioxidants in Biology. Santa Barbara, California.; 2008

Oxygen Club of California. Oxidants and Antioxidants in Biology

Hypovolemic state induced by acute hemorrhage triggered a heterogeneous and dynamic nitric oxide synthases (NOS) activation. An increased cardiac endothelial NOS expression is an early molecular response to regulate heart rate after blood loss. The inducible NOS become a major source of cardiac NO production in the later stages, which could be determinant of the heart dysfunction after 120 min of sustained hemorrhagic shock. Our aim was to evaluate the involvement of mitochondrial NOS (mtNOS) activity in the cardiovascular adaptation to hemorrhagic shockc after 120 min of bleeding in conscious and anesthetized rats. Groups of animals (n=5 per group): C: normotensive conscious and anesthetized rats; CH: conscious hemorrhaged rats (20% blood loss); AH: anesthetized hemorrhage rats. No differences in the succinate-supported state 4 and 3 respiration (ng-at O/min.mg protein) were observed among the experimental groups (Cst4 = 130±9.8, Cst3 = 234±16; CHst4 = 112±10, CHst3 = 204±15; AHst4 = 158±11, AHst3 = 240±11). Bleeding did not modify heart mitochondrial hydrogen peroxide production (nmol H2O2/min.mg protein) compared with C (C=0.577±0.05; CH=0.569±0.1; AH=0.524±0.06). However, the hypovolemic state modified heart mtNOS functional activity determined by enhancing H2O2 production (C=59%; CH=85%; AH=67%). Taking into account that changes in mtNOS functional activity reflect variations in mitochondrial NO production and steady state concentration, higher mitochondrial NO levels would be involved in the cardiovascular adaptation to vol