Reference : Ruminal, cardiorespiratory and adrenocortical sequelae of Na2EDTA-induced hypocalcemia i...
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
Life sciences : Anatomy (cytology, histology, embryology...) & physiology
http://hdl.handle.net/2268/57233
Ruminal, cardiorespiratory and adrenocortical sequelae of Na2EDTA-induced hypocalcemia in calves
English
Desmecht, Daniel mailto [Université de Liège - ULg > Département de morphologie et pathologie > Pathologie spéciale et autopsies >]
Linden, Annick mailto [Université de Liège - ULg > Département des maladies infectieuses et parasitaires > Santé et pathologies de la faune sauvage >]
Lekeux, Pierre mailto [Université de Liège - ULg > Département de sciences fonctionnelles > Physiologie - Doyen de la Faculté de Médecine vétérinaire >]
1996
Veterinary Research Communications
Kluwer Academic Publishers
20
47-60
Yes (verified by ORBi)
International
0165-7380
Dordrecht
The Netherlands
[en] Calf ; cortisol ; hypocalcaemia ; pathophysiology ; rumen
[en] A study was undertaken to provide further information on the ruminal, cardiorespiratory and hypothalamo-pituitary-adrenocortical (HPAC) physiological sequelae of hypocalcaemia in dairy calves. The functional picture observed in standing calves experiencing Na2EDTA-induced progressive hypocalcaemia showed a biphasic pattern. During the first phase (Ca2+ varying between 1.20 +/- 0.09 and 0.64 +/- 0.15 mmol/L, mean +/- SD), the animals became dull and lethargic, shifting their weight from one hind limb to the other, with cool extremities and hypersalivation. Their ventilation was slightly increased but their heart rate, thoracoabdominal pressure, pulmonary mechanics, haemoglobin and temperature remained constant. Conversely, their systemic arterial pressure (SAP) and the amplitude of their ruminal contractions (RCA) were severely decreased. During the second phase (Ca2+ < 0.64 +/- 0.15 mmol/L), there was restlessness, tachycardia, hypertension, polycythaemia and, finally, inability to stay upright. It is suggested that the diminished Ca2+ availability caused smooth-muscle and myocardial dysfunctions which could explain the RCA and SAP changes recorded during the first phase, whereas neural and/or humoral sympathetic discharge probably accounted for the reversal in SAP and heart rate when Ca2+ was decreased further. Serum cortisol increased regularly and remained significantly correlated with Ca2+ in each animal. Moreover, regression of delta cortisol/delta Ca2+ on delta Ca2+/delta Na2EDTA was significant (p < or = 0.001). It was concluded that mild asymptomatic hypocalcaemia severely impairs ruminal function, which will progressively worsen the Ca2+ deficit; that the inability to maintain posture in hypocalcaemia is not due to hypotension; and that the higher the HPAC response to hypocalcaemia, the higher the resistance to its effects. An asymptomatic periparturient cow with barely detectable ruminal activity may merit preventive calcium borogluconate therapy. Also, the physiological role of hypotension in explaining the clinical picture may be less important than other processes, such as neuromuscular failure. Finally, the present results imply a possible HPAC exhaustion in cows with periparturient paretic hypocalcaemia
IRSIA Grant 5475A, Brussels, Belgium
Researchers ; Professionals ; Students
http://hdl.handle.net/2268/57233

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