Effects of sources and amounts of potassium on feed palatability and on potassium toxicity in dairy calves.
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Biomedical subjects
Publications and source records attributed to W J Miller.
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Calves were fed a corn-skim milk or a purified diet to determine if the large differences in manganese metabolism in rats fed such diets also occurred in ruminating calves. The calf purified diet was similar to the rat purified diet but with potassium bicarbonate and sodium bicarbonate added as buffers to be suitable for ruminating calves. In contrast to the huge differences in rats, retention of manganese-54 was the same in calves fed the corn-skim milk diet as in calves fed the purified diet. It is unlikely that the minor differences in the diets caused such large differences in effects between calves and rats. A likely reason for the difference is the functional rumen in the calf. The active rumen may metabolize ingredient(s) that affect manganese absorption in the rat and, therefore, would not be in the small intestine to affect absorption by the calf.
Control (.5% chloride) or low-chloride (.038% chloride) practical diets and low-chloride (.00038% chloride) well water were fed to male Holstein calves for 7 wk. Substantial alterations in characteristics of blood associated with acid-base balance developed in those fed the low-chloride diet. Along with reduced potassium in plasma, concentrations of chloride in synovial fluid, saliva, and plasma also were reduced. Solids in plasma, blood pH, packed cell volume, carbon dioxide pressure (PCO2) in blood, and bicarbonate were increased. Most of the changes in plasma occurred within 1 wk with little change thereafter, indicating an adaptation by the calves to the low-chloride diet. The adaptation by the low-chloride calves was primarily due to a tremendous reduction in urinary chloride excretion. Change in blood factors was insufficient to cause severe alkalosis in calves. The low-chloride diet had no significant effect on sodium absorption, retention, or distribution in body fluids. Potassium in plasma and aqueous humor were reduced in calves fed the low-chloride diet, but potassium concentrations in other body fluid were not affected significantly.
Fifteen male Holstein calves were fed diets containing .25 (control), .7, or 1.15% magnesium (from supplemental magnesium oxide) for 28 days. Feed consumption and growth rate were not affected adversely by .7% magnesium but were depressed with 1.15% magnesium. Fecal dry matter percentage was reduced slightly with .7% magnesium and substantially decreased with 1.15% magnesium. However, feces from calves fed .7% magnesium were more fluid in consistency. Urinary and fecal magnesium content increased in calves fed .7 and 1.15% magnesium, with changes closely related to dietary magnesium. Magnesium in plasma increased slightly with .7% magnesium and materially with 1.15%. Magnesium in liver, kidney, and heart was not affected by diets. Apparently calves can tolerate safely .7% magnesium, but 1.15% is detrimental. On day 21 of treatment, all calves received zinc-65 orally and were killed 7 days later. Calves fed .7 and 1.15% magnesium excreted less zinc-65 and retained more, especially in liver and large intestine. Liver and kidney of calves receiving higher percents magnesium had elevated stable zinc. Calcium and copper in tissue were not elevated. The effect of high dietary magnesium on zinc metabolism appears to be systemic in tissues.
Raw milk from goats and cows (bovine) was combined with sodium selenite (.5 muCi/10 ml milk) and incubated at 39 C to allow selenium binding to milk components. After incubation intervals between .5 and 24 h, samples were separated into cream, whey, and casein fractions by centrifugation and acid precipitation. When samples were incubated up to 6 h, the aqueous whey fraction contained the highest amounts of radioactivity, the casein substantially less, and the cream contained little senenium-75. Twenty-four hours of incubation at 39 C caused the samples to curdle, resulting in a major shift of radioactivity from the aqueous phase to the acid precipitable (casein) fraction. This shift occurred in all curdled samples irrespective of time or temperature of incubation. Acidifying milk samples with lactic acid in the presence of a bacterial inhibitor also increased selenium binding by the casein fraction. Samples of whey fractions were applied to a Sephadex gel filtration column for further separation. Most of the selenium-75 was recovered in low molecular weight fractions. Radioaactive selenium appeared to remain largely in the unbound ionic form when added to noncurdled goats' or cows' milk. Most of the selenite added to milk does not combine with proteins at normal pH but increasingly does so as pH falls below 6.0.
A method was developed by which radioactive manganese, manganese-54 carbonate (with a high specific activity), could be produced. This was accomplished by reacting manganese-54 chloride, manganese chloride tetrahydrate, and sodium bicarbonate. This reaction produced manganese-54 carbonate (specific activity .35 mCi/mg manganese mixed with stable manganese. The purity of the manganese carbonate (manganese-54 carbonate) was determined by the use of x-ray diffraction methods. One method compared "d" spacings (distance in angstroms between lattice planes of a crystal) with standard and index values for pure manganese carbonate. Another method compared x-ray diffractograms of the synthesized product with standard manganese carbonate. By both methods all material was the carbonate form of manganese (manganese-54 carbonate).
Young dairy calves were fed diets containing 40 or 640 ppm zinc with 0 or 5 ppm aflatoxin for 3 wk. The aflatoxin mixture contained 80.5% B1, 19.5% G1, and less than .1% B2 and G2. The aflatoxin-fed calves exhibited characteristic signs of aflatoxicosis which included reduced feed intake, weight gains, nitrogen balance, pulse rate, and respiration rate. Feed intake and weight gains recovered some during the 3rd wk. No gross abnormalities were observed in the liver or other organs at autopsy. Addition of 600 ppm zinc to diets containing aflatoxin did not alleviate the toxic conditions. Effects of aflatoxin or zinc metabolism were investigated during the 3rd week of treatment through oral dosing of zinc-65. Absorption of zinc-65 was slightly lower in aflatoxin-fed calves. However, the aflatoxin effect on absorption of zinc-65 was less than that of high dietary zinc. Retention of zinc-65 in small intestinal tissue was increased in aflatoxin-fed calves, but concentrations in other tissues were not affected. Stable zinc was reduced in liver and increased in kidney and three sections of the small intestine. Further research is needed to define more clearly the relationship of zinc to aflatoxin in dairy calves.
