Effects of D,L-2-difluoromethylornithine and indomethacin on mammary tumor promotion in rats fed high n-3 and/or n-6 fat diets.

Virgin female Sprague-Dawley rats (50 days of age) were administered a single intragastric 10-mg dose of 7,12-dimethylbenz(a)anthracene (DMBA). Twenty-one days later they were placed on diets containing either 20% corn oil (CO), 15% menhaden oil plus 5% corn oil (MO + CO), 20% CO plus 0.5% w/w of the irreversible ornithine decarboxylase inhibitor, D,L-2-difluoromethylornithine (CO + DFMO), 20% CO plus 0.004% w/w of the cyclooxygenase inhibitor indomethacin (CO + INDO), 20% CO + 0.004% INDO + 0.5% DFMO (CO + INDO + DFMO), or 15% MO + 5% CO + 0.5% DFMO (MO + CO + DFMO). The incidence of DMBA-induced mammary tumors was significantly reduced in rats fed diets containing DFMO but not in rats fed the diet containing indomethacin. Incidences of mammary tumors at 16 weeks post-DMBA were 86% in rats fed the CO diet, 83% in rats ingesting the diet containing CO + INDO, 28% in rats fed CO + DFMO, 32% in rats fed diet containing CO + INDO + DFMO, 59% in rats fed the MO + CO diet, and 24% in rats fed the MO + CO + DFMO diet. The average number of tumors and tumor burden per tumor-bearing rat were reduced and tumor latency was increased in all rats fed diets containing DFMO. Body weight gain, but not food intake, of rats fed the 20% fat + 0.5% DFMO diets was significantly less than in rats fed the 20% fat diets. Prostaglandin E and leukotriene (LTB4) syntheses, ODC activity and mammary tumorigenesis were significantly inhibited by feeding the diet containing menhaden oil or by adding 0.5% DFMO to any of the high fat diets. Feeding a 20% CO diet containing 0.004% INDO significantly reduced prostaglandin synthesis and ODC activity and increased LTB4 synthesis of mammary tumors but did not inhibit mammary tumorigenesis. This study suggests that the 5-lipoxygenase product LTB4 may be involved in mammary tumor production. Whereas a decrease in LTB4 appears to be associated with a decrease in tumorigenesis, an increase (as seen in the indomethacin group) was not associated with any change in the tumorigenic response.

Effects of dietary primrose oil on mammary tumorigenesis induced by 7,12-dimethylbenz(a)anthracene.

The mammary tumor-promoting effect of a high-fat diet containing 20% evening primrose oil (PO) was compared to that of a 20% corn oil (CO) diet. Mammary tumors were induced in female Sprague-Dawley rats using 10 mg (Study 1) and 5 mg (Study 2) 7,12-dimethylbenz(a)anthracene (DMBA). The 10 mg dose of DMBA gave a total mammary tumor incidence of 47% in rats fed the PO diet and 80% for those fed the CO diet. When only adenocarcinomas were counted, the malignant mammary tumor incidences were 41% in rats fed the PO diet and 73% in rats fed the CO diet. In a second study using 5 mg DMBA to induce mammary tumors, total tumor incidences were 50% for PO-fed rats and 63% for those receiving a CO diet. Again, when only adenocarcinomas were counted, tumor incidences were 27% for PO- and 63% for CO-dieted rats. Analysis of plasma fatty acid profiles indicated that animals fed a 20% PO diet showed significant increases in 18:3 and 20:4 fatty acids and significant decreases in 16:0 and 18:1 compared to animals fed a 20% CO diet. These results indicate that the mammary tumor promoting effect of a diet containing 20% fat can be diminished by substituting PO for CO. Moreover, the promoting effect on mammary cancer by a high-fat diet could be depressed by feeding a source of gamma-linolenic acid (GLA).

Eicosanoid synthesis in 7,12-dimethylbenz(a)anthracene-induced mammary carcinomas in Sprague-Dawley rats fed primrose oil, menhaden oil or corn oil diet.

