Metabolic acid-base disorders.

Acid-base homeostasis is an important determinant of many physiologic functions. Nowhere is understanding the mechanisms and significance of hydrogen ion (H+) imbalance more important than in critical care management, where patients are threatened with a physiochemical disorder that is often as complex as it is dangerous. Although there may be contentious issues yet unresolved concerning acid-base homeostasis, the incontrovertible fact is that the body at least seems to defend H+ balance as vigorously as it does oxygen transport or perfusion pressure. Equally, there seems to be an important and predictable relation between this balance and other physiochemical variables such as concentrations of other ionic species, carbon dioxide, and plasma proteins. The prudent clinician strives to understand whether or not and how acid-base imbalances are affecting his or her patient and what to do about it.     

Metabolic epidermal necrosis in a dog associated with pancreatic adenocarcinoma, hyperglucagonaemia, hyperinsulinaemia and hypoaminoacidaemia

A case of metabolic epidermal necrosis associated with a pancreatic carcinoma is described. Normoglycaemia, reduced serum fructosamine, and hypoaminoacidaemia were identified. Hyperinsulinaemia and hyperglucagonaemia were documented. Immunohistochemistry documented strong tumour expression of both insulin and glucagon supporting combined paraneoplastic production of both hormones by the tumour. Enteral protein and fatty acid supplementation and parenteral amino acid supplementation proved ineffective. Metastasis to regional lymph nodes was identified and the patient was euthanased.     

Organophosphorus compounds. II. Metabolic considerations

Organophosphorus compounds are esters of alcohols with phosphoric acids or anhydrides of phosphoric acids with some other acids. The most important groups are the phosphates, phosphorothionates, phosphorothioates, phosphoroamidates, phosphorochloridate and phosphonates. The metabolism of phosphorothionates and phosphorothioates involves initial activation (oxidative desulphuration) followed by hydrolysis of the active metabolites. Activation is carried out by the action of microsomal oxidases, and degradation is performed by different types of hepatic and plasma esterases.     

Metabolic hoof horn disease. Claw horn disruption.

Low-quality hoof horn is a frequent underlying cause of lameness in cattle. Because the lesions that are observed are the result of insults that affect horn production at the cellular level, the term claw horn disruption has been proposed to describe the disease process. Although claw horn disruption may result from multiple etiologies, the response of the keratinocytes is relatively nonspecific in that lesions often appear the same regardless of cause. To solve herd problems, the investigation of possible etiologies must be integrated with a basic understanding of the anatomic and physiologic features of hoof horn production.     

Metabolic acidosis: a quick reference.

This article serves as a quick reference for metabolic acidosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.     

Metabolic alkalosis: a quick reference.

This article serves as a quick reference for metabolic alkalosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.     

Metabolic effects of amylin in lactating goats.

The objective of this study was to investigate the role of amylin (a pancreatic hormone) in regulating metabolism in support of lactation. Rat amylin was infused (320 pmol.kg LW(-1).h(-1)) for 6 h via an external pudic (mammary) artery into six lactating goats. This dose of amylin led to a sixfold increase in plasma concentrations of amylin relative to baseline. Amylin infusion increased plasma concentrations (jugular) of glucose and NEFA up to 16 and 168%, respectively, relative to saline infusion. In contrast, plasma concentrations of Ca and PO4 during amylin infusion were reduced by 18 and 30%, respectively, relative to saline infusion. Plasma concentrations of IGF-I, insulin, and Mg were not different between the two treatments, although IGF-I concentrations in the amylin-infused group, 1 and 6 h postinfusion, were significantly higher than those in the saline-infused group. Similarly, amylin infusion failed to affect milk yield and major constituents of milk except protein; milk protein content decreased progressively until the end of amylin infusion and remained low thereafter. Amylin also had no effect on minerals in milk (Ca, PO4, Mg, Fe, Sr, S, K, or Na) except Zn, which was significantly decreased from 56.8+/-5.8 micromol/L at 0 h to 44.5+/-2.4 micromol/L at 6 h postinfusion. Mammary blood flow (measured with a transit-time blood flow probe) increased up to 26% during amylin infusion, although this effect lasted only for the first 3 h. In conclusion, amylin increased plasma concentrations of glucose and NEFA, and mammary blood flow, while decreasing plasma concentrations of Ca and PO4. Despite these metabolic changes, amylin infusion did not increase milk yield of lactating goats.     

Pathophysiological effects of endotoxins in ruminants. 2. Metabolic aspects

Metabolic disturbances following intravenous and intramammary administration of endotoxins in ruminants are described. In contrast to the similarity in response of blood biochemical parameters after intravenous and intramammary administrations of endotoxins, responses in plasma concentrations of enzyme activities, the thyroid hormones, cortisol, and somatotropin differ markedly. Biochemical changes in blood after endotoxin administration are predominantly dose-dependent; thus some of the biochemical parameters - especially plasma concentrations of Fe and Zn - serve also to evaluate the effects of certain drugs in endotoxin models. Changes in milk composition have been documented only after intramammary infusion of endotoxins and can partly be explained by the increased permeability of the blood/milk barrier. Appearance and production of milk returns to normal within a week after intramammary endotoxin treatment, indicating that the mammary gland is only temporarily damaged by endotoxin-induced mastitis.     

