Desensitization of rabbit myometrium to oxytocin and prostaglandin F2 alpha.

The desensitizing effects of oxytocin (OT) and prostaglandin F2 alpha (PGF2 alpha) were investigated in the uteri of rabbits. Uterine motility was measured in anesthetized rabbits infused intravenously with either PGF2 alpha (50 micrograms/min) or OT (100 mU/min) alternately. The treatment sequence was saline (30 min), first drug (OT or PGF2 alpha, 90 min), second drug (OT if PGF2 alpha was first drug and vice versa, 90 min), and first drug (repeated) 60 min. Both OT and PGF2 alpha infusions increased motility approximately 200% within 5-10 min. Thereafter, motility decreased linearly to base-line value. Fifty percent desensitization was completed at 35-45 min and 100% at 90 min. A tenfold increase in the infusion rate caused no further increase in motility. However, OT infusion into a PGF2 alpha desensitized uterus (and vice versa) elicited an immediate uterokinetic response. Oxygen consumption and glucose oxidation rate of uterine slices measured at different stages (preinfusion, maximal motility, and desensitized) of uterine motility showed no difference (P greater than 0.05) between the two experimental treatments. It was concluded that either OT or PGF2 alpha infusions specifically desensitized the uterus.

Uterotonic effect of prostaglandin F2 alpha and oxytocin on the postpartum cow.

Uterine motility was measured in 6 mixed-breed beef cows 48 to 72 hours after parturition, using an intrauterine balloon technique. Baseline uterine motility was measured for 30 minutes after a stabilization period. After 25 mg of prostaglandin F2 alpha (PGF2 alpha) was given IM, motility was recorded for 2 to 4 hours. After PGF2 alpha injection, 200 IU of oxytocin was given IM and motility was recorded for 2 to 4 hours. Twenty-four hours later, oxytocin treatment was administered, and 2 to 4 hours later, PGF2 alpha was given. The tension-time index was calculated. When PGF2 alpha was given initially, it did not affect (P greater than 0.05) uterine motility. However, oxytocin after PGF2 alpha increased uterine motility an average of about 225% of that of base line 20 minutes after injection. When oxytocin was given before PGF2 alpha treatment, the average increment of uterine motility was 875% above base line 20 minutes after oxytocin injection. The injection of PGF2 alpha did not affect uterine motility significantly (P greater than 0.05), whether given before or after oxytocin treatment. There was a linear decrease in the uterotonic effect of oxytocin between 10 minutes and 2 hours. When oxytocin was injected first, the correlation coefficient for the time-response relationship was -0.98. When oxytocin was injected after PGF2 alpha, the correlation coefficient was -0.84. Seemingly, PGF2 alpha should not be used as a uterotonic agent in the postpartum cow; however, oxytocin was an effective uterotonic agent.

Retention of calcium in intestinal wall of the rabbit by treatment with a glucocorticoid.

In this work, consideration was given to the possibility that increased retention of Ca in the intestinal wall may have resulted in the glucocorticoid-treated animal. Rabbits were treated with pharmacological doses of either dexamethasone, estrogen, or progesterone during 1 wk. Two milliliters of solution containing Ca (plus Mg, K, and Na) were infused into a double-ligated (4 cm apart) gut loop (jejunum). In addition, an adjacent loop was double ligated but received no infusion. Uterine horns were treated in the same way as the gut and were used as controls to test for organ specificity. After the organs were infused with the calcium solution, they were returned into the abdominal cavity for a 4-h period. Dexamethasone treatment was given to a different group of rabbits in which neither surgery was performed nor mineral solution was infused into the lumen of the intestine; in this experiment calcium concentrations were measured in the mucosa, submucosa, and serosa layer obtained from the duodenum, midjejunum, and distal jejunum. In rabbits subjected to surgery, the concentration of Ca in the whole wall of the intestine of the dexamethasone-treated rabbits (45.4 +/- 2.6 mM/kg dry tissue) was twice as large as in controls (22.6 +/- 3.2 mM/kg dry tissue) (P less than 0.05). Mg concentrations were moderately (17%) increased (P less than 0.05). In the group of rabbits receiving dexamethasone but not subjected to surgery, the concentration of Ca in the duodenum (mucosa, submucosa, and whole wall), midjejunum (whole wall), and distal jejunum (submucosa) was significantly (P less than 0.05) elevated as compared with controls. In these rabbits, the duodenum was the most affected segment of the intestine. The effect of dexamethasone was both organ and steroid specific but not mineral specific. This result suggests that one of the effects of the glucocorticoid (dexamethasone) treatment on the intestinal wall was to increase the retention of Ca.

Inhibition of gastric hydrochloric acid secretions in the rat given Ostertagia ostertagi (a gastric parasite of cattle) extract.

