Metabolic and inflammatory responses to pulmonary exacerbation in adults with cystic fibrosis.

BACKGROUND: We hypothesized that increased resting energy expenditure in adults with cystic fibrosis was related to chronic inflammation secondary to pulmonary infection and could be modified by treatment of the underlying infection. METHOD: To determine the relationship between resting energy expenditure and the inflammatory and metabolic responses, we studied 22 adults with cystic fibrosis and chronic Pseudomonas aeruginosa infection before and after treatment of a respiratory exacerbation. Resting energy expenditure was measured by indirect calorimetry. Spirometry and circulating concentrations of C-reactive protein, neutrophil elastase alpha1-antiproteinase complex, catecholamines, non-esterified fatty acids and glycerol were determined. RESULTS: The mean (95% confidence interval)% predicted FEV1 was 28.5% (20.6, 36.4) and mean body weight 50.7 kg (47.4, 54.1). Following treatment, 1-s forced expiratory volume (FEV1) and weight increased, while C-reactive protein (P<0.0001) and neutrophil elastase alpha1-antiproteinase complex concentrations (P<0.0001) were reduced. Resting energy expenditure decreased from 6.8 (6.3, 7.2) to 6.25 (5.9, 6.6) MJ day-1 by day 15 (P<0.001). Changes in resting energy expenditure and C-reactive protein were related (r = 0.66, P< 0.0001). Weight gain was inversely related to resting energy expenditure (r = 0.43, P = 0.02) and unrelated to energy intake (r = 0.02, P = 0.47). Post-treatment reduction in norepinephrine was related to changes in heart rate (r = 0.57, P<0.01), resting energy expenditure (r = 0.51, P = 0.001) and non-esterified fatty acids (r = 0.42, P< 0.05). CONCLUSIONS: A parallel reduction in the host inflammatory and catabolic responses followed treatment of a respiratory exacerbation and may have contributed to weight gain.

An analysis of the susceptibilities of several populations of Rattus norvegicus to warfarin.

An analysis was made of the dose-response of several populations of Rattus norvegicus fed upon baits containing 0.005% warfarin for various numbers of days. Warfarin-susceptible populations fell within a narrow range, with LFP 50s and LFP 98s (lethal feeding periods in days to obtain 50% and 98% mortalities respectively) of up to 3.0 and 5.0 days respectively. The probability of an individual rat from these populations surviving a six-day feeding period was estimated at 0.003 or less. Populations with responses falling beyond these limits were regarded as warfarin-resistant.Six of nine populations of R. norvegicus, from England, Germany and the United States, were determined to be warfarin-susceptible within the narrow limits given above. In all six cases, no animals survived the six-day WHO feeding test for anticoagulant susceptibility. In three populations from the United States, where rats survived six days feeding, their population responses clearly fell outside the measures given above. It is suggested, tentatively, that anticoagulant-resistant Norway rat populations be defined as those whose LFP 50 and LFP 98 exceeds 3.0 and 5.0 days respectively, and in which the probability of an individual animal surviving a six-day feeding upon 0.005% warfarin is 0.01 or more.

Anticoagulant resistance in wild Norway rats in New York.

Wild Norway rats (Rattus norvegicus) from several habitats were tested for their susceptibility and resistance to warfarin. Animals were fed 0.005% warfarin in ground oatmeal for periods varying from 1 to 12 days. Rats having no prior exposure to anticoagulants were shown to be susceptible, none having survived a 6-day feeding period. Resistant rats were found on two farms where anticoagulant materials had been used intensively for about 20 years.