The comparative effects of high-fat diets (20%, w/w) on eicosanoid synthesis during mammary tumor promotion in 7,12-dimethylbenz(a)anthracene (DMBA)-induced rats were studied using diets containing 20% primrose oil (PO), 20% menhaden oil (MO) or 20% corn oil (CO). Sprague-Dawley rats fed the PO or MO diet had 21% of 24% fewer adenocarcinomas, respectively, than rats fed the CO diet. Histologically (i.e., mitotic figures, inflammatory cell infiltration and necrosis), the CO-fed rats exhibited the highest frequency of changes within tumors. Plasma fatty acid composition was significantly altered by diet, reflecting the composition of the oils which were being fed. Only the plasma of PO-fed rats contained detectable levels of gamma-linolenic acid (GLA). Arachidonic acid (AA) levels were significantly higher (p less than 0.05) in PO-fed than in CO- or MO-fed rats. MO-fed rats had significantly higher levels of plasma palmitic acid, while palmitoleic, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were detected only in MO-fed rats. As expected, linoleic acid (LA) and AA levels were lower (p less than 0.05) in the MO-fed rats than in PO- or CO-fed groups. The plasma of the CO-fed rats contained significantly higher levels of oleic acid. Eicosanoid synthesis in mammary carcinomas of rats fed the 20%-fat diets was 2-10 times higher than in mammary fat pads of control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Generalized Equine Cutaneous Mastocytosis.

A newborn foal developed generalized cutaneous mastocytosis characterized by multiple elevated nodules of mast cells in skin and basophil hyperplasia in bone marrow. Skin lesions began as small aggregates of mast cells that progressively enlarged, ulcerated, and regressed spontaneously. Eosinophil infiltration, collagen necrosis, and fibroplasia were characteristic of advanced lesions. Many new lesions developed during the first month of life but numbers progressively diminished. Large numbers of mast cells were present in biopsies of lymph node, spleen and bone marrow. Discrete aggregates of mast cells were present in the bone marrow postmortem but no other significant change was seen. Mast cells contained large amounts of histamine but little serotonin. Ultrastructurally, their cytoplasmic granules were chiefly granular with few dense forms. In cell culture, mast cells from early lesions maintained mitotic activity through 14 passages. Cells obtained from older lesions were rapidly overgrown with fibroblasts. An equine herpesvirus isolated from cultures of cutaneous mast cell lesions and of spleen was not thought to be related to the disease.

Hemostatic indices in healthy foals from birth to one month of age.

Hemostatic indices were determined in 45 healthy light breed foals, from birth to 1 month of age, and in 20 healthy adult (> 2 years of age) light breed horses. Blood samples were obtained from each foal at 4 ages: 1) < 24 hours, 2) 4-7 days, 3) 10-14 days, and 4) 25-30 days. The following hemostatic indices were determined: platelet count; prothrombin and activated partial thromboplastin times; activity concentrations of protein C, antithrombin III, plasminogen, alpha-2 antiplasmin, tissue plasminogen activator, and plasminogen activator inhibitor-1; plasma protein C antigen and fibrinogen concentrations; and serum fibrin degradation products concentration. Prothrombin and activated partial thromboplastin times were significantly longer at birth than in older foals. The plasma concentrations of the following were significantly lower at birth than in older foals: antithrombin III, plasminogen and tissue plasminogen activator activities, protein C antigen, and fibrinogen. Concentrations of the following were significantly higher at birth than in older foals: protein C and plasminogen activator inhibitor-1 activities and fibrin degradation products. These results indicate that hemostatic indices of neonatal foals differ significantly from those of older foals and adults. With the exceptions of antithrombin III and tissue plasminogen activator activities, all hemostatic indices measured in foals at 1 month of age were equivalent to adult values.

Hematologic values in calves infected with Sarcocystis cruzi.

Calves were inoculated with 2 X 10(5) Sarcocystis cruzi sporocysts. Red cell mass decreased dramatically between Days 21 and 35 post-infection and plasma volume increased concurrently, so that blood volume did not change significantly. Mild reticulocytosis and increased pyrimidine 5' nucleotidase activity in erythrocytes occurred between Days 35 and 42. Antiglobulin tests with anti-bovine IgG, IgM and C3 were negative, with the exception of a positive test for C3 in 1 of 6 infected calves.

Regulation of equine fibrinolysis in blood and peritoneal fluid based on a study of colic cases and induced endotoxaemia.

