2008
DOI: 10.1016/j.cveq.2008.03.005
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Clinical Pathology of the Foal

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Cited by 82 publications
(102 citation statements)
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References 60 publications
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“…Conversely, other studies [1] reported that urea and creatinine levels are high at birth, but rapidly decrease to values similar to those reported for adult animals. These variations were not observed in the present study.…”
Section: Discussionsupporting
confidence: 59%
“…Conversely, other studies [1] reported that urea and creatinine levels are high at birth, but rapidly decrease to values similar to those reported for adult animals. These variations were not observed in the present study.…”
Section: Discussionsupporting
confidence: 59%
“…Statistical differences were found between sampling time for MCV, while no differences were observed for MCH and MCHC. It can be hypothesized that the decrease in MCV may be related to a physiological fetal erythrocyte disruption/elimination from the bloodstream and an increase in microcytes production, as occurring in foals (Harvey et al, 1984;1987;Axon and Palmer, 2008).…”
Section: Discussionmentioning
confidence: 99%
“…The K3EDTA samples collected at 24 h of life were processed in the same way. The differential count was used to calculate Neutrophil-Lymphocyte ratio (N/L) in order to verify the maturity of calves, as previously reported in foals (Axon and Palmer, 2008). Calves with N/L >2 were considered mature.…”
Section: Methodsmentioning
confidence: 99%
“…Hospitalized foals with critical disorders such as sepsis, pneumonia, enterocolitis, neonatal encephalopathy (NE), and prematurity/dysmaturity frequently develop acid–base, fluid, electrolyte and plasma protein disturbances 1, 2. Possible mechanisms for these disturbances include reduced perfusion because of hypovolemia and hypotension,3, 4, 5, 6 activation of hormonal mechanisms including the renin angiotensin aldosterone system and vasopressin,7, 8, 9 tubular damage,10, 11 and perturbation of the hypothalamic–pituitary–adrenal axis 12.…”
mentioning
confidence: 99%
“…Possible mechanisms for these disturbances include reduced perfusion because of hypovolemia and hypotension,3, 4, 5, 6 activation of hormonal mechanisms including the renin angiotensin aldosterone system and vasopressin,7, 8, 9 tubular damage,10, 11 and perturbation of the hypothalamic–pituitary–adrenal axis 12. Plasma protein alterations might be caused by increased capillary leakage,12, 13 altered intravascular and tissue albumin distribution, imbalances between albumin synthesis and degradation14, 15 and failure of transfer of passive immunity (FTPI) 2…”
mentioning
confidence: 99%