Vascular hyporeactivity to vasoconstrictor agents and hemodynamic decompensation in hemorrhagic shock is mediated by nitric oxide.

@article{Thiemermann1993VascularHT,
  title={Vascular hyporeactivity to vasoconstrictor agents and hemodynamic decompensation in hemorrhagic shock is mediated by nitric oxide.},
  author={Christoph Thiemermann and Csaba Szab{\'o} and Jane A Mitchell and John R. Vane},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={1993},
  volume={90 1},
  pages={267-71}
}
This study investigates the role of nitric oxide (NO) and the induction of a calcium-independent NO synthase (NOS) in development of vascular hyporeactivity to norepinephrine (NE) and vascular decompensation associated with hemorrhagic shock (HS) in the anesthetized rat. HS for 120 min caused a time-dependent reduction of the pressor responses to NE. This hyporeactivity is mediated by an enhanced release of NO by the constitutive NOS, for it was reversed by NG-nitro-L-arginine methyl ester… CONTINUE READING

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