Much of the pathophysiology associated with equine gastrointestinal diseases is attributed to the effects of endotoxin on haemostasis. Because little is known about the responses of the equine fibrinolytic system to endotoxin, regulation of the system was investigated. Tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type-1 (PAI-1) were identified as the primary plasminogen activator and plasminogen activator inhibitor, respectively, in equine blood. Under experimental conditions, the equine fibrinolytic system responded to endotoxin in a manner similar to that reported in man, with an early, transient increase in t-PA activity followed by an overwhelming and prolonged increase in activity of PAI-1. To investigate the response of the equine fibrinolytic system to clinical endotoxaemia, endotoxin concentrations were measured in plasma and peritoneal fluid, and activities of t-PA and PAI-1 were compared between healthy horses (n = 38) and horses with naturally occurring gastrointestinal diseases (n = 150). It was observed that plasma PAI-1 and peritoneal t-PA were increased concurrently in abnormal horses; and that these increases were associated with the presence of endotoxin. The results of this study suggest that 1) fibrinolysis is regulated in horses in a manner similar to that in man; 2) regulation of fibrinolysis is altered in endotoxaemic horses with gastrointestinal diseases; 3) events occurring in the vascular system may not reflect those in the peritoneal cavity; and 4) t-PA activity is increased in the peritoneal fluid of endotoxaemic horses with gastrointestinal diseases.

Hemostatic and fibrinolytic indices in neonatal foals with presumed septicemia.

Thirteen coagulation tests evaluating hemostatic and fibrinolytic indices and serum cytokine and plasma endotoxin concentrations were obtained in 34 foals with a positive sepsis score (septic group) and 46 age-matched healthy foals. Compared to healthy foals, the prothrombin, activated partial thromboplastin, and whole blood recalcification times were significantly longer in septic foals. The fibrinogen and fibrin degradation products concentrations, percent plasminogen, alpha-2 antiplasmin, and plasminogen activator inhibitor activities, and tumor necrosis factor and interleukin-6 activities were greater in septic foals. Protein C antigen and antithrombin III activity were significantly lower in septic foals. Blood cultures were positive for growth and endotoxin was detected in 19 of 29 and 15 of 30 septic foals, respectively. In septicemic foals with detectable endotoxin in the plasma, the prothrombin and activated partial thromboplastin times were significantly longer and the plasminogen and antithrombin III activities were significantly less than in septic foals in which endotoxin was not detected. Twenty-three of the 34 septic foals did not survive. Septic foals that did not survive were most likely to have a positive blood culture in which a gram-negative organism was isolated. Histopathologic evidence of hemorrhage was evident in 11 foals at postmortem examination and thrombosis was identified in 2 foals. The prothrombin time was significantly longer in foals that had multisite hemorrhage at postmortem examination. The results of this study indicate that clinically relevant alternations in hemostatic and fibrinolytic indices occur in neonatal foals with septicemia and that derangements can be correlated with the presence of endotoxin in plasma. Derangements in hemostatic or fibrinolytic indices were helpful in identification of septic foals with increased risk of coagulopathy, but were not helpful in predicting hemorrhage as compared to thrombus formation. Survival of septicemic foals was correlated with gram-negative bacteremia, but not with the presence of endotoxin or coagulopathy.

Hypercoagulable state associated with a deficiency of protein C in a thoroughbred colt.

Protein C is a vitamin K-dependent serine protease with anticoagulant and profibrinolytic activity which is synthesized in the liver. Decreased protein C activity was detected in a Thoroughbred colt with clinical and histopathologic evidence of recurrent venous thrombosis. Although protein C activity was reduced, protein C antigen concentration was normal. Consumptive coagulopathies produce a decrease in both the functional and antigenic concentrations of protein C, thus a defect in protein C synthesis was suspected. Inhibition of gamma-carboxylation secondary to vitamin K antagonism results in the synthesis of a protein C molecule with antigenicity, but without biological activity. However, there was no evidence of vitamin K antagonism. The hypercoaguable state resulting from the reduced activity of protein C in this colt was associated with uncomplicated renal disease, rather than a protein C consumptive process such as endotoxemia. A primary hypercoagulable state due to a deficiency of protein C activity was diagnosed. Primary deficiencies of protein C activity have not been previously documented in horses.

Microcytosis and iron status in dogs with surgically induced portosystemic shunts.

Microcytosis is common in dogs with congenital portosystemic shunts (PSS) and acquired liver disease. The objective of this study was to determine if microcytosis could be induced in normal dogs by surgical creation of PSS, and to characterize the changes in hematology and iron status. Hematocrit, mean cell volume, mean cell hemoglobin, and mean cell hemoglobin concentration decreased linearly from 45.5%, 69.1 fL, 22.8 g/dL and 33.1% to 39.5%, 55.9 fL, 17.8 g/dL and 31.9%, respectively, 18 weeks after creation of PSS. The erythrocyte count did not change, but red cell distribution widths indicated a shift to a heterogenous population with decreased volume. Mean cell volume and mean cell hemoglobin decreased rapidly after induction of PSS and were significantly (P < .05) different from presurgery values within 2 weeks. Serum iron and copper concentrations and total iron binding capacity were decreased in dogs with PSS. Liver iron concentration doubled after creation of PSS, with the majority of stainable iron located in Kupffer cells. The changes in erythrocyte indices and measures of iron status in dogs with surgically induced PSS were similar to those in dogs with congenital PSS. Microcystosis developed rapidly in dogs after induction of PSS. These results indicate that iron deficiency was not the cause of microcytosis in these dogs.

