Iodine in milk and meat of dairy cows fed different amounts of potassium iodide or ethylenediamine dihydroiodide.

Relationships between I intake by lactating Holstein cows and iodine concentrations in milk and meat were investigated. Six treatment groups with seven cows assigned to each treatment were fed a basal diet containing .8 mg I/kg alone or supplemented with I at 1, 2, or 4 mg/kg in four 5-wk periods. Basal alone was fed in the first and third periods and the I supplement was potassium iodide in the second period and ethylenediamine dihydroiodide in the fourth period. Iodine concentrations in milk increased with each increase in dietary I from 205 ng/ml for basal periods to 404, 477, and 757 ng/ml when 1, 2, or 4 mg/kg I was fed as potassium iodide; and 467, 535, and 869 ng/ml when 1, 2, or 4 mg/kg I was fed as ethylenediamine dihydroiodide. Concentrations of I in skeletal muscle after the fourth period were not affected by 2 mg/kg I and only increased from 166 to 199 ng/g when supplemental I was 4 mg/kg. Moderate changes in dietary I are quickly reflected in milk I, but I in meat is relatively stable.

Effect of minoxidil on platelet function and the synthesis of prostaglandins in platelets.

At the 12.5 micrograms level, minoxidil prevents the irreversible aggregation of platelets by 2 x 10(-6) mol/L adenosine diphosphate (ADP). Levels of minoxidil greater than 12.5 micrograms cause a reversal of primary aggregation by 2 x 10(-6) mol/L ADP. Aggregation of platelets in response to 125 micrograms of arachidonic acid is measurably reduced by 12.5 micrograms of minoxidil and totally suppressed by 30 micrograms. Concurrent with the inhibition of platelet aggregation, increasing concentrations of minoxidil cause a gradual reduction in the synthesis of prostaglandin E2 (PGE2) and thromboxane B2 (TxB2). In the presence of 100 micrograms of minoxidil, PGE2 is reduced from a control value of 87.7 +/- 2.2 pg/ml to 23.9 +/- 3.2 pg/ml. At this level of minoxidil, TxB2 drops from 105 +/- 3.3 ng/ml to 10.5 +/- 2.6 ng/ml. The effect of minoxidil on platelet aggregation is not associated with increased cyclic adenosine monophosphate synthesis. All data support the conclusion that minoxidil functions (in platelet metabolism) primarily as a cyclooxygenase inhibitor.

Effects of hypothyroidism and short-term aging on whole blood thromboxane and arterial prostacyclin synthesis.

Hypothyroidism results in decreased platelet aggregation and has unique effects on the development of atherosclerosis and angina pectoris. Because prostacyclin and thromboxane A2 profoundly influence platelet function and vascular tone and are thought to be important in the development of atherosclerosis and angina pectoris, we studied the effects of hypothyroidism in rats on the in vitro elaboration of prostacyclin passively by aortic tissue and of thromboxane A2 by thrombin-stimulated whole blood. Hypothyroidism induced by iodine 131 (given at age 7 weeks) persistently caused a mild decrease in platelet count (P less than 0.01) and 30% decrease in immunoreactive thromboxane B2 (the hydrolysis product of thromboxane A2) generation per platelet (P less than 0.01) compared with age-matched euthyroid rats. Between 20 and 23 weeks of age immunoreactive 6-ketoprostaglandin F1 alpha (the hydrolysis product of prostacyclin) generation decreased by 30% in euthyroid rats. In hypothyroid rats less than 23 weeks of age, 6-ketoprostaglandin F1 alpha production was the same as that of age-matched euthyroid rats. With further aging, 6-ketoprostaglandin F1 alpha production did not decrease as it did in euthyroid rats. Hypothyroid rats more than 20 weeks old had, therefore, significantly greater 6-ketoprostaglandin F1 alpha production than age-matched euthyroid rats (P less than 0.005). L-Thyroxine given daily for 28 days to 23-week-old hypothyroid rats caused a rapid increase in platelet count and a delayed normalization of the thromboxane synthetic abnormality. 6-Ketoprostaglandin F1 alpha production transiently increased in response to L-thyroxine, but decreased to the euthyroid level after 28 days of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of excessive iodide administered in the dry period on thyroid function and health of dairy cows and their calves in the periparturient period.

Experiments were conducted in three successive years in which iodide (I) doses of 1.25, 2.5, 5.0 and 7.5 mg/kg body weight were given to 47 dairy cows during the dry period, compared with 16 control cows on basal diets of 1 ppm I. Effects on cows dosed at 1.25 and 2.5 mg I/kg (50 and 100 ppm dry feed) were not different from controls in terms of vitality of calves, changes in plasma thyroxine (T4), plasma triiodothyronine (T3), thyroxine secretion rate and 10-mo milk yields of the lactation after treatment. Cows dosed with 5 and 7.5 mg I/kg (200 and 300 ppm dry feed) averaged 272.8 d gestation, which was significantly shorter than 279.5 d for all cows on lesser I intakes. Abnormal calves at birth were 25% from the two highest I dosages vs 8% from controls plus the two lowest I dosages. Average plasma T4 and T3 decreased on the day of calving by about 30%, while plasma total I increased about 20%. Changes were greatest in cows fed high I dosages for the longest period prepartum. Plasma I and T3 of calves at birth were about three times the concentrations in their dam's plasma and plasma T4 of neonatal calves was four to five times greater than their dams. Highest dosages of I for dams tended to depress plasma T4 and T3 in neonatal calves.

