Summary
In horses with hepatic necrosis, lipidosis, neoplasia and cirrhosis, progression of the disease was studied by serial measurements of total serum bile acid concentrations and of plasma glutamate dehydrogenase (GD) and γ glutamyl transferase (γGT) and by liver biopsy. Plasma ammonia concentrations were significantly elevated compared to clinically normal horses, but such changes were not always accompanied by a decline in plasma urea concentration. A fall in plasma glucose concentration carried a guarded prognosis. These were all invaluable aids in early diagnosis and throughout the disease course. The study suggests that other factors, such as hypokalaemia, alkalosis, short chain volatile fatty acids, false and true neurotransmitters, may be important in the pathogenesis of hepatic coma in the horse.
There is a paucity of information on the metabolic effects of undernutrition of the ewe carrying multiple fetuses in late pregnancy. In the present study the effects of induction of ketosis from 132 d gestation in ewes carrying twin fetuses were compared with a control group. The ewes were well fed up to 132 d. Ketotic ewes showed a loss of condition score from 3.7 (SE 0.11) at 130 d gestation to 3.0 (SE 0.15) 10 d later after clinical recovery, compared with control twin-pregnant ewes (P < 0-01). The weight loss during the same time period was from 706 (SE 2.7) kg at 130 d to 64.2 (SE 2.7) kg at 140 d gestation. As expected, both groups lost weight and condition score in the first 28 d of lactation. Induction of ketosis caused a significant shortening of the gestation period to 142.8 (SE 0.7) d compared with 150 (SE 0.4) d in normal twin-pregnant ewes (P < 0.001). Ewes with induced ketosis recovered clinically and showed a normal feed intake by 3.4 (SE 007) d; three required treatment. Induction of ketosis resulted in reduction of hepatic uptake of bromosulphthalein (P < 001) and its biliary excretion (P c 0.05), metabolic clearance rate (P < 0.001), fractional clearance (P c 0.001) and 15 and 30 min retention compared with control twin-pregnant ewes. Most values had returned to normal by the first week of lactation. It is thought that in human pregnancy similar changes in bromosulphthalein clearance may be related to reduced binding sites for bromosulphthalein in the liver caused by increased circulating oestrogens.Induction of ketosis resulted in a significant hypoglycaemic (P c O-Ol), ketotic (P < 0.001) state compared with well-fed twin-pregnant ewes. These changes could be correlated with the severity of the clinical signs, together with a significant rise in plasma urea (P c 0.001) and NH, (P i 0.05) concentrations. Again, the return of most of these values to normal by the first week of lactation lends support to the reversibility of hepatic lesions caused by fatty infiltration of the liver. The seventy of this condition in naturally occurring cases suggests that factors other than undernutrition may be contributory, such as the general body condition of the ewe and glucose metabolism by the liver, including the conversion of propionate to glucose.
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