Abstract:
Subarachnoid hemorrhage (SAH) may cause neurogenic
pulmonary edema (NPE), and chylomicron metabolism
may be destroyed in injured lungs. We aimed to investigate
the effect of neurogenic pulmonary edema (NPE), if
present, on the development of cerebral fat embolism. This
study has been conducted on 20 rabbits. Experimental SAH
has been applied to half of the animals by injecting homologous
blood into the cisterna magna, and the remaining half
was applied only isotonic saline solution in the same manner
under general anesthesia. After 20 days, all animals
were killed. Their lungs and brains were examined histopathologically.
Six animals died of SAH between 16 and
20 days, and foamy hemorrhagic parenchymal lesions and
intra-alveolar hemorrhage were observed in their lungs. Fat
globules were abundantly found in cerebral arteries of six of
all the non-surviving animals. But, minimal histopathological
changes were found in the lungs and brains of the surviving
animals. Cerebral fat embolism was detected in only
one animal that was given isotonic solution. SAH may cause
NPE and result in lung tissue destruction. Chylomicron
metabolism may be disordered in the destructed lungs and
leakage of chylomicrons into systemic circulation may be
facilitated via destroyed lung barrier. These pathologic processes
may lead to cerebral fat embolism.
