Ammonia Toxicity in Cattle. II. Changes in Carotid and Jugular Blood Components Associated with Toxicity

Davidovich, A.; Bartley, E.E.; Chapman, T. E.; Bechtle, R. M.; Dayton, A. D.; Frey, R A

doi:10.2527/jas1977.444702x

Cited by 36 publications

(27 citation statements)

References 11 publications

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“…1973; Davidovich et al 1977;Dave 1980 andBlood et al 1983). 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.…”

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confidence: 99%

“…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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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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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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“…0.50). The correlations between blood pH and HCO 3 À concentrations or urine pH were very high (R ! 0.80), correlations between blood pH and L-lactate concentrations were high (R = 0.73), and correlations between blood pH and pCO 2 were low.…”

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confidence: 99%

“…During blood alkalosis, increased filtration of HCO 3 À without modification of proton (H + ) excretion is described, inducing alkaline urine. 17 The decreased urine pH from H 40 (experiment 1) or H 52 (experiment 2) is consistent with acidic urine observed only 96 hours after blood alkalosis induced by duodenal obstruction in cattle.…”

Section: Urine Regulation and Compensationmentioning

confidence: 99%

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Experimental Soybean Meal Intoxication in Cattle

Raboisson

Ferrières

Nicot

et al. 2012

Veterinary Internal Medicne

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Background: Cattle are commonly fed soybean meal (SBM) and accidental intoxication sometimes occurs. Objectives: To describe the biologic and clinical features of SBM intoxication. Animals: Four steers with ruminal cannula. Methods: Controlled experimental trial. SBM was administered once at 1 and 2% of body weight (BW) via cannula at 2-month intervals.Results: This study showed a 2-phase pathogenic course for 2% BW SBM intoxication. The 1st phase (until 10 hours post-administration) is restricted to ruminal modification with volatile fatty acid overproduction and moderate ruminal ammonia concentration. In the 2nd phase (12-22 hours post-administration), ruminal pH returned to initial values and marked ammonia accumulation occurred in blood, inducing severe metabolic alkalosis with hyperglycemia, hyperinsulinemia, and delayed aciduria (30-40 hours post-administration). Among the clinical signs, nervous signs were only observed during the period with increased plasma ammonia concentration. At 1% BW, ruminal and blood modifications were less pronounced than at 2% BW, and clinical signs were not observed.Conclusions and Clinical Relevance: Ammonia accumulation in blood during the second phase is the consequence of continued ammonia production, decreased carbohydrate fermentation, and overwhelming of hepatic detoxifying capacity. Because ammonia accumulation is associated with the clinical signs, treatment of SBM intoxication could be similar to treatment of urea intoxication, including rumenotomy, oral administration of cold water and vinegar, and measurement of ruminal pH.

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Cerebral ammonia metabolism in normal and hyperammonemic rats

Cooper

Lai

1987

Neurochemical Pathology

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Brain ammonia is generated from many enzymatic reactions, including glutaminase, glutamate dehydrogenase, and the purine nucleotide cycle. In contrast, the brain possesses only one major enzyme for the removal of exogenous ammonia, i.e., glutamine synthetase. Thus, following administration of [13N]ammonia to rats [via either the carotid artery or cerebrospinal fluid (csf)], most metabolized label was in glutamine (amide) and little was in glutamate (plus aspartate). Since blood-and csf-borne ammonia are converted to glutamine largely, if not entirely, in the astrocytes, it is not possible from these types of experiments to predict with certainty the metabolic fate of the bulk of endogenously produced ammonia. By comparing the specific activity of L-[13N]glutamate to that of L-[amine-13N]glutamine following intracarotid [13N]ammonia administration it was concluded that metabolic compartmentation is no longer intact in the brains of rats treated with the glutamine synthetase inhibitor L-methionine-SR-sulfoximine (MSO) and that blood and brain ammonia pools mix in such animals. In MSO-treated animals, recovery of label in brain was low (approximately 20% of controls), and of the label remaining, a prominent portion was in glutamine (amide) (despite an 87% decrease in brain glutamine synthetase activity). These data are consistent with the hypothesis that glutamine synthetase is the major enzyme for metabolism of endogenously--as well as exogenously--produced ammonia. The rate of turnover of blood-derived ammonia to glutamine in normal rat brain is extremely rapid (t1/2 less than or equal to 3 s), but is slowed in the brains of chronically (12-14-wk portacaval-shunted) or acutely (urease-treated) hyperammonemic rats (t1/2 less than or equal to 10 s). The slowed turnover rate may be caused by an increased astrocytic ammonia, decreased glutamine synthetase activity, or both. In the hyperammonemic rat brain, glutamine synthetase is still the only important enzyme for the removal of blood-borne ammonia. Hyperammonemia causes an increase in brain lactate/pyruvate ratios and decreases in brain glutamate and brainstem ATP, consistent with an interference with the malate-aspartate shuttle. In vitro, pathological levels of ammonia also inhibit brain alpha-ketoglutarate dehydrogenase complex and, less strongly, pyruvate dehydrogenase complex. The rat brain does not adapt to prolonged hyperammonemia by increasing its glutamine synthetase activity.(ABSTRACT TRUNCATED AT 400 WORDS)

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Ammonia Toxicity in Cattle. II. Changes in Carotid and Jugular Blood Components Associated with Toxicity

Cited by 36 publications

References 11 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

Experimental Soybean Meal Intoxication in Cattle

Cerebral ammonia metabolism in normal and hyperammonemic rats

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