Ammonia Toxicity in Cattle. I. Rumen and Blood Changes Associated with Toxicity and Treatment Methods2

Bartley, E.E.; Davidovich, A.; Barr, G. W.; Griffel, G. W.; Dayton, A. D.; Deyoe, C. W.; Bechtle, R. M.

doi:10.2527/jas1976.434835x

Cited by 89 publications

(62 citation statements)

References 6 publications

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“…It was observed that intensity and duration of symptoms in the buffalo calves appeared to be longer though with delayed onset as compared to other species of animals which is similar to the observations of Dave (1980). The degree of manifestation of clinical symptoms in the present study was related to the concentration of ammonia in the rumen as well as blood which is similar to the observations of Bartley et al (1976) and Da vidovich et al (1977). The findings of Chalupa (1968) that the difference in the duration of the clinical symptoms might be related to the difference in the blood ammonia levels attained at each stage of the disease also confirms the present observations.…”

Section: Resultssupporting

confidence: 92%

“…Animals were not responding to external stimuli ending with their death at this stage. These clinical findings are similar to those reported by Chalupa 1968;Bartley et al 1976;Davidson et al 1977 andChoudhuri et al 1981. It was observed that intensity and duration of symptoms in the buffalo calves appeared to be longer though with delayed onset as compared to other species of animals which is similar to the observations of Dave (1980).…”

Section: Resultssupporting

confidence: 92%

“…Though clinico--biochemical and pathological studies have been conducted in cattle (Oltjen et al 1963;Morris and Payne, 1970;Bartley et al 1976;Davidovich et al 1977 andSethuraman andRathor 1979) but no systematic information is available on the effect of urea-induced ammonia intoxication on hepatic, renal and cardiovascular systems in buffaloes as well as in cattle. Hence the present study was undertaken to investigate and correlate physiological, biochemical and histopathological alterations in experimentally urea-induced rumen alkalosis in buffalo calves.…”

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confidence: 99%

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Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

Randhawa¹,

Dhaliwal²,

Gupta³

et al. 1989

Acta Vet. Brno

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Randhawa S. S., P. S. Dhaliwal, P. P. Gupta, A. K. Ahuja, S. S. R a th 0 r : Studies on Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves. Acta vet. Brno, 58, 1989: 225-243. Peracute rumen alkalosis was induced by intraruminal administration of urea @ 1.25 g/kg. b. wt. as a single dose in six healthy male Murrah buffalo calves of about 1 -2 years age. Peracute ammonia toxicity resulted in profuse salivation, ruminal stress, incoordination, recumbency followed by clonic convulsions, frequency of which increased with the progression of the condition, dyspnea, hyperpnea, tachycardia, opisthotonus, pupillary dilatation followed by death of the animals between 60-150 mts. It was observed that a linear relationship exists between death time and body weight of the calf with the same dose rate. Electrocardiographic studies revealed ventricular fibrillation with superimposition of P wave over T wave. The cardiac potentials gave rise to random osci11ations. Studies on liver function tests revealed that ammonia toxicity markedly affects the functional status of the liver as indicated by increase in serum enzymatic activities of arginase, glutamic oxalotransaminase, glutamic pyruvic transaminase, lactate dehydrogenase and glutamate dehydrogenase with increase in the half life of B.S.P. excretion rate which was subsequently confirmed by histopathological observations. Histopathological changes in the digestive system revealed exfoliation of the epithelial lining of the mucous membrane of the rumen, lymphocytic abomasitis, and necrotic enteritis. Other significant histopathological alterations were follicular cholecystitis, meningo-encephalitis, lymphocytic nephritis and cystitis, and alveolar emphysema. Intoxication, ECG, rumen liquor, blood, urineSudden changes in the dietary constituents with consumption of excess amounts of protein-rich concentrates and/or non-protein nitrogenous compounds has resulted in frequent occurrence of rumen alkalosis in ruminants. The disease is characterised by excessive production of ammonia in the rumen which may produce gastrointestinal, hepatic, renal, circulatory and nervous disturbances (Chalupa 1968; Parkins et aI.