The immersion of freshly collected Ostertagia ostertagi adults into saline solution (NaCl, 0.9%; pH 1.0) resulted in 100% mortality of worms within a 10-minute period. At pH 7.0, mortality was 58% after 270 minutes. At pH 2.2, which approximates the usual abomasal pH, 100% mortality resulted within 60 minutes. In the stomach of rats injected with an extract of O ostertagi (from the abomasum of cattle), there were decreased total secretion of hydrogen ions and volume of secretion (P less than 0.05) and increased mean pH of gastric secretion (P less than 0.05). These effects were similar to those found in stomach of rats treated with cimetidine. Results indicated that the pH of the abomasum was detrimental to parasitic survival and that hypochlorhydria found during ostertagiosis may be mediated partially by a chemical released from the parasite.

Internal vomiting in the ruminant: effect of apomorphine on ruminal pH in sheep.

Five sheep, with a rumen fistula inserted, were each injected (IV) with apomorphine (18 mg) and ruminal pH was measured every 5 minutes during a 1-hour period. During the base-line period (30 minutes) that preceded apomorphine injection, pH was constant in individual sheep and te group mean (+/- SD) was 7.1 +/- 0.35. After apomorphine was injected, group mean was 6.9, 6.0, 6.3, 6.3, 6.3, 6.4, 6.4, 6.5, 6.7, 6.9, 6.9, and 7.1 at 5, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, and 60 minutes, respectively. The pH reduction of ruminal content was recorded in 4 of the sheep. Maximal reduction occurred in the 10-minute period after apomorphine was injected. The pH returned to control value within 40 to 50 minutes after injection. Vomitus was not expelled through the mouth by any of the sheep. It was concluded that expulsion of acidic abomasal contents back into the preabomasal compartment (internal vomiting) was the cause of acidification of the rumen after apomorphine was injected.

Altering iodine metabolism in the calf by feeding iodine-binding agents.

Effects of feeding cottonseed meal and anion-exchange resin on iodine absorption and excretion by calves were investigated. Each additional amount of resin fed from .3 to 3.5 g/kg body weight further increased fecal excretion from single oral iodine-131 and intravenous iodine-125 doses. By feeding 3 to 10 g cottonseed meal/kg body weight, excretion of oral iodine-131 given daily was increased 7 to 94% in feces and reduced as much as 35% in urine, but plasma iodine-131 was not changed. Introducing 1 g resin/kg body weight daily into the diet increased fecal iodine-131 excretion three to five times that with cottonseed meal alone and reduced both plasma and urinary iodine-131. The same amount of resin fed daily had similar effects on excretion of iodine-131 injected subcutaneously each day. Although iodine depletion by a highly efficient iodine binder (resin) in the gastrointestinal tract is probable, iodine binding by a natural feed constituent (cottonseed meal) was relatively inefficient.

Magnesium movement in hypothyroid sheep.

We described magnesium transport in hypothyroid and normal sheep with an eight-compartment biomodel fitted by a least-squares technique to data from multiple compartments and routes of entry of 28-Mg. Isotopic equilibrium was not attained during this period of observation in hypothyroid or control sheep. Hypothyroidism reduced transfer coefficients for absorption (P less than 0.01) of 28-Mg from the GI tract but did not change the rate coefficient for endogenous 28-Mg losses to feces (P less than 0.05). Nutritional balance data indicated higher absorption and retention of Mg in hypothyroid sheep, and the observed decrease in rate of passage of digestive residues suggested that mean retention time of GI tract contents had a definite effect on the availability of Mg.

Effect of thyroid status and thiocyanate on absorption and excretion of iodine by cattle.

Effects of throidectomy or iodine-131, thyroprotein feeding, and thiocyanate dosing on radioiodine metabolism in the bovine were studied in 34 animals. Two thyroidectomized calves excreted 44% more radioiodine in urine and 38% less in feces than two thyroid-tact calves. Oral thiocyanate increased urinary radioiodine 32% in throidectomized and 46% in intact calves while reducing fecal radioiodine 48% in throidectomize and 11% in intact calves. Urninary radioiodine clearance of two heifers was increased 52% by thiocyanate, but urine flow was not affected. Percentages of radioiodine doses cycled through the abomasum daily and recovered from digestive tracts at slaughter, respectively, were: 12 thyroid-intact cows, 468 and 77; two intact cows fed 10 g sodium thiocyanate daily,64 and 41; 10 thyroid-damagedcows, 506 and 149; and four thyroid-damaged cows fed 8 g thyroprotein daily, 372 and 93. Thyroid damage had little effect on gastric radioiodine secretion but increased total digestive tract radioiodine because of greater volume of tract contents. Inhibition of gastric radioiodine secretion by thiocyanate reduced the digestive tract radioiodine pool. The digestive tract iodine pool may conserve iodine by reducing loss in urine.