The role of endotoxin in the pathogenesis of progressive liver disease is receiving increasing attention, but remains controversial. Similarly, although alcoholic hepatitis is now recognized as the transitional link between alcoholic fatty liver and advanced alcoholic liver disease, the aetiology of liver cell necrosis in alcoholic hepatitis is not known. Rats fed a nutritionally adequate liquid alcohol diet according to the formula of Lieber and DeCarli developed fatty livers. Littermates fed an identical diet and challenged with small IV doses (1 microgram/g body weight) of E. coli lipopolysaccharide endotoxin (LPS) developed focal necrotizing hepatitis. Control littermates fed an identical calorie balanced but alcohol free diet and challenged with identical doses of LPS did not develop any liver lesions. The hepatocyte necrosis with associated inflammatory changes induced by LPS in fatty livers has some features of early human alcoholic hepatitis and suggests that progressive alcohol induced damage may be multifactorial in origin.

Luminal narrowing was assessed in 238 transverse segments obtained from coronary arteries removed at postmortem. In each segment, narrowing was assessed by gross visual estimation before and after fixation, and on histological sections by stereological point counting and computer-assisted planimetry. Computer-assisted planimetry was found to be accurate and reliable but the equipment needed is expensive, and requires specialized software and an experienced user. Morphometric measurement by stereologic point counting was accurate, rapid, simple, and inexpensive. In comparison with computer-assisted planimetry visual estimation was found to be neither accurate nor reliable. Our results indicate point counting as the method of choice for assessment of coronary artery luminal narrowing by atherosclerosis.

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