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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute laminitis-hypertension was produced by carbohydrate overloading of the gastrointestinal tract in 12 adult horses. Obel grade 3 (OG3) lameness developed 40 hours (+/- 3.5, SEM) after overfeeding. At OG3 lameness, mean plasma volume was significantly decreased (P less than 0.005) when compared with base-line values. Before OG3 lameness, transient decreases in serum phosphorus and calcium were recorded. Mild hyponatremia also developed before OG3 lameness and persisted. After establishment of OG3 lameness, persistent hypokalemia and increased plasma aldosterone concentration occurred coincidently. Transient increase in plasma hydrocortisone (cortisol) and renin activity and transient hypochloremia were also recorded during the syndromal phase. Changes in plasma volume and serum electrolytes are discussed and related to the pathogenesis of acute equine laminitis. The alterations in plasma renin activity and aldosterone concentration were interpreted as homeostatic adjustments to fluid and electrolyte imbalances. Differences between the horse and pony during onset of experimental alimentary laminitis are also discussed.
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PMID:Plasma volume, electrolyte, and endocrine changes during onset of laminitis hypertension in horses. 675 27

Nine adult female sheep were each surgically fitted with an Ivan and Johnston reentrant cannula in the cranial part of the duodenum just distal to the pylorus. By diversion (loss) of abomasal outflow, this model has been shown to consistently induce hypochloremic, hypokalemic metabolic alkalosis, accompanied by hyponatremia and dehydration. Each sheep was subjected to 3 treatment trials, each preceded by a 24-hour prediversion period, and a diversion period during which a syndrome of hypochloremia (68 +/- 2 mEq/L), hypokalemia, hyponatremia, and metabolic alkalosis was induced. Development of this syndrome was attributable to losses of large amounts of acid and electrolytes in the abomasal effluent. Mean total electrolyte contents of the effluent were: Cl-, 650 +/- 27 mEq; Na+, 388 +/- 23 mEq; and K+, 123 +/- 12 mEq, with total volume loss ranging from 3.6 to 10.0 L of gastric contents and pH ranging from 3 to 5. Decreases in plasma electrolyte concentrations also can be attributed to decreased intake, because anorexia developed shortly after the onset of diversion. Electrolyte losses in urine during diversion were minimal for Cl- (mean +/- SEM, 12.0 +/- 5.1 mEq), but were greater for Na+ (124.2 +/- 14.5 mEq) and K+ (185.1 +/- 31.2 mEq). Treatments consisted of 0.9% NaCl (300 mosm/L), 3.6% NaCl (1,200 mosm/L), and 7.2% NaCl (2,400 mosm/L) administered over a 2-hour period, with the administered volume determined by the estimated total extracellular fluid Cl- deficit. Significant difference was not found among treatments, with all solutions resulting in return of clinicopathologic and physical variables to prediversion values within 12 hours of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of 0.9, 3.6, and 7.2% NaCl for correction of experimentally induced hypochloremic, hypokalemic metabolic alkalosis in sheep. 836 15