02707naa a2200397 a 450000100080000000500110000800800410001910000160006024500550007626000090013152017680014065000190190865000220192765000200194965000100196965000150197965000090199465000120200365000100201565000120202565000220203765000100205965000170206965000100208665000120209665000170210865000110212565000120213665300160214865300190216465300180218365300220220165300140222365300190223777300530225615227772025-07-24       1958    bl uuuu     u00u1 u    #d1 aREID, R. L.  aPregnancy toxaemia in ewes.h[electronic resource]  c1958  aAbstract : Some biochemical and physiological aspects of undernutrition, the fetus as a parasite and stress as etiological factors in pregnancy toxaemia of ewes are reviewed. The supply of carbohydrate to the fetus is maintained at the expense of maternal blood glucose, which increases after lambing and when the fetus dies in utero. The role of acetyl coenzyme A is discussed with reference to hyperketonaemia in undernourished pregnant ewes; it is suggested that utilization of glucose by the ewe is depressed. Plasma hydrocortisone concentration increased in ewes showing signs of pregnancy toxaemia. Experiments are described brieflywhich indicate that although fasting alone did not necessarily cause pregnancy toxaemia, fasting coupled with some other form of stress did, but the relative importance of environmental and nutritional stress depends upon the nutritional status of the ewe. The hypothesis is advanced that undernutrition leads to hypoglycaemia, which in turn and when prolonged causes hyperactivity and hypertrophy of the adrenal glands; the weight of the glands may be doubled. When hypertrophy has taken place the response to a sudden stress is greater than normal. The maintenance of sufficiently increased plasma hydrocortisone values during and after stress leads to a depression of utilization of glucose by the tissues. Clinical signs of pregnancy toxaemia will occur only when the depression of glucose utilization is reinforced by the depressing effect of hypoglycaemia per se on utilization of glucose by brain tissue. Clinical signs may occur with normal blood glucose values if depression of hydrocortisone is sufficiently severe. The accuracy and sequence of events of the above hypothesis have yet to be verified experimentally.  aAdrenal glands  aAnimal physiology  aBlood chemistry  aBrain  aCoenzyme A  aEwes  aFasting  aFetus  aLambing  aPregnancy toxemia  aSheep  aObstetrícia  aOvino  aPrenhez  aReprodução  aStress  aToxemia  aBlood sugar  aHydrocortisone  aHypoglycaemia  aNutritional state  aPatologia  aUndernutrition  tAgricultural Reviewgv. 4, n. 2, p. 21-25, 1958.