Study of morbid anatomy material from dead
patients suffering from HIV-related illnesses, including
hepatitis С, provided an opportunity to identify substantial
pathological changes in the structural elements liver that
suggested other pathogenetic mechanism of development
changes in patients with HIV and hepatitis С associated
with impaired metabolism in erythrocytes that are
collapsing, hemoglobin in the plasma of blood blood vessels
of the liver. As a result of the destruction of erythrocytes,
free, not associated with erythrocytes, hemoglobin
cannot carry carbon dioxide from cells, hypoxia ensues
the structural elements of the liver and cells are forced
to use the free dissolved in plasma oxygen, which further
exacerbates the occurrence of hypoxia and Anoxia and then
the appearance of intoxication of the massive destruction
of hemoglobin and the advent of plasma transferrin. The
last captured by macrophages. The free hemoglobin in
the bloodstream increases its toxic effect on tissue cells,
causing cell death in the resultant ischemia, thus worsening
the oxygen supply of them. As a result of the subsequent
destruction of haemoglobin are formed its decay products in
the form of iron рorphyrin, bilirubin, The latter contributed
to the development of jaundice or acute porfirii owing to the
death of hepatocytes, which manifest is to develop cirrhosis
or cancer
Calcium Peroxide-Containing Polydimethylsiloxane-Based Microwells for Inhibiting Cell Death in Spheroids through Improved Oxygen Supply
