Left ventricular dysfunction after acute intracranial hypertension is associated with increased hydroxyl free radical production, cardiac ryanodine hyperphosphorylation, and troponin I degradation.

@article{Hall2005LeftVD,
  title={Left ventricular dysfunction after acute intracranial hypertension is associated with increased hydroxyl free radical production, cardiac ryanodine hyperphosphorylation, and troponin I degradation.},
  author={Sean R R Hall and Louie Wang and Brian Milne and Murray Hong},
  journal={The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation},
  year={2005},
  volume={24 10},
  pages={1639-49}
}
BACKGROUND In addition to generating free radicals, stress-induced activation of the sympathetic nervous system results in hyperphosphorylation of the cardiac ryanodine receptor (RyR2)/calcium (Ca2+) release channel on the sarcoplasmic reticulum, causing leaky channels. These events may contribute to cytosolic Ca2+ overload and activation of Ca2+-dependent cytotoxic processes. Because myocardial dysfunction associated with intracranial hypertension is catecholamine mediated, we sought to… CONTINUE READING