Effects of aerosolized methylprednisolone on experimental neurogenic pulmonary injury.

  title={Effects of aerosolized methylprednisolone on experimental neurogenic pulmonary injury.},
  author={H. Edmonds and H. Cannon and H. Garretson and G. Dahlquist},
  volume={19 1},
We examined the effects of graded doses of methylprednisolone sodium succinate (MPSS)--0.05 (low), 0.5 (medium), and 5 mg/kg/hour (high)--on the development of neurogenic pulmonary injury in rabbits. The aerosolized drug was administered intratracheally for 5 hours beginning 10 minutes after a 2-minute elevation of the cerebrospinal fluid pressure (Pcsf) to 250 mm Hg. Compared to untreated control animals, the percentage of increase in pulmonary capillary permeability, as determined by 51Cr… Expand
Protective effect of erythropoietin on type II pneumocyte cells after traumatic brain injury in rats.
Erythropoietin protects the ultrastructure of pneumocyte type II cells against damage after traumatic brain injury and significantly reduced both the Ultrastructural pathologic changes and the lipid peroxidation levels in the treatment group. Expand
The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor
It is concluded that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension, and management of the brain‐dead donor with early anti‐inflammatory treatment and vasoconstrictors is warranted. Expand
Neurogenic Pulmonary Edema
Neurogenic pulmonary edema occurs as a complication of acute neurologic illness and may mimic acute lung injury of other etiology and implications for organ donation after brain death. Expand
Rat donor lung quality deteriorates more after fast than slow brain death induction
It is demonstrated that fast BD induction deteriorates quality of donor lungs more on a histological level than slow BD induction, reflected by higher mean arterial pressures during the BD induction period and an increased need for hemodynamic support during theBD stabilization phase. Expand
Ultrastructural changes in pneumocyte type II cells following traumatic brain injury in rats.
The data suggested that ultrastructural damage is obvious at 2 h and deteriorates with time and the electron microscopic scoring model worked well in depicting the traumatic changes, which were supported by lipid peroxidation. Expand
Pulmonary Transplantation: the role of brain death in donor lung injury
An understanding of the mechanism of donor lung injury could lead to the development of new treatment strategies for the donor to reduce lung injury, increase the number of donors with acceptable lungs, and improve the results of transplantation. Expand
Muerte encefálica: repercusión sobre órganos y tejidos
The development of the knowledge regarding the pathways that interrelate brain death with the inflammatory organ response provides us with an important area of knowledge, which allow for future therapeutic strategies aimed at modulating the systemic response to brain death to improve the quality of the organs obtained for transplant and also to increase graft survival of the solid organ transplant recipients. Expand
Apoptosis-related gene bcl-2 in lung tissue after experimental traumatic brain injury in rats.
The oxidative stress imposed on lung tissue, as seen by high levels of lipid peroxidation, after brain injury was significantly attenuated by MPSS treatment. Expand
Early Hemodynamic Injury During Donor Brain Death Determines the Severity of Primary Graft Dysfunction after Lung Transplantation
Postreperfusion, lungs retrieved early from untreated brain‐dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha‐blockade‐treated donors. Expand
Neurogenic pulmonary edema
Neurogenic pulmonary edema remains poorly understood because of the complexity of its pathophysiologic mechanisms involving hemodynamic and inflammatory aspects. Expand