Vascular leakage induced by histamine, bradykinin, serotonin and prostaglandin E2 in Greyhounds

SUMMARY Vascular leakage induced by intradermal injection of histamine, bradykinin and serotonin alone and co-injected with prostaglandin E₂ was measured in Greyhounds using ¹²⁵Iodine-labelled human serum albumin (¹²⁵I-HSA) as a marker in the blood. Histamine and bradykinin produced dose-dependent vascular leakage. At equimolar concentrations, histamine was more than twice as potent as bradykinin. Serotonin did not induce vascular leakage and was irritant. Prostaglandin E₂ did not induce significant vascular leakage (maximum 5μL) when injected alone, but when co-injected with histamine and bradykinin, the vascular leakage of both histamine and bradykinin was increased. This effect was more pronounced if lower concentrations of histamine and bradykinin were injected. The induced vascular leakage was greatest during the first five minutes of lesion development for histamine, during the second five minutes of lesion development for bradykinin, and the synergistic effect of prostaglandin E₂ was maximal during the third five minute period of lesion development.     

Bioavailability of threonine in soybean meal for rats and chicks.

The bioavailability of threonine in soybean meal and the effects of the excess amino acids in soybean meal on the estimate were measured using rats and chicks in slope-ratio assays. In Exp. 1, a corn-based diet containing .23% threonine was supplemented with 0 to 45% L-threonine in .05% increments. The growth rate of weanling rats fed these diets increased quadratically (P less than .001) with L-threonine addition, the increase being essentially linear up to the .10% addition. In Exp. 2, the basal diet was supplemented with 0, .025, .050, .075, or 100% threonine from L-threonine, simulated soybean meal (a mixture of crystalline amino acids with a pattern designed to simulate soybean meal), or soybean meal. Regressions of partitioned weight gain and body N gain of rats vs supplemental threonine intake were calculated for each source using multiple regression. Slope ratios (soybean meal:L-threonine) were .91 for weight gain and .92 for body N gain. The additional amino acids in simulated soybean meal did not affect the estimate. For Exp. 3, a corn-soybean meal-based diet containing .48% threonine was supplemented with 0 to 60% L-threonine in .10% increments. The growth rate of broiler chicks fed the diets increased quadratically (P less than .001) with L-threonine addition. The increase was essentially linear up to the .10% addition. In Exp. 4, the basal diet was supplemented as in Exp. 2. Regressions of partitioned weight gain of chicks vs supplemental threonine intake were calculated for each source. The slope ratio for soybean meal:L-threonine was 1.03; however, the model exhibited fundamental invalidity and therefore the estimate should be interpreted with caution. The additional amino acids in the simulated soybean meal did not affect the value.     

Zinc-amino acid complexes for swine

Two experiments were conducted to determine the effect of sources of dietary zinc on gain, feed conversion and blood and bone traits of swine. In the first experiment 96 pigs were used in a 28-d study. The pigs were fed diets with no supplemental Zn or with either 9 or 12 ppm supplemental Zn from zinc sulfate (ZnSO4), zinc methionine (ZnMet) or zinc methionine with picolinic acid (ZnMet w/PA), each with or without 5% added corn oil. There were differences (P less than .05) in average daily gain (ADG) and average daily feed intake (ADFI) between the pigs fed the two organic Zn sources, with those fed ZnMet w/PA showing the better gains and feed conversion. However, neither organic Zn source resulted in pig performance that was different from either the diet with no supplemental Zn or the diets supplemented with Zn from ZnSO4. In the second experiment the same dietary Zn sources and treatments were fed as in Exp. 1 except that corn oil was deleted as a variable. No differences in ADG, ADFI, feed/gain (F/G) or in changes in serum Zn or Cu were observed among treatments during either the 21-d nursery or the 56-d growing periods. During the subsequent 56-d finishing period ADG and ADFI were greater (P less than .01) for pigs fed the Zn-supplemented diets than for those fed the diets without supplemental Zn. There were no differences among treatments in F/G during the finishing period. Zn content of bone ash was lower (P less than .01) in the non-Zn-supplemented pigs. These data suggest that the Zn sources used are of similar biological value and do not support the theory that picolinic acid aids Zn absorption.     

