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- Author or Editor: Ramiro E. Toribio x
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Abstract
Most homeostatic systems in the equine neonate should be functional during the transition from intra- to extrauterine life to ensure survival during this critical period. Endocrine maturation in the equine fetus occurs at different stages, with a majority taking place a few days prior to parturition and continuing after birth. Cortisol and thyroid hormones are good examples of endocrine and tissue interdependency. Cortisol promotes skeletal, respiratory, cardiovascular, thyroid gland, adrenomedullary, and pancreatic differentiation. Thyroid hormones are essential for cardiovascular, respiratory, neurologic, skeletal, adrenal, and pancreatic function. Hormonal imbalances at crucial stages of development or in response to disease can be detrimental to the newborn foal. Other endocrine factors, including growth hormone, glucagon, catecholamines, ghrelin, adipokines (adiponectin, leptin), and incretins, are equally important in energy homeostasis. This review provides information specific to nutrition and endocrine systems involved in energy homeostasis in foals, enhancing our understanding of equine neonatal physiology and pathophysiology and our ability to interpret clinical and laboratory findings, therefore improving therapies and prognosis.
Abstract
OBJECTIVE
To compare the effects of 7.2% hypertonic and 0.9% isotonic saline (sodium chloride) solutions on cardiovascular parameters and plasma arginine vasopressin (AVP) concentrations in healthy, isoflurane-anesthetized horses.
ANIMALS
8 healthy horses.
PROCEDURES
In a prospective, randomized, crossover study, horses were anesthetized with isoflurane twice with a 14-day washout period between anesthetic episodes. While anesthetized, horses received a bolus (4 mL/kg) of 7.2% hypertonic saline solution (HS) or 0.9% isotonic saline solution (IS). Heart rate; systolic, mean, and diastolic arterial blood pressures; and central venous and pulmonary artery pressures were measured every 5 minutes; cardiac output was measured by means of thermodilution every 15 minutes. Systemic vascular resistance (SVR) was calculated. Blood samples were collected before and during anesthesia, and plasma AVP concentrations were determined with a validated ELISA. Data were analyzed with repeated-measures ANOVA and Pearson correlations.
RESULTS
HS caused an increase in systolic (P = .003) and mean (P = .023) arterial blood pressures that lasted for 30 minutes. The SVR was increased (P < .001) for 45 minutes with HS compared with the SVR after IS administration. Mean plasma AVP concentration increased (P = .03) 15 minutes after HS administration, with the increase lasting 90 minutes.
CLINICAL RELEVANCE
A bolus of HS resulted in a clinically relevant increase in blood pressure in healthy, isoflurane-anesthetized horses. This effect was attributed to volume recruitment and an increase in SVR. Administration of HS offers an option for improving arterial blood pressure in anesthetized horses.
Abstract
Objective—To clone and sequence cDNA for equine insulin-responsive glucose transporter (glucose transporter type 4 [GLUT-4]) and determine effects of glycogen-depleting exercise and meal type after exercise on GLUT-4 gene expression in skeletal muscle of horses.
Animals—Muscle biopsy specimens from 7 healthy adult horses.
Procedure—Total RNA was extracted from specimens, and GLUT-4 cDNA was synthesized and sequenced. Horses were exercised on 3 consecutive days. On the third day of exercise, for 8 hours after exercise, horses were either not fed, fed half of daily energy requirements as hay, or fed an isocaloric amount of corn. The GLUT-4 mRNA was determined by use of realtime reverse transcriptase-polymerase chain reaction in muscle biopsy specimens obtained before 3 consecutive days of exercise and within 10 minutes and 4, 8, and 24 hours after the third exercise bout.
Results—A 1,629-bp segment was sequenced, of which 1,530 bp corresponded to the coding region and encoded a protein of 509 amino acids. Expression of GLUT-4 gene increased by 2.3, 4.3, 3.3, and 2.6 times 10 minutes and 4, 8, and 24 hours after exercise, respectively, compared with that prior to exercise. No differences were observed in GLUT-4 gene expression among conditions of feed withholding, corn feeding, and hay feeding during the 8 hours postexercise.
Conclusions and Clinical Relevance—Lack of increase of GLUT-4 gene expression after grain feeding and exercise may explain the apparently slower rate of glycogen synthesis after exercise in horses relative to that of other species. (Am J Vet Res 2005;66:379–385)
Abstract
Objective—To determine effects of experimentally induced hypercalcemia on serum concentrations and urinary excretion of electrolytes, especially ionized magnesium (iMg), in healthy horses.
Animals—21 clinically normal mares.
Procedures—Horses were assigned to 5 experimental protocols (1, hypercalcemia induced with calcium gluconate; 2, hypercalcemia induced with calcium chloride; 3, infusion with dextrose solution; 4, infusion with sodium gluconate; and 5, infusion with saline [0.9% NaCl] solution). Hypercalcemia was induced for 2 hours. Dextrose, sodium gluconate, and saline solution were infused for 2 hours. Blood samples were collected to measure serum concentrations of electrolytes, creatinine, parathyroid hormone, and insulin. Urine samples were collected to determine the fractional excretion of ionized calcium (iCa), iMg, sodium, phosphate, potassium, and chloride.
Results—Hypercalcemia induced by administration of calcium gluconate or calcium chloride decreased serum iMg, potassium, and parathyroid hormone concentrations; increased phosphate concentration; and had no effect on sodium, chloride, and insulin concentrations. Hypercalcemia increased urinary excretion of iCa, iMg, sodium, phosphate, potassium, and chloride; increased urine output; and decreased urine osmolality and specific gravity. Dextrose administration increased serum insulin; decreased iMg, potassium, and phosphate concentrations; and decreased urinary excretion of iMg. Sodium gluconate increased the excretion of iCa, sodium, and potassium.