Neutrophilic movement of a Basenji with Pelger-Huët anomaly.

Random and chemotactic neutrophilic movements in a Basenji with Pelger-Huët (P-H) anomaly was compared with such movement in 5 healthy control dogs. Duplicate samples of neutrophils were quantitated after 5, 10, 15, 30, and 45 minutes of incubation. On the basis of population mean responses, no significant difference (P greater than 0.05) was found between P-H and control neutrophils for any type of movement at any time interval examined. These findings indicate that the movement of neutrophils with P-H anomaly may be unaffected by the nuclear abnormality.

Chromogenic assays for equine coagulation factors VII, VIII:C, IX, and X, and C1-esterase inhibitor.

OBJECTIVES: To adapt manual human chromogenic assays for coagulation factors VII (F.VII), VIII:coagulant (F.VIII:C), IX (F.IX), and X (F.X), and C1-esterase inhibitor (C1-INH) for use with an automated analyzer, and to measure the activity of these proteins in horses. ANIMALS: 10 healthy horses were used to determine ranges for the assays. Pooled plasma for standards was collected from an additional 20 healthy horses. PROCEDURE: A computer-assisted analyzer was programmed from the manual method for commercially available human F.VII, F.VIII:C, F.IX, F.X, and C1-INH chromogenic assay kits. Standards were prepared from pooled citrated equine plasma for the F.VII, F.VIII:C, and F.X assays, and from commercial pooled citrated human plasma for F.IX and C1-INH assays. RESULTS: Mean +/- SD activities in citrated equine plasma from 10 horses were 226 +/- 19% for F.VII; 209 +/- 31% for F.VIII:C; 149 +/- 38% for F.IX; 88 +/- 12% for F.X; and 18.4 +/- 8.4% for C1-INH. Intra-assay coefficients of variation (CV) were 5.3% for F.VII; 2.1% for F.VIII:C; and 3.0% for C1-INH. Interassay CV were 5.7% for F.VII; 7.4% for F.VIII:C; 3.8% for F.IX; 14.4% for F.X; and 22.0% for C1-INH. CONCLUSIONS: Human chromogenic assay kits can be automated and used to measure F.VII, F.VIII:C, F.IX, F.X, and C1-INH activities in citrated equine plasma. CLINICAL RELEVANCE: Human chromogenic assays can be routinely used to measure F.VII, F.VIII:C, F.IX, F.X, and C1-INH in horses, and may be useful in evaluation of horses with disorders of hemostasis.

Analysis of coagulation proteins as acute-phase reactants in horses with colic.

OBJECTIVES: To measure coagulation factor VIII:coagulant (F.VIII:C) and C1-esterase inhibitor (C1-INH), hemostasis-associated acute-phase reactant proteins and coagulation factors VII (F.VII), IX (F.IX), and X (F.X), hemostasis proteins not associated with an acute-phase response, in a select population of horses with colic and hemostasis abnormalities, and presumed to have acute-phase changes. To compare these values and other routine hemostasis test results in the horses with colic with values for a population of healthy horses. To correlate the values of known equine acute-phase reactants, F.VIII:C and fibrinogen, to those of other tests of hemostasis. To identify hemostasis-associated acute-phase reactant proteins and gain insights into the effects the acute-phase response has on hemostatic abnormalities in horses with colic syndrome. SAMPLE POPULATION: 54 plasma samples from horses with colic attributable to inflammatory (n = 39) or strangulating (n = 15) intestinal disorders. PROCEDURE: Plasma samples were evaluated for activities of F.VII, F.VIII:C, F.IX, F.X, C1-INH, antithrombin III, protein C, plasminogen, and alpha 2-antiplasmin (alpha 2AP); fibrinogen concentration; and prothrombin (PT) and activated partial thromboplastin (APTT) times. RESULTS: Horses with colic had significantly higher fibrinogen concentration, greater alpha 2AP and protein C activities, and longer PT and APTT than did healthy horses. Horses with colic also had significantly lower mean F.VII activity than did healthy horses. Significant positive correlations between fibrinogen concentration and F.VIII:C, C1-INH, and alpha 2AP values, and between F.VIII:C activity and fibrinogen, C1-INH, alpha 2AP, and plasminogen values were identified. CONCLUSIONS: An acute-phase response contributes to changes observed in coagulation proteins in horses with colic attributable to inflammatory and strangulating intestinal disorders. The data suggest that plasminogen, alpha 2AP, and C1-INH, should be considered equine acute-phase proteins.

