The Biomicroscopic Observation of the Effect of Experimental Toxic Liver Injury on the Intrahepatic Blood Circulation

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Abstract
From the results obtained in the present experiments, it is considered that decrease in the optical transmission, observed by biomicroscope, i.e., the fog phenomenon, in the liver at the initial phase of hepatic injury is due to the dissociation of lipid in the liver cells. The explanation is based on the following facts. According to the rule of optics, when fine granules of a high refractive index are present in a substrate, the optical transmission decreases by light scattering. The substances which can affect the optical transmission in liver cells are lipids and proteins. The refractive index of proteins, however, is much lower than that of lipids and almost equal to the index of water. Therefore, it seems that proteins do not have as great an effect on changes in the optical transmission as do lipids. In fractionization there were no changes in the amount of total lipid and neutral fat fatty acid of the liver at the initial phase of injury, and there was a slightly decreased tendency in the amount of total phospholipid. From these facts it may possibly be concluded that the decrease in the optical transmission of liver at the initial hepatic injury, the fog phenomenon, is caused by the dissociation of lipid in hepatic cells. Although it has been stated that the injured hepatic cells become stainable with various vital stainings because of the change in their permeability, in the present experiment no such evidence was confirmed. In the electron micrographs, swelling in ergastoplasm was recognized, but there were no discernible changes in mitochondria, nucleolus, nuclear membrane and cell membrane. The same results were obtained in the livers at 1, 2, or 3 hours after the hepatic injury. Finally, although it has been considered that there is a close relationship between hepatic injury and the blood circulation in liver (the author has published a paper supporting this) the experimental results recently obtained by the author showed no relation between the blood circulation in liver and the initial change of hepatic injury. In other words, the blood circulation in liver does not play a main role in toxic hepatic injury. This was also confirmed by the experiment with electropolarograph; the oxygen partial pressure did not change even after the liver was injured. In this paper, several experimental findings on the pathologic physiology of the initial phase of hepatic injury were described, which were obtained by studies mainly on the living materials, and especially by biomicroscopic observations.