Concentrations of ovarian and pituitary hormones following prostaglandin F2 alpha-induced luteal regression in ewes varies with day of the estrous cycle at treatment

Prostaglandin F2 alpha (PGF2 alpha) was injected on d 5, 8 or 11 postestrus in ewes to determine how stage of the estrous cycle would affect PGF2 alpha-induced changes in concentrations of ovarian and pituitary hormones and intervals to the onset of estrus and the preovulatory surge of luteinizing hormone (LH). Initial concentrations of progesterone and average values during the 12 h after PGF2 alpha were related positively to the day of cycle on which PGF2 alpha was administered. Patterns of decline in progesterone after injection of PGF2 alpha were similar among the 3 d. Concentrations of LH in plasma increased in a similar manner from 0 to 12 h in all ewes. After 12 h LH continued to increase, plateaued or declined in ewes treated on d 5, 8 or 11, respectively. Initial concentrations of follicle stimulating hormone (FSH) in plasma were related positively to day of treatment. After treatment with PGF2 alpha, FSH increased within 2 h on d 5 but declined by that time on d 8 or 11. Concentrations of estradiol following treatment did not vary with day. The onset of estrus and the preovulatory surge of LH occurred at 36 and 35, 40 and 45, and 48 and greater than 48 h in ewes treated on d 5, 8 or 11, respectively. It is concluded that: 1) the initial increase in LH is dependent on a decrease in plasma progesterone and 2) differences in patterns of secretion of gonadotropins before the preovulatory surge of LH might be caused by differences in progesterone or progesterone:-estradiol ratio when luteal regression is induced on different days of the estrous cycle.     

Effects of interrupted lighting regimens on the feeding activity of the laying fowl

Segmentation of the main light period of an 8L:4D:2L:10D regimen into 30 min light, 30 min dark did not affect total feeding activity, rate of feeding or total intake of laying hens. When 15 min light and 45 min dark was provided each hour feeding activity and food intake were reduced, while rate of feeding and feeding during the dark periods increased. No feeding occurred in the 10 h 'night'. Hens subjected to interrupted lighting showed less feeding activity than those on a 14L:10D regimen. Insertion of a 4 h dark period in the 14 h subjective day of laying hens increased their rate of feeding, but reduced total intake. The pattern of feeding activity depended on the position of the 4 h dark period. The largest modification of feeding activity occurred on a 8L:4D:2L:10D regimen; 20% of activity occurred in the last 2 h of the apparent day. Feeding occurred during the 4 h dark period, but not during the 10 h 'night'.     

Pitfalls in immunofluorescence testing in canine dermatology

Indirect immunofluorescence testing for pemphigus-like antibodies was performed on 100 dogs: 50 dogs with various nonpemphigus dermatologic diseases, 25 dogs with various nondermatologic diseases, and 25 normal dogs. One dog (generalized demodicosis) was positive for pemphigus-like antibodies at a titer of 1:10. It was concluded that canine pemphigus-like antibodies are a potential source of misinterpretation and misdiagnosis in indirect immunofluorescence testing. Direct immunofluorescence testing for IgG, IgA, IgM, and C3 was performed on the footpads of 11 normal dogs. Granular deposition of IgM at the basement membrane zone was demonstrated in 5 of the 11 dogs. It was concluded that direct immunofluorescence testing of canine footpads using only polyvalent immunoglobulin antisera or anti-IgM antisera may lead to misinterpretation and misdiagnosis in up to 45% of all dogs tested.     

Plasma Taurine Concentrations in Normal Dogs and in Dogs With Heart Disease

Plasma taurine concentrations were determined in 76 dogs with dilated cardiomyopathy (DCM), 28 dogs with acquired valvular disease (AVD), and 47 normal (control) dogs. The data were collected at 2 referral centers. The Animal Medical Center, New York, NY (AMC), and the University of California, Davis (UCD), and the studies were conducted independently. Different anticoagulants (sodium citrate at AMC and lithium heparin at UCD) were used to collect the plasma samples. Paired analysis of samples showed a significant difference in plasma taurine concentrations, depending on the anticoagulant used. Consequently, results from each clinic were analyzed separately. Plasma taurine concentrations were significantly higher in dogs with AVD (median, 133 nmol/mL; range, 25 to 229 nmol/mL) than in control dogs (median, 63 nmol/mL; range 44 to 224 nmol/mL) and dogs with DCM (median, 72 nmol/mL; range, 1 to 247 nmol/mL) at AMC (P= .001). The number of dogs with AVD at UCD was too small to draw meaningful conclusions. At UCD, the median plasma taurine concentration was 98 nmol/mL (range, 28–169 nmol/mL) in dogs with AVD, 75 nmol/mL (range, 0.1–184 nmol/mL) in dogs with DCM, and 88 nmol/mL (range 52–180 nmol/mL) in control dogs. There were no significant differences in plasma taurine concentrations between dogs with DCM and the control dogs at either hospital. Congestive heart failure and administration of cardiac medication had no significant effect on plasma taurine concentrations. Plasma taurine concentration was low (<25 nmol/mL) in 17% (13/76) of the dogs with DCM. Seven of the 13 dogs with low plasma taurine concentrations were Cocker Spaniels or Golden Retrievers. It was concluded that most dogs with DCM do not have low plasma taurine concentrations. However, certain breeds or individual dogs may have low plasma taurine concentrations in association with DCM. Whether this association is causal or not is unknown. The significance of the high plasma taurine concentrations in dogs with AVD is also unknown.