Metabolic acid-base disorders in the critical care unit.

The recognition and management of acid-base disorders is a commonplace activity in the critical care unit, and the role of weak and strong acids in the genesis of metabolic acid-base disorders is reviewed. The clinical approach to patients with metabolic alkalosis and metabolic acidosis is discussed in this article.     

Metabolic aspects in the etiology of displaced abomasum.

Results of studies on metabolic variables that exist prior to the diagnosis of displaced abomasum (DA) indicate that subclinical ketosis is a risk factor for DA. Serum aspartate aminotransferase activity, serum and milk betahydroxybutyric acid concentrations, and milk fat-to-protein ratios were often elevated before the diagnosis of DA, and these variables may be used to predict DA. Prevention of subclinical ketosis may prevent DA.     

Metabolic and electrolyte disturbances in acute canine babesiosis.

Arterial blood pH, PCO2, bicarbonate, base excess/deficit, and lactate, as well as serum sodium, potassium, and chloride were measured in clinically normal dogs and in dogs with acute canine babesiosis. Metabolic acidosis developed in dogs with fatal as well as nonfatal Babesia canis infection. In the fatal group, the acidosis was uncompensated; among survivors, base deficit and blood lactate were significantly lower, and pH, PCO2, and bicarbonate values were significantly higher. Serum potassium values were significantly lower, and serum chloride values were significantly higher in dogs with acute babesiosis than in clinically normal dogs. The shock resulting from acute canine babesiosis is best viewed as anemic shock. Treatment should include an alkalizing agent, a blood transfusion, fluid therapy, and a babesicidal drug.     

The equine metabolic syndrome peripheral Cushing's syndrome.

Certain management practices tend to promote the development of obesity (metabolic syndrome) in mature horses as they enter their teenage years. These management practices include the provision of starch-rich (high glycemic index) and fat-supplemented rations to healthy horses that are relatively inactive. Some horse breeds and ponies appear to be genetically predisposed to metabolic syndrome. The accretion of intra-abdominal adiposity by equids is associated with the development of insulin insensitivity (hyperinsulinemia), glucose intolerance, dyslipidemia, hypertension, and insidious-onset laminitis. Omental adipocytes are metabolically active, secreting free fatty acids and hormonally active mediators including cortisol, leptin, and resistin that might contribute to persistence and worsening of insulin refractoriness and the obese phenotype. We have hypothesized that obesity-associated laminitis arises as a consequence of vascular changes and a hypercoagulable state, similar to the development of atherosclerosis in human type 2 diabetes. Several molecular mechanisms that might serve to explain the development of insulin insensitivity as a result of excessive adiposity have been incriminated. Little investigation into the relationship between obesity, insulin insensitivity, and laminitis in horses has been reported to date. Insulin sensitivity and glucose tolerance can be improved by dietary restriction and exercise aimed at reversing omental obesity. Management practices that promote the development of obesity are likely initiated during the first 10 years of the horse's life. Veterinarians and horse owners must recognize that mature-onset obesity in adult horses is associated with a risk for development of laminitis. Obesity and insulin insensitivity might be prevented if horse owners can be educated to feed rations with a relatively lower glycemic index to inactive horses. Investigative research pertaining to the development of antiobesity drugs for human patients is continuing. Greater than 30 new pharmaceuticals are in various stages of research. However, it will likely take many years before any of these drugs are shown to be useful and safe in horses. Lifestyle changes in the form of diet and exercise patterns are still the crux of therapy for both human and equine patients.     

Metabolic responses to ammonium acetate infusion in exercising horses.

The relationship between elevated plasma ammonia (NH3) levels, fatigue development and muscle metabolism were examined in horses during a submaximal fatigue test. Eight Quarter Horse mares were intravenously infused prior to exercise with either sodium acetate (control) or ammonium acetate (AMINF), and exercised to fatigue on an 11% grade treadmill, carrying 27 kg of lead. Time to fatigue was not different (P greater than 0.05) between groups. Intramuscular NH3 and lactate increased (P less than 0.001) during exercise; however, the treatment did not (P greater than 0.05) affect either. A treatment by exercise interaction (P less than 0.01) occurred for plasma NH3. The reciprocal relationship between changes in plasma and intramuscular alanine (ala) and glutamate (glu) indicated activation of the glucose-alanine cycle. Plasma glutamine (gln) increased (P less than 0.001) during exercise; however intramuscular gln was not (P greater than 0.05) altered. The excretion of urea-N was depressed as a result of exercise while the orotic acid/creatinine ratio did not (P greater than 0.05) change. The amino acids and urinary metabolites were not (P greater than 0.05) affected by treatment. These results did not show any metabolic evidence for a role of increased plasma NH3 levels in fatigue development. However this study did provide insight into other aspects of nitrogen metabolism during exercise in the horse.