In the course of observations on the r61e of the liver in blood formarion and destruction, we have had occasion to ligate portal branches to the organ. The ensuing changes have been of such striking character as to merit study for their own sake; and the present paper is concerned with them. There already exists, of course, a considerable literature on so obvious a theme. For the moment it m a y suffice to state in this connection that according to the generally accepted view occlusion of a portal branch to the liver has no effect on the organ save when a grave derangement of the systemic circulation is also present. The complete local parenchymal atrophy that in our experiments regularly followed such occlusion was unforeseen, as was the further observation that the atrophy is conditional, being dependent upon a compensatory hypertrophy of the remainder of the organ. Method.The liver of the rabbit is singularly adapted for experiments involving the blood vessels and bile ducts, since it consists of two separate masses, each with its own vessels and ducts. The rabbit may indeed for operative purposes be said to possess two livers. They are of very unequaI size, the larger, or main liver, as we shall call it, formed of the left anterior and posterior lobes and the right anterior lobe with the gall bladder, being three times as big as the smaller, or lobe mass, which consists of the right posterior and caudate lobes. The lobe mass contains just enough parenchyma, as Ponfick 1 showed, to suffice for the
The relation of the portal blood to liver maintenance.
There are excellent reasons for employing the rabbit in an experimental analysis of the biliary factor in liver lesions; and it is possible to obtain in this animal results uncomplicated by infection or by intercurrent cirrhosis. Ligation of the common duct of the rabbit results in a mixed lesion from injury throughout the entire length of the bile channels. By obstructing single ducts and altering the portal stream we have produced cirrhoses of pure monolobular and diffusely intralobular types. The character of the connective tissue changes is determined by the path of escape of bile from the collecting system, which in turn is largely conditional upon the secretory activity, while this again is dependent upon blood flow. The portal flow is largely diverted from regions of local stasis through encroachment on the stream bed by the dilated ducts. There is a large margin of safety in bile elimination by the normal hepatic tissue. Less than a quarter of the liver of the rabbit, and this deprived of its entire portal stream, will suffice to keep the organism free from clinical jaundice and healthy when the remainder of the liver, which receives all of the portal blood, has its ducts ligated. The vicarious elimination thus illustrated is of great importance for regions of local stasis by keeping the blood relatively free from bile, thus preventing resecretion into such regions and facilitating exchange from them into the body fluids. Our experimental monolobular and intralobular cirrhoses are the result of the limitation of biliary lesions to special levels of the duct system. Their resemblance to the different forms of "biliary" cirrhosis associated with Hanot's name is close, and the diverse liver lesions of Hanot's disease are readily explained on the assumption that the stasis, with or without infection, which is indubitably here present, has its situation at different levels in different cases. There are reasons for the view that bile stasis per se may sometimes be a prime cause of the malady. Certainly such stasis must be thought of as acting to complicate many chronic liver lesions. In a later paper experiments on the dog will be described essentially similar in result to those on the rabbit as here set forth.
In examining the gastrointestinal tract of rats which were being used for other experiments, our attention was directed to the frequent occurrence of lesions in the tureen or esophageal portion of the stomach. Since these lesions were found only in rats on variously deftd e n t diets, it seemed interesting to pursue the subject further in the hope of defining the particular factor concerned.Before describing the lesions encountered, the normal structure of the non-glandular portion of the rat stomach m a y be briefly recalled.
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