Conclusions and Clinical Relevance—Hypercalcemia resulted in hypomagnesemia, hypokalemia, and hyperphosphatemia; increased urinary excretion of calcium, magnesium, potassium, sodium, phosphate, and chloride; and induced diuresis. This study has clinical implications because hypercalcemia and excessive administration of calcium have the potential to increase urinary excretion of electrolytes, especially iMg, and induce volume depletion.
Abstract
Objective—To evaluate the diagnostic value of serum concentrations of total magnesium (tMg) and ionized magnesium (iMg), concentrations of magnesium (Mg) in muscle, intracellular Mg (icMg) concentrations, urinary Mg excretion (EMg), Mg clearance (CMg), and fractional clearance of Mg (FCMg) in horses fed diets with Mg content above and below National Research Council recommendations.
Animals—9 young female horses.
Procedures—6 horses were fed a reduced-Mg diet for 29 days followed by an Mg-supplemented diet for 24 days. Control horses (n = 3) were fed grass hay exclusively. Blood, urine, and tissue samples were collected, and an Mg retention test was performed before and after restriction and supplementation of Mg intake. Serum tMg, serum iMg, muscle Mg, icMg, and urine Mg concentrations were measured, and 24-hour EMg, CMg, and FCMg were calculated.
Results—Reductions in urinary 24-hour EMg, CMg, and FCMg were evident after 13 days of feeding a reduced-Mg diet. Serum tMg and iMg concentrations, muscle Mg content, and results of the Mg retention test were not affected by feeding the Mg-deficient diet. Spot urine sample FCMg accurately reflected FCMg calculated from 6- and 24-hour pooled urine samples. Mean ± SD FCtMg of horses eating grass hay was 29 ± 8%, whereas mean FCtMg for horses fed a reduced-Mg diet for 29 days was 6 ± 3%.
Conclusions and Clinical Relevance—The 24-hour EMg was the most sensitive indicator of reduced Mg intake in horses. Spot sample FCMg can be conveniently used to identify horses consuming a diet deficient in Mg. (Am J Vet Res 2004;65:422–430)
Abstract
Objective—To evaluate calcium balance and parathyroid gland function in healthy horses and horses with enterocolitis and compare results of an immunochemiluminometric assay (ICMA) with those of an immunoradiometric assay (IRMA) for determination of serum intact parathyroid hormone (PTH) concentrations in horses.
Animals—64 horses with enterocolitis and 62 healthy horses.
Procedures—Blood and urine samples were collected for determination of serum total calcium, ionized calcium (Ca2+) and magnesium (Mg2+), phosphorus, BUN, total protein, creatinine, albumin, and PTH concentrations, venous blood gases, and fractional urinary clearance of calcium (FCa) and phosphorus (FP). Serum concentrations of PTH were measured in 40 horses by use of both the IRMA and ICMA.
Results—Most (48/64; 75%) horses with enterocolitis had decreased serum total calcium, Ca2+, and Mg2+ concentrations and increased phosphorus concentrations, compared with healthy horses. Serum PTH concentration was increased in most (36/51; 70.6%) horses with hypocalcemia. In addition, FCa was significantly decreased and FP significantly increased in horses with enterocolitis, compared with healthy horses. Results of ICMA were in agreement with results of IRMA.
Conclusions and Clinical Relevance—Enterocolitis in horses is often associated with hypocalcemia; 79.7% of affected horses had ionized hypocalcemia. Because FCa was low, it is unlikely that renal calcium loss was the cause of hypocalcemia. Serum PTH concentrations varied in horses with enterocolitis and concomitant hypocalcemia. However, we believe low PTH concentration in some hypocalcemic horses may be the result of impaired parathyroid gland function. ( Am J Vet Res 2001;62:938–947)
Abstract
Objective—To clone and sequence the cDNA for feline preproparathyroid hormone (preproPTH) and to compare that sequence with other known parathyroid hormone (PTH) sequences.
Sample Population—Parathyroid glands from 1 healthy cat.
Procedure—A cDNA library was constructed in λ phage from feline parathyroid gland mRNA and screened with a radiolabeled canine PTH probe. Positive clones were sequenced, and nucleic acid and deduced amino acid sequences were analyzed and compared with known preproPTH and PTH sequences.
Result—Screening of approximately 2 X 105 recombinant plaques revealed 3 that hybridized with the canine PTH probe; 2 clones comprised the complete sequence for feline preproPTH. Feline preproPTH cDNA consisted of a 63-base pair (bp) 5'-untranslated region (UTR), a 348-bp coding region, and a 326-bp 3'-UTR. The coding region encoded a 115-amino acid peptide. Mature feline PTH consisted of 84 amino acids. Amino acid sequence analysis revealed that feline PTH was > 83% identical to canine, bovine, swine, equine, human, and macaque PTH and 69, 71, and 44% identical to mouse, rat, and chicken PTH, respectively. Within the region responsible for hormonal activity (amino acids 1 to 34), feline PTH was > 79% identical to other mammalian PTH sequences and 64% identical to the chicken sequence.
Conclusions and Clinical Relevance—The amino acid sequence of PTH is conserved among mammalian species. Knowledge of the cDNA sequence for feline PTH may be useful to investigate disturbances of calcium metabolism and alterations in PTH expression in cats. (Am J Vet Res 2002;63:194–197)
