Pathological studies of the animals replaced totally with the artificial heart. Part II Concerning liver, gastrointestinal tract, kidney, and general discussion.
Twenty-eight goats with an artificial heart (AH) were studied pathologically. Being continued from the previous report, the liver, gastrointestinal tract, and kidneys were taken up in this paper and finally, general discussion was done to get our ideas in shape concerning the pathophysiological status of the goat. Central necrosis of the liver was always observed in the goats which survived for over 140 hours. This finding seemed to be caused mainly by circulatory insufficiency of the portal vein at the latter half of the survival time. Microscopic findings of degeneration, necrosis, and edema were commonly observed at the walls of gastrointestinal tracts, when goats showed poor apetite, mucous feces and constipation. But these problems have been improved by application of a new control method to regulate the output of AH system within a goat's physiological range since October 1974. The lesions seen in the kidneys are classified into 5 groups. The most important findings of them are lower nephron nephrosis and cortical necrosis, both of which indicate the occurrence of long standing vasoconstriction of proximal renal arteries. By means of microangiographic method and others, thrombi were detected frequently in the kidneys. The vascular walls, where thrombi were attached to, were often damaged. Therefore, these thrombi were thought to be formed in the local vessels in situ through renal circulatory insufficiency. The renal pathological lesions have been also improved and severe renal failure from which the previous goats could not escape, has been lessened since the application of a new AH control method. As a whole, the main pathophysiological status of the animals replaced by the AH are thought conclusively to be peripheral circulatory insufficiency. This would be caused by abnormal hemodynamics, so that, the essential clinical etiology is thought to be AH function itself.
D000818:Animals; D001201:Ascites / Q000473:pathology; D004064:Digestive System / Q000098:blood supply / Q000473:pathology*; D005234:Fatty Liver / Q000473:pathology; D006041:Goats; D006354:Heart, Artificial / Q000009:adverse effects* / Q000401:mortality; D007238:Infarction / Q000473:pathology; D007416:Intestinal Perforation / Q000473:pathology; D007668:Kidney / Q000473:pathology*; D008099:Liver / Q000473:pathology*; D009336:Necrosis; D009929:Organ Size; D011168:Portal System / Q000473:pathology; D011183:Postoperative Complications / Q000473:pathology*; D012077:Renal Artery / Q000473:pathology; D013927:Thrombosis / Q000473:pathology