Technetium-99m sulfur colloid scintigraphy was used to study alterations of reticuloendothelial function in 7 dogs with experimentally induced biliary cirrhosis and portosystemic shunting. Scintigraphic studies were performed before and 6 weeks after common bile duct ligation. Radiocolloid plasma clearance rate was determined by measuring activity in plasma samples and by analyzing the rate of liver uptake on dynamic scintigraphic image sequences. Percentage of uptake in the liver, spleen, and lungs, as well as the ratio of hepatic-to-extrahepatic uptake, was determined from static equilibrium images. Relative to preoperative values, there were significant decreases in plasma clearance rate, percentage of liver uptake, and ratio of hepatic-to-extrahepatic uptake and significant increases in percentage of spleen and lung uptake on postoperative studies. The mechanism of technetium-99m-labeled sulfur colloid extraction by the liver is different from that of other radiocolloids; it does not require active phagocytosis or pinocytosis. Thus, liver uptake of this tracer principally reflects effective liver blood flow. Portosystemic shunting was documented in these dogs at the time of the postoperative radiocolloid scans, and we believed was responsible for the decrease in liver reticuloendothelial activity. Possible mechanisms for the increased splenic and pulmonary reticuloendothelial activities are discussed.

Eighteen healthy dogs were allotted to 3 groups (n = 6 dogs each). All dogs were evaluated at the beginning of the study by complete physical examination; total and differential WBC counts; serum biochemical analysis (alanine transaminase and alkaline phosphatase activities and bilirubin and albumin concentrations); sulfobromophthalein excretion, ammonia tolerance, and glucagon response testing; portal and intraparenchymal pressure determinations; operative mesenteric portography; and histologic assessment of hepatic biopsy specimens. The left hepatic vein was ligated completely in dogs of groups 1 and 2. Group-3 (control) dogs had a ligature placed loosely around the left hepatic vein. Dogs of groups 1 and 3 were reevaluated 24 hours after surgery by use of the aforementioned hematologic and biochemical tests. Group-1 dogs were reevaluated by use of portal and intraparenchymal pressure determinations, jejunal vein portography, and complete necropsy at 48 hours after surgery. At 4 weeks after surgery, dogs of groups 2 and 3 were reevaluated by use of all aforementioned tests. Results indicated transient hepatic congestion, which resolved by the fourth postoperative week. Longstanding effect on hepatic structure, circulation, or function was not found. We concluded that left hepatic vein ligation in clinically normal dogs does not cause severe or permanent liver damage.

Blood flow to the semitendinosus muscle was studied in 12 dogs after ligation of either the proximal or distal vascular pedicle and elevation of the muscle from its normal position. Using 25-micrometer-diameter radioactive microspheres, flow was measured at rest, h and 18 days after muscle elevation and pedicle ligation. Mean blood flow in the proximal region of the muscle 6 and 18 days after ligation of the caudal gluteal (proximal) pedicle was not significantly different from mean blood flow calculated in the middle and distal regions of the muscle. There was also no significant difference in mean blood flow among proximal, middle, and distal regions of the muscle, 6 and 18 days after ligation of the distal caudal femoral (distal) pedicle. There was significantly (P < 0.05) increased blood flow between group-A (ligation of caudal gluteal artery) and group-C (operated-control) muscles, 6 and 18 days after surgery. There was no loss of muscle fiber striations or nuclei, or presence of fibrous tissue that might have indicated ischemic necrosis in any of the experimental groups. These results indicate that the entire semitendinosus muscle can be sustained by the blood flow from either of its 2 vascular pedicles, which reinforces its potential as a muscle flap.

Alterations in serum lipid and lipoprotein concentrations in ponies with experimentally induced liver disease were investigated. Hepatocellular damage was induced, using a nonlethal dose of carbon tetrachloride. In a separate group of ponies, obstructive jaundice was induced by surgical ligation of the common bile duct. Over a 6-day period, blood samples were obtained from ponies after treatment with carbon tetrachloride and for 12 days in ponies subjected to surgery. Serum cholesterol and triglyceride concentrations were unaffected in both groups of ponies, except for significantly (P < 0.01) high triglyceride concentration in ponies of the ligated group during the second postsurgical week. This increase was most likely attributable to anorexia observed during that period. Hyperbilirubinemia was observed early in ponies of the ligated group; most of the bilirubin was of the conjugated type. Using electrophoretic and ultracentrifugal methods, serum lipoprotein alterations were detected only in ponies of the ligated group. Increases of very low-density and low-density hpoprotein cholesterol concentrations and decrease in high-density lipoprotein cholesterol concentration were found. Although no changes were seen in total serum cholesterol concentration, a redistribution of lipoprotein cholesterol was observed in ponies of the ligated group. Similar alterations in lipoprotein distribution have been found in dogs, rats, and human beings with obstructive jaundice and cholestasis. The association between serum lecithin:cholesterol acyl transferase activities and these lipoprotein alterations remains to be elucidated.

To determine blood supply in the area, dye or radioopaque contrast material was injected into the named arteries supplying the terminal colon and rectum in 10 dogs. The cranial rectal artery appeared to supply most of the blood to the terminal colon and rectum. The middle and caudal rectal arteries supplied variable and relatively insignificant amounts. The intrapelvic rectum had a less adequate blood supply than did the terminal colon or proximal rectum. A ventral midline laparotomy and pubic osteotomy were performed in an additional 11 dogs to provide access to the terminal colon and rectum. When the cranial rectal artery was ligated and the colorectal junction was transected and anastomosed, the intrapelvic rectum developed marked congestion, edema, and discoloration. Rectal fluorescence, after IV administration of fluorescein, was either poor or absent. Histologically, partial- to full-thickness mucosal necrosis was evident in most tissue specimens taken from the rectum, and muscle necrosis was evident in some. These findings suggest that, in dogs, the cranial rectal artery should be preserved if at all possible and, if the cranial rectal artery is ligated, most of the intrapelvic rectum should be resected to ensure adequate blood supply to the anastomosis.