Effects of excessive intakes of iodine upon growth and thyroid function of growing Holstein heifers.

Thirty Holstein heifer calves averaging 120 days of age and 102 kg of body weight were allocated to one control and four treatment groups of six each. Iodine, as ethylenediamine dihydriodide, was mixed 1:9 with dextrose and administered once daily atop feed at .625, 1.25, 2.5, or 5.0 mg iodine per kilogram body weight. Calves were housed individually in unheated, well-ventilated barns and fed complete mixed feeds containing less than 1 ppm iodine. Feed intakes were recorded daily and body weights weekly. Jugular venous blood was collected from iodine treated calves at 0, 4, 8, and 12 wk of the experiment and analyzed for iodine, thyroxine, and triiodothyronine of plasma. Feed intake per unit body weight and per unit gain were not significantly different between treated and control calves. However, daily feed intake and average daily gain decreased slightly at the highest iodine intake. Thyroxine and triiodothyronine were not different among treatments. Thyroxine declined in all calves from 0 to 12 wk. Thyroxine of calves fed 5.0 mg of iodine per kilogram body weight decreased more than of calves fed less iodine. Iodine intake as high as 5.0 mg/kg body weight was tolerated without morbidity, although a minor effect on performance and thyroid activity was indicated.

Mammary gland development of dairy heifers during their first gestation.

Mammary gland development was determined by analysis of udders at thirteen stages of the first gestation of nine pairs of identical twin dairy heifers. Stained sagittal sections of udders showed that gland parenchyma spread into and displaced adipose tissue so that total udder weight does not reveal extent of gland development. Changes in composition of mammary gland during gestation reflected gross and histological changes. Percentages of fat and deoxyribonucleic acid decreased while percentages of nitrogen, water, dry fat-free tissue, and ribonucleic acid increased. Development of the portion of the udder which was mammary gland appeared to be a continuous exponential process through gestation, and increases in quantitative development followed the general formula for organ growth, Y = Aekt (In Y = In A + kt), in which k is the rate constant for growth by months (t). Analysis of variance showed in addition to stage of gestation that body weight and pairs, but not age, affected the regression. Adjusting for body weight only produced rate constants for growth similar to those from adjusting for pairs and weight. Rates of development were approximately 33% per month for nitrogen, dry fat-free tissue, and internal surface area of mammary glands, and approximately 25% for parenchyma weight and deoxyribonucleic acid. Average rate of increase in total udder weight was only about .5 that for mammary glands only.

Serum thyrotropin, thyroxine, and tri-iodothyronine in dairy cows fed varying amounts of iodine.

The objective was to determine whether dairy cows fed supplemental iodine daily at 2.5 or 5.0 mg per kg body weight for 49 wk had altered thyroid status relative to controls fed no supplemental iodine. Average daily dose of iodine was 1.6 and 3.3 g. Iodine as ethylene diamine dihydriodide was fed to Holstein cows beginning at 8 to 10 wk of lactation, for the remainder of that lactation, through the dry period, and into the next lactation. On day 341 after onset of iodine feeding, each cow was injected intravenously with 15 microgram thyrotropin releasing hormone per 100 kg body weight. Thyrotropin in jugular blood collected before injection of releasing hormone averaged 7.6, 6.1, and 8.2 ng/ml for cows given 0, 2.5, and 5.0 mg iodine/kg body weight; there were no differences between means. Releasing hormone increased thyrotropin, thyroxine, and tri-iodothyronine in serum of all cows, but increases were not affected by quantity of dietary iodine.

Iodine absorption, excretion, recycling, and tissue distribution in the dairy cow.

Research on iodine metabolism was reviewed with special reference to cattle and milk secretion. Iodine metabolism in the fetus and thyroid activity as related to milk secretion and iodine feeding have also been considered. Between 70 and 90% of dietary iodine is absorbed directly from the bovine rumen, reticulum, and omasum. In the abomasum, rate of iodide secretion is approximately 18 times the rate of absorption. Circulating thyroxine is not secreted into the abomasum but enters the small intestine in the bile. Most of the iodide secreted into the abomasum is reabsorbed from the small and large intestines; absorption of thyroxine averages less than 10%. The thyroid usually contains an amount of iodine equal to the daily dietary intake; extrathyroidal tissues concentrate only .006 to .04% as much radioiodine per unit weight as the thyroid. At normal iodine intake (less than 10 mug/kg body weight daily), iodine losses average 30% of the daily intake in feces, 40% in urine, and 8% in milk. Milk iodine is influenced by amount and chemical form of dietary iodine, stage of lactation or milk yield, seasonal effects, goitrogens, and thyroid status. Cows secrete less iodine into milk than most other species and have an efficient iodine recycling system via the gastrointestinal tract which conserves iodine and can protect them against low dietary iodine.

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.

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.