Induction of fertile oestrus during the anoestrous season in mature lactating and dry ewes is possible with the proper sequence of hormone treatments. Wagner (1964) found 0\m=.\5or 1\m=.\0 mg of 6-chloro-6-dehydro-17\g=a\acetoxyprogesterone (CAP) per head per day in the feed for 16 days and 1000 i.u. pregnant mare's serum gonadotrophin (pmsg) injected 36 hr and 18 days later to be effective in producing fertile matings. The best regimen resulted in 77% of the treated ewes lambing. Hansel (1964) observed that treating lactating Western White-faced ewes with 750 i.u. of pmsg on Days 1 and 15 and feeding 60 mg of 6-methyl-17-acetoxyprogesterone (MAP) daily from Days 7 to 14 resulted in 65% of the treated ewes lambing. Hulet & Foote (1967), testing various combinations of CAP, MAP and pmsg on dry and lactating anoestrous ewes, found CAP and MAP, fed from Days 1 to 14 followed by pmsg injected on Days 15 and 31, resulted in 60% of the treated ewes lambing. However, little work has been done on the induction of fertile oestrus in ewe lambs. Foote & Bennett (1968) induced oestrus in eighty-four ewe lambs at 5 and 8 months of age, using a combination of 1 mg of oestradiol-17\g=b\ on Day 1 followed by daily injections of 12 mg of progesterone for 14 days and 600 i.u. of pmsg 2 days after the last injection of progesterone. Using this treatment, 87% of the ewe lambs at 8 months were in oestrus and ovulated. By 25 days after mating, 60% were pregnant. * Contribution from the Montana Agricultural Experiment Station, Journal Series No. 146.
Background: Hyperglycaemia is a common finding and an independent risk factor for increased morbidity and mortality in aneurysmal subarachnoid haemorrhage (SAH). Although in these patients hyperglycaemia is commonly ascribed to insulin resistance, there is little understanding of underlying mechanisms. Aims: To prospectively study temporal disturbances of glucose metabolism after aneurysmal SAH in patients without known abnormalities of glucose metabolism and to explore possible correlations with markers of stress. Methods: In consecutive aneurysmal SAH patients not subjected to insulin therapy, in-hospital and follow-up oral glucose tolerance tests (OGTTs) and assessments of insulin resistance, pancreatic β-cell function, free fatty acids (FFA) and cortisol were performed and compared with reference values. Results: We included 13 patients. In the first 2 weeks of admission, median fasting glucose and FFA levels were elevated while insulin levels were not. OGTTs were indicative of glucose intolerance in all patients at days 3 and 7, while on follow-up 1 patient had glucose intolerance and all patients had normal fasting glucose levels. Pancreatic β-cell function was impaired throughout the first week and insulin resistance from day 4 to 10. Levels of cortisol correlated with higher fasting glucose and increased FFA. FFA in turn correlated with pancreatic β-cell dysfunction. Conclusions: Aneurysmal SAH patients have transient abnormalities of glucose metabolism. During the first week, it appears to result predominantly from transient pancreatic β-cell dysfunction, in combination with insulin resistance.
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