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A major obstacle in the quest for health care quality improvement is physician acceptance of clinical practice guidelines. Typically objective and autonomous, physicians do not readily "buy-in" to standards that challenge their judgement. In this article, the authors identify the necessary conditions for physician acceptance if not active participation in the development and promulgation of these living documents.

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Many hospitals, disappointed with their quality programs, are starting to ask, "What went wrong?" This article identifies five early warning signs of failing programs--and what to do about them.

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Free fatty acids (FFA) are believed to play a role in the genesis of the fat embolism syndrome (FES). Levels of plasma FFA, glucose, insulin, and the stress hormones cortisol, growth hormone, prolactin, glucagon, and catecholamines were measured on admission to hospital in: a) 14 patients with long bone fractures at risk of developing FES, b) 14 patients with soft-tissue injuries of comparable severity, and c) 20 healthy fasting subjects. The findings were similar in both groups of injured patients and in keeping with the hormonal and substrate responses to the stress of trauma; plasma FFA levels were raised but in neither group was the rise pronounced. Plasma FFA levels of the fracture patients were only moderately higher than the values of the healthy fasting subjects. These findings suggest that mobilized FFA from peripheral adipose tissue are not important in the genesis of the FES, but do not exclude a role for FFA derived mainly from hydrolysis of triglyceride emboli in the lung.

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To assess the possible effect of the calcium antagonists nifedipine and nimodipine on the anterior pituitary responses to thyrotropin releasing hormone (TRH), seven normal males were studied in a double-blind placebo-controlled trial. The rise from basal levels of thyroid stimulating hormone (TSH) and prolactin was similar following the administration of a single therapeutic dose of either of these agents as compared to placebo. Nifedipine and nimodipine do not affect the anterior pituitary release of TSH and prolactin in response to TRH.

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The aim of this study was to assess the acute effects of clonidine, an alpha 2-adrenergic agonist, on hormonal responses to graded exercise in 8 healthy young men. After fasting overnight, each subject was tested on 2 mornings, 1 week apart. On one occasion he was given 200 micrograms clonidine orally and on the other identical placebo tablets, the order being randomized in a double-blind fashion over the 2 days. Thereafter each subject performed 2 successive treadmill runs, equivalent to 60 and 100%, respectively, of maximal aerobic power. Clonidine pretreatment blunted the maximal increase in plasma catecholamines by more than 60% of the control response (p less than 0.01), without significantly altering the rise of plasma cortisol or ACTH. Furthermore, clonidine significantly reduced the exercise-induced maximal rise in plasma glucose, without modifying the slight decline in mean plasma insulin or increase in pancreatic glucagon levels. The drug did not affect the maximal increments in plasma growth hormone or prolactin occurring after exercise. It was concluded that a single dose of clonidine suppressed peripheral sympathetic responses, without altering central (pituitary) alpha-adrenergic-mediated hormonal responses, to short-term exercise in healthy men.

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This study was designed to assess whether transcendental meditation (TM) could influence various endocrine responses in 10 experienced male meditators. Nine matched subjects, uninformed of the TM procedure, acted as controls. Meditators successfully practised their technique for 40 min in the morning while controls relaxed for this period. No significant differences emerged between these 2 groups with respect to carbohydrate metabolism (plasma glucose, insulin and pancreatic glucagon concentrations), pituitary hormones (growth hormone and prolactin) or the 'stress' hormones, cortisol and total catecholamines-although meditators tended to have higher mean catecholamine levels. Plasma free fatty acids were significantly elevated in meditators 40 min after completing the period of TM. No clear evidence was thus obtained that any of the stress, or stress-related, hormones were suppressed during or after meditation in the particular setting examined.