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Potassium chloride and sodium chloride were infused into the reticulorumen of male Holstein calves, approximately 6 mo of age and 260 kg, at .29, .58, 1.15, 1.73, 2.31, or 2.88 g potassium per kilogram body weight or 1.35, 2.12, or 2.16 g sodium per kilogram in equal volumes of water. Paired controls were infused with water. Calves were monitored for physiological changes for 6 h at 15, 30, or 60-min intervals. Potassium and total solids of plasma and packed cell volume were increased at potassium doses greater than .29 g of potassium per kilogram body weight within 1 h after dosing. At the higher doses of potassium, sodium content of plasma increased about 1 h after the increase in plasma potassium. Respiration rates within a potassium treatment varied with respect to time after dosing, but generally they increased, and associated variables of carbon dioxide pressure, pH, and bicarbonate in blood were decreased accordingly. Clinical toxicity signs, including excess salivation, muscular tremors of legs, and excitability were observed with potassium doses greater than .58 g of potassium per kilogram body weight. Three of five calves given 1.73 g of potassium per kilogram, three of four calves given 2.31 g of potassium per kilogram, and one calf given 2.88 g of potassium per kilogram body weight died. With a small number of calves, oral sodium infusions increased plasma sodium in proportion to the dose, but plasma potassium remained relatively constant. Sodium infusions of 2.12 and 2.16 g of sodium per kilogram body weight were fatal.
Young male Holstein calves were fed either a control (.5% chloride) or a low-chloride (.038% chloride) practical diet for 7 wk. Both groups received low-chloride (.00038% chloride) well water. Feeding the low-chloride diet did not produce definite clinical symptoms of chloride deficiency. Neither body weight gains, feed intake, feed digestibility, nor body retention of chloride, sodium, potassium, or nitrogen were effected adversely. Although the chloride intake of the low-chloride calves was only one-sixteenth that of controls, body chloride retention was similar for the two groups. The similar retention of body chloride was due to effective homeostatic mechanisms in which urinary chloride excretion was reduced by 95% in the low-chloride calves. Low-chloride calves consumed more water and excreted more urine than control calves. Although the exact minimum chloride requirement for growth in calves was not established, .038% chloride was adequate for normal growth for the 7 wk.
Holstein bull calves were fed 1, 2, and 4% supplemental magnesium as magnesium oxide. The control diet contained .3% magnesium and consisted of ground corn, soybean meal, cottonseed hulls plus mineral, vitamin, and antibiotic supplements. Diarrhea was the most obvious effect of high intake of magnesium. The extent and intensity of the diarrhea was related closely to the dietary magnesium content. High (2 and 4%) magnesium reduced feed consumption and weight gains. Although there were traces of blood in feces, no abnormalities were observed at autopsy. Large tubular sections of mucus were voided in the feces with a greater prevalance among calves fed 2 and 4% supplemental magnesium. Magnesium in plasma rose sharply in response to the increased intake of magnesium. In calves receiving the 4% added magnesium, the plasma values were triple those of controls. When high magnesium was fed, magnesium increased much more in urine than in plasma. Within 1 wk after calves were returned to control diet, magnesium in urine and plasma declined to control.
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A satisfactory animal model has been found for laboratory studies of human hepatitis A-namely, the white-moustached marmoset (Saguinus mystax). With this species it has been possible to perform serum-neutralization tests and to develop immune-adherence and complement-fixation tests demonstrating antigen and antibody to the virus. The recent work in marmosets has also led to determination of the agent's characteristics: it most closely resembles the enteroviruses of the picornavirus family. These advances open the way for development of a routine serologic test for diagnosis of the disease, of a human immune globulin for general use that would be precisely standardized for hepatitis A antibody, and, ultimately, of a vaccine. They also provide bases for epidemiologic studies that could reveal nonspecific measures for the disease's control. In addition, there is indication that marmosets could be used for safety control of the hepatitis B vaccine that has already been developed. An adequate supply of S. mystax-threatened by recent embargoes on their exportation-is essential to continuation of this work. The question of marmoset supply, both in the short term and over the long range, deserves serious review.
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The zinc homeostatic control breakdown in cattle fed a high but nontoxic amount of zinc was investigated. Liver copper was decreased by the 600 ppm added dietary zinc indicating altered copper metabolism. However, duodenal copper, liver and duodenal iron and manganese were not affected. Zinc-65 in blood was reduced 90% by the high dietary zinc 48 h following oral zinc-65 dosing. The 600 ppm supplemental zinc increased zinc by 500% in liver, 20 times in pancreas and kidney, and 100% in the duodenum. The increased liver and duodenal zinc was confined largely to the soluble cell fraction. This concentrating of excess tissue zinc in the soluble fraction may be an adaptive mechanism which detoxifies large quantities of zinc and prevents disruption of normal cellular activity.
Zinc-65 was injected directly into various sites throughout the small intestine of Holstein calves fed a low zinc diet. Zinc absorption was determined by comparing zinc-65 content of blood, liver, kidney, lung, heart, pancreas, rib, muscle, and other tissues. Tissue zinc-65 was plotted against site of injection expressed as percentage of intestinal length from proximal to distal ends. Zinc absorption occurred throughout the small intestine with the amount absorbed per centimeter of length about equal throughout the small intestine. This is in contrast to conclusions from studies of rats indicating more absorption in the proximal part of the small intestine. The difference appears to have been due to artifacts in the procedures with rats. However, species and dietary differences may have affected relative findings between this and earlier work.