Use of enzyme-linked immunosorbent assay to measure thrombin-antithrombin III complexes in horses with colic.

OBJECTIVES: To evaluate new ELISA for measurement of thrombin-antithrombin III (TAT) concentration, and to correlate the values to other tests of hemostasis in horses with colic. DESIGN: Plasma TAT concentration and 8 other hemostasis analytes were measured in horses with colic at hospital admission and during the next 4 days. Retrospectively, data were analyzed by outcome, broad-category diagnosis, and clinical management, and for correlation between TAT and other assays. ANIMALS: 100 horses with colic. PROCEDURE: Plasma samples were evaluated for TAT, fibrinogen, and fibrin degradation products concentrations; antithrombin III (ATIII), protein C, alpha 2-antiplasmin, and plasminogen activities; prothrombin time (PT); and activated partial thromboplastin time. RESULTS: Changes were indicative of a hypercoagulable state, most severe in nonsurviving horses, characterized by increased TAT concentration; decreased ATIII, protein C, and plasminogen activities; and increased PT. Nonsurvivors had significantly increased TAT concentration compared with that in survivors, without regard to sample collection time; however, compared over time, TAT was significantly increased only at admission. Highest TAT concentration was in nonsurvivors with inflammatory intestinal lesions. There was significant negative correlation between TAT and ATIII, protein C, alpha 2-antiplasmin, and plasminogen values, and significant positive correlation between TAT and PT, and fibrin degradation products values. CONCLUSIONS: Plasma TAT reflects the current state of coagulation system activation and is a good assay for early diagnosis of the hypercoagulable state in horses with the most severe forms of colic. CLINICAL RELEVANCE: Measurement of equine TAT provides further information to characterize the hypercoagulable state in horses to aid in case management.

Chromogenic assay for equine plasminogen.

A functional assay for equine plasminogen was established, using urokinase as the activator, a synthetic chromogenic substrate, a computer-assisted centrifugal analyzer, and acidified/neutralized plasma. One documented effect of plasma acidification appears to be inactivation of alpha-2-antiplasmin. Intra- and interassay precision testing yielded coefficients of variation of 4.1% (n = 10) and 5.6% (n = 26), respectively. Plasminogen was stable in equine plasma stored up to 1 week at 4 C and up to 5 months at -70 C. Plasminogen in nonacidified equine plasma was not activated by urokinase, streptokinase, tissue plasminogen activator, or tissue plasminogen activator plus soluble fibrin. Streptokinase also failed to activate plasminogen in acidified/neutralized equine plasma.

Effects of exploratory laparotomy on plasma and peritoneal coagulation/fibrinolysis in horses.

Plasma and peritoneal fluid samples were collected before and after surgery from 6 horses undergoing a ventral midline exploratory laparotomy and from 6 anesthetized control horses. Coagulation/fibrinolytic components measured in the plasma and peritoneal fluid of these horses included the functional activity of antithrombin III, alpha-2 antiplasmin, plasminogen, and protein C, and the concentrations of fibrinogen and fibrin degradation products. Peritoneal fluid antithrombin III, fibrin degradation products, and plasminogen values were significantly increased after surgery (over time) in principal horses. Compared with control horses, postoperative peritoneal fluid from horses undergoing laparotomy had significantly increased antithrombin-III activity at 12 and 72 hours, alpha-2 antiplasmin activity at 24 hours, fibrin degradation product concentrations at 6, 12, 24, 72, 96, and 144 hours, plasminogen activity at 6, 12, 24, 48, 72 and 96 hours, and protein-C activity at 12, 24, 72, and 96 hours. There were no significant changes in the peritoneal fibrinogen concentration in principal horses. Plasma plasminogen activity was significantly decreased at 24 hours after surgery in principal horses, compared with controls. Changes were minimal in the remaining plasma coagulation/fibrinolytic components of horses undergoing laparotomy. Plasma and peritoneal fluid values of anesthetized control horses did not change.

Use of newly developed assays for protein C and plasminogen in horses with signs of colic.

