The objective of this study was to define, in detail, the anatomy of the portal and hepatic veins in the dog in order to establish a procedure for the systematic evaluation of the liver by ultrasonography. Anatomical details were obtained from the formalin fixed livers of ten dogs. The hepatic and portal veins were removed intact from these livers so that a detailed pattern of distribution could be established and the numbers of branches could be counted. Silastic casts were also made of the hepatic and portal veins of two livers, one in situ and one in which it had been removed. The former was to enable the relationship of the portal to the hepatic veins to be established as closely as possible within the animal and the other to provide a model of the distribution of each venous system within the liver. Contrast medium was infused into two other livers and radiographs taken to establish the relationship of each branch to each lobe. It was found that there was a consistent pattern of venous branching to each lobe of the liver in the dog with little variation between individual specimens. All liver lobes contained definite venous branches so that the left lateral and medial, quadrate, right medial and lateral, caudate and papillary veins could be distinguished in each venous system. We believe that an appreciation of this venous distribution will aid in the systematic evaluation of the liver during ultrasonography by enabling identification of each liver lobe. It should be of value for differentiating portal from hepatic veins and veins from dilated bile ducts.
A method for systematic examination of the livers was developed, based on identification of the hepatic and portal veins in sixteen dogs. The right medial, quadrate, left medial and lateral hepatic veins and the hepatic branches of the portal veins were easily located with the dog in dorsal recumbency. The right lateral and caudate hepatic veins were identified more easily from the right side with the transducer positioned between the ninth to the eleventh intercostal spaces. Visibility was affected by the fullness of the stomach but this effect could be minimized by changing the position of the transducer to select a more suitable anatomical approach. Identification of the two systems depended on their echogenicity, the anatomical position of the main branches and their pattern of distribution. As in humans, the portal veins were in general, more echogenic than the hepatic veins and the hepatic veins could be traced from their junctions with the caudal vena cava. Identification of the branches of the hepatic and portal veins was complicated by the anatomical shape, the nutritional status and respiratory stage of the animal. A systemic approach based on a knowledge of the distribution patterns produced by the hepatic and portal veins ensures that all liver lobes are identified and all important structures are assessed.
Recent research in our laboratory has demonstrated that basic fibroblast growth factor (bFGF) is a permissive mitogen for epiphyseal growth plate chondrocytes. Immunocytochemistry demonstrated the presence of bFGF in the proliferative and hypertrophic zones of normal epiphyseal growth plates of 4-wk-old broiler chickens. The purpose of this investigation was to extend this research to include examination of the status of bFGF in the cartilage lesion associated with tibial dyschondroplasia (TD). Immunocytochemistry revealed that the distribution of bFGF in the growth plate proximal to the TD lesion was similar to that observed with normal growth plate. However, the intensity of immunofluorescence was greatly diminished in the TD lesion. The number of chondrocytes staining positive for bFGF was also reduced. In the peripheral edges of the lesion where cartilage was being actively resorbed, the staining intensity was greatly increased when compared to the rest of the TD lesion. Similar patterns were observed in all TD tissues examined whether the lesions were spontaneous or induced by dietary treatments or genetic selection. It is hypothesized that the decrease in bFGF, a potent angiogenic factor, may be responsible for the poor vascularization of the TD lesion.
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