IQUIMEFA   05518
INSTITUTO QUIMICA Y METABOLISMO DEL FARMACO
Unidad Ejecutora - UE
artículos
Título:
Nitric oxide synthases are involved in the modulation of cardiovascular adaptation in hemorrhaged rats
Autor/es:
BALASZCZUK A.; ARRECHE N.; MC LAUGHLIN; ARRANZ C.; FELLET A.
Revista:
VASCULAR PHARMACOLOGY
Editorial:
Elsevier Science
Referencias:
Lugar: New York, EEUU; Año: 2006 vol. 44 p. 417 - 426
ISSN:
1537-1891
Resumen:
Aim: Nitric oxide has been implicated in the cardiovascular adaptation to hemorrhagic shock. Our aim was to study the potential role of nitric oxide synthases (NOS) in the cardiovascular response in hemorrhagic hypotension produced experimentally in anesthetized rats.Nitric oxide has been implicated in the cardiovascular adaptation to hemorrhagic shock. Our aim was to study the potential role of nitric oxide synthases (NOS) in the cardiovascular response in hemorrhagic hypotension produced experimentally in anesthetized rats. Methods: groups of animals (n=14, per group): (a) normotensive ; (b) hypovolemic (20% blood loss); (c) normotensive and pretreatment with NG-nitro-L-arginine methyl ester (LNAME); (d) hypovolemic and pretreatement with L-NAME.groups of animals (n=14, per group): (a) normotensive ; (b) hypovolemic (20% blood loss); (c) normotensive and pretreatment with NG-nitro-L-arginine methyl ester (LNAME); (d) hypovolemic and pretreatement with L-NAME.G-nitro-L-arginine methyl ester (LNAME); (d) hypovolemic and pretreatement with L-NAME. Results: L-NAME restored the hypotension induced by hemorrhage. Blood loss decreased heart rate in the first stage increasing at 60 and 120 min. L-NAME blunted this effect. Right atria and left ventricle histochemical NOS activities increased at 60 and 120 min (atria 8 and 24%, respectively; ventricle 21 and 45 %, respectively). This activity increased 17% in smooth muscle at 120 min. Heart endothelial NOS protein levels increased in heart at 60 min being attenuated at 120min. Inducible NOS protein levels raised significantly in right atria, left ventricle and aorta at 120 min.L-NAME restored the hypotension induced by hemorrhage. Blood loss decreased heart rate in the first stage increasing at 60 and 120 min. L-NAME blunted this effect. Right atria and left ventricle histochemical NOS activities increased at 60 and 120 min (atria 8 and 24%, respectively; ventricle 21 and 45 %, respectively). This activity increased 17% in smooth muscle at 120 min. Heart endothelial NOS protein levels increased in heart at 60 min being attenuated at 120min. Inducible NOS protein levels raised significantly in right atria, left ventricle and aorta at 120 min. Conclusion: Hemorrhagic shock induced a time-dependent and specific NOS activation modulating cardiovascular function. The inhibition of nitric oxide system appears to prevent the acceleration of heart rate during late phases after acute hypovolemic state induced by blood loss.Hemorrhagic shock induced a time-dependent and specific NOS activation modulating cardiovascular function. The inhibition of nitric oxide system appears to prevent the acceleration of heart rate during late phases after acute hypovolemic state induced by blood loss.