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Section: Resultssupporting

confidence: 92%

Section: Resultssupporting

confidence: 92%

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confidence: 99%

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Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

Randhawa¹,

Dhaliwal²,

Gupta³

et al. 1989

Acta Vet. Brno

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“…Plasma ammonia levels typically associated with clinical ammonia toxicity range between 500 and 800 mmol/l (Bartley et al, 1976;Symonds et al, 1981), well in excess of the peak values recorded here at approximately 50 mmol/l. Ammonia produced in the rumen that is in excess of microbial requirement may be absorbed across the ruminal epithelium and converted to urea in the liver (Lobley et al, 1995), with the liver having the ability to remove ammonia added to the portal blood up to a maximum of 182 mg/min before peripheral blood concentrations increase (Symonds et al, 1981).…”

Section: Discussioncontrasting

confidence: 41%

“…Rumen bacteria can, depending on the diet, derive between 40% to 95% of their N from ammonia, the balance being from peptides and amino acids (Nolan, 1993). There is, however, a reluctance to include urea in the diet of high-producing dairy cows due to the potential negative effects of high plasma ammonia and/or urea levels on intake and fertility, or even death by ammonia toxicity if it is inappropriately mixed with the rest of the ration or included at too high a level -E-mail: lsinclair@harper-adams.ac.uk (Bartley et al, 1976). This has lead to the development of several methods aimed at reducing the rate of urea-N release in the rumen that include calcium chloride-bound urea, biuret, isobutylidene diurea, acetyl urea, tung-and linseed-oil-coated urea, formaldehyde treated urea and natural zeolite.…”

Section: Introductionmentioning

confidence: 99%

The partial replacement of soyabean meal and rapeseed meal with feed grade urea or a slow-release urea and its effect on the performance, metabolism and digestibility in dairy cows

Sinclair

Blake

Griffin

et al. 2012

Animal

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The objectives of the study were to determine the effect of the partial replacement of soyabean meal and rapeseed meal with feed grade urea or a slow-release urea on the performance, metabolism and whole-tract digestibility in mid-lactation dairy cows. Forty-two Holstein-Friesian dairy cows were allocated to one of three dietary treatments in each of three periods of 5 weeks duration in a Latin square design. Control (C) cows were offered a total mixed ration based on grass and maize silages and straight feeds that included 93 g/kg dry matter (DM) soyabean meal and 61 g/kg DM rapeseed meal. Cows that received either of the other two treatments were offered the same basal ration with the replacement of 28 g/kg DM soyabean and 19 g/kg DM rapeseed meal with either 5 g/kg DM feed grade urea (U) or 5.5 g/kg DM of the slow-release urea (S; Optigen R ; Alltech Inc., Kentucky, USA), with the content of maize silage increasing. There was no effect (P . 0.05) of dietary treatment on DM intake, which averaged 22.5 kg/day. Similarly, there was no effect (P . 0.05) of treatment on daily milk or milk fat yield but there was a trend (P 5 0.09) for cows offered either of the diets containing urea to have a higher milk fat content (average of 40.1 g/kg for U and S v. 38.9 g/kg for C). Milk true protein concentration and yield were not affected by treatment (P . 0.05). Milk yield from forage and N efficiency (g milk N output/g N intake) were highest (P , 0.01) in cows when offered S and lowest in C, with cows receiving U having intermediate values. Cows offered S also tended to have the highest live weight gain (0.38 kg/day) followed by U (0.23 kg/day) and C (0.01 kg/day; P 5 0.07). Plasma urea concentrations were higher (P , 0.05) at 2 and 4 h post feeding in cows when offered U and lowest in C, with animals receiving S having intermediate values. There was no effect (P . 0.05) of treatment on whole-tract digestibility. In conclusion, the partial replacement of soyabean meal and rapeseed meal with feed grade urea or a slow-release urea can be achieved without affecting milk performance or diet digestibility, with the efficiency of conversion of dietary N into milk being improved when the slow-release urea was fed.

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Nutrition and Metabolic Diseases

Smith

Sherman

2009

Goat Medicine

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Ammonia Toxicity in Cattle. I. Rumen and Blood Changes Associated with Toxicity and Treatment Methods2

Cited by 89 publications

References 6 publications

Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

Studies of Clinico-biochemical and Pathological Changes in the Urea-Induced Acute Rumen Alkalosis in Buffalo Calves

The partial replacement of soyabean meal and rapeseed meal with feed grade urea or a slow-release urea and its effect on the performance, metabolism and digestibility in dairy cows

Nutrition and Metabolic Diseases

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