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The aim of this study was to assess whether the potent calcium antagonist nifedipine was capable of modifying the hormonal response to graded exercise in 7 healthy young men. After fasting overnight, each subject came to the laboratory on 2 consecutive mornings. On one day he was given 10 mg of nifedipine sublingually and on the other an identical placebo capsule; the order was randomised in a double-blind fashion over the 2 days. Thereafter each subject performed 2 successive short treadmill runs, equivalent to 60 and 100%, respectively, of maximal aerobic power. While significantly blunting the rise in mean systolic blood pressure and inducing a greater fall in diastolic blood pressure during and after exercise compared with the placebo, nifedipine did not impair the brisk response to pituitary-adrenal hormones (ACTH, cortisol and total catecholamines). Nifedipine also did not modify the effects of short-term exercise in raising mean plasma glucose levels, stimulating pancreatic glucagon secretion and producing a delayed increase in plasma insulin concentrations. Nor did the drug blunt the significant rise of growth hormone and prolactin levels occurring during and after the treadmill run. It was concluded that, apart from inducing significant changes in blood pressure, a single dose of nifedipine does not appear to suppress the counterregulatory hormonal responses to short-term physical activity in healthy men.

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The acute metabolic changes after drinking ethanol have been studied in 11 fasting, healthy, nonobese, medical students, 6 of whom consumed 40 g ethanol diluted with 750 ml of a sugar-free soft drink over 1 h. The other 5 drank the same volume of soft drink alone. Blood levels of ethanol, glucose, immunoreactive insulin and growth hormone were measured over the ensuing 8 h, as well as the plasma concentrations of prolactin, cortisol and triiodothyronine. After ingesting ethanol, the mean plasma glucose concentration declined, but not to hypoglycemic levels (the nadir was 3.9 mmol/l at 6 h), insulin levels fell gradually and the mean growth hormone concentration showed a modest late rise. Other hormones did not change significantly. We conclude that, in the particular setting examined, the oral administration of ethanol does not cause hypoglycemia or other adverse effects on carbohydrate metabolism.

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Alcohol may provoke reactive hypoglycaemia when drunk with a sucrose mixer (gin and tonic) but not in the form of a starch-based beverage. In the present study alcohol-potentiated reactive hypoglycaemia was shown to depend on the nature of the carbohydrate ingested together with the alcohol. When 14 men (9 normal weight and 5 obese) aged between 20 and 50 years consumed a 50 g glucose load together with 50 g ethanol over an hour, their early plasma insulin response was significantly higher and their later fall in plasma glucose significantly lower than after drinking the same amount of a starch solution (maize meal) and alcohol. In four subjects (3 of them non-obese) plasma glucose concentrations dropped below 2.8 mmol/l after drinking the glucose-alcohol solution. Obesity seemed to be associated with features of peripheral insulin resistance. We conclude that the common social custom of drinking alcohol together with a simple sugar mixer should probably be modified.

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Alcohol may provoke reactive hypoglycaemia when drunk with a sucrose mixer ('gin and tonic') but does not do so when taken in the form of a starch-based beverage like sorghum beer. We examined the hypoglycaemic potential of bottled beer (Lion Lager; South African Breweries), which differs from sorghum beer in that it contains less carbohydrate (polysaccharides and simple sugars) and has a higher alcohol content. After an overnight fast 5 Black men each drank 2 litres of Lion Lager over an hour. Over the ensuing 5 hours their plasma insulin, glucose and alcohol concentrations were compared with the responses previously documented before and after consuming the same volume of sorghum beer or a 100 g control carbohydrate solution. Bottled beer elicited a prompt but short-lived rise in plasma insulin (mean +/- SEM, 37 +/- 7 mU/l at 1 hour), which was significantly greater than that produced by sorghum beer but less sustained than after drinking the control carbohydrate solution. After drinking bottled beer plasma glucose levels fell to a mean nadir of 3,6 mmol/l at 2 hours (compared with 5,4 mmol/l for sorghum beer), thereafter slowly returning to the basal value, while a substantial rise in the blood alcohol concentration occurred. We conclude that the development of alcohol-induced reactive hypoglycaemia is largely determined by the nature of the carbohydrate ingested together with alcohol.

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