Protein C content and plasminogen activity were measured in plasma from 100 horses with signs of colic. Data were analyzed by grouping horses 4 ways. Each horse was allotted to 1 of 2 outcome groups (survivors and nonsurvivors), 1 of 3 broad-category diagnosis groups (inflammatory disorders, strangulating obstructions, and all other gastrointestinal disorders), and 1 of 2 clinical management groups (medical and surgical). In a fourth grouping, all horses (although numbers of horses included in each subgroup were small) were assigned either to specific diagnostic groups that had high expectation for activated hemostasis (intestinal ischemia, endotoxemia, jugular thrombosis, peritoneal adhesions, and laminitis) or to a control group, in which active hemostasis was unlikely. Within 2 to 24 hours after admission, nonsurvivors developed lower protein C content than did survivors. Protein C content and plasminogen activity became low during hospitalization in horses with strangulating obstructions and in horses having surgery. The results from the grouping by specific diagnosis must be considered pilot data because the numbers of horses in each subgroup were small. Although not statistically significant, trends were noticed in protein C and plasminogen: (1) horses with intestinal ischemia and endotoxemia developed low protein C content and plasminogen activity, (2) protein C content became low in horses that developed peritoneal adhesions or laminitis, and (3) plasminogen activity became low in horses that developed jugular thrombosis. Low protein C content or low plasminogen activity, or both, may be useful as predictors for outcome and for these specific complications of equine colic.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline phosphatases in tissues and sera of cats.

The numbers and widths of bands of alkaline phosphatase (ALP) activity in polyacrylamide gels and the comparison of their electrophoretic mobility to that of a reference substance (Rf value) were found to be reliable aids in the identificaiton of various isoenzymes in in serum and organ extracts from cats. The hepatic isoenzyme was identified in sera of clinically normal adult cats, pregnant cats late in gestation, and cats with common bile duct occlusion. In addition to the hepatic isoenzyme, placental ALP was found late in gestation in sera from queens. Sera from kittens less than 15 weeks of age contained only the osseous ALP isoenzyme.

Thiacetarsamide in dogs with Dirofilaria immitis: influence of decreased liver function on drug efficacy.

The influence that decreased functional hepatic mass had on blood arsenic concentrations in dogs after they were treated with thiacetarsamide, on the clearance of indocyanine green (ICG), on arsenic concentrations in the heartworm (Dirofilaria immitis), and on drug efficacy was studied. Dogs which were partially hepatectomized and treated with thiacetarsamide (1.76 mg/kg, 2 times a day for 2 days) had a significantly (P less than 0.01) reduced ICG clearance, significantly (P less than 0.01) higher arsenic levels in heartworms, and a significantly (P less than 0.01) higher proportion of heartworms killed than did dogs that were sham operated and treated with thiacetarsamide or sham operated and untreated. There were no significant differences in blood arsenic (thiacetarsamide) concentrations 2 minutes after injection between hepatectomized and nonhepatectomized groups. More male heartworms were killed than were female worms in the thiacetarsamide-treated groups. Indocyanine green half-life was longer (12.43 minutes) in the hepatectomized group than it was in the nonhepatectomized sham-operated groups (5.09 and 4.94 minutes). Indocyanine green clearance rate was lower in the hepatectomized group (0.54 ml/min/kg) than that in the nonhepatectomized groups (1.36 and 1.56 ml/min/kg). A parallel seemed to exist between ICG and thiacetarsamide removal from the blood by the liver. This parallel also was suggested in the higher worm arsenic (thiacetarsamide) concentrations for the hepatectomized group vs that for nonhepatectomized groups. Apparently, the slower the removal of thiacetarsamide from the blood by the liver, the higher the worm arsenic level and, consequently, the higher the worm kill.

Antigenic assay for protein C determination in horses.

An antigenic assay was developed for determination of protein C in horses. Protein C, a natural, vitamin K-dependent anticoagulant component in blood, was isolated from equine plasma, a specific antibody was produced in goats, and a rocket electroimmunophoresis assay was established. Tests were performed to verify the identity of the isolated protein C and to determine the purity of the antibody. Protein C antigen was measured in plasma from 34 clinically normal horses, and values were compared with amidolytic function values. The mean (+/- SD) values for the 2 test methods were similar (antigen content, 104.5 +/- 13.8%; amidolytic activity, 104.6 +/- 17.5%), but the correlation coefficient was 0.1. Four horses given Na coumarin had markedly decreased plasma protein C amidolytic activity and minimal decrease in protein C antigen content.