Impaired glucose tolerance(IGT) occurs in 40-60% of individuals with CF. The standard approach to describe IGT has not included simultaneous height and weight ages, skin fold thickness, ponderal index,%FVC and glycosylated hemoglobin(HbAIc)in CF. We employed these parameters in addition to standard oral glucose tolerance testing as an aid in identification of IGT in 18 fasted calorically prepared,sweat chloride proven CF patients with a x̄ age of 17 yrs. IGT was defined as fasting glucose(G)<140mg/dl and 2°G>140mg/dl. G was done by glucose oxidase,insulin(I)by radioimmunoassay,dialyzed HbAIc by mini-column and fetal Hb by alkaline denaturation. No anthropometric data correlated with IGT. %FVC correlated with HbAIc(r=-.47p<.05).Fetal Hb levels were normal. Anthropometrics did not identify IGT.↓%FVC correlates with ↑HbAIc p<.05. Fasting dialyzed HbAIc was a useful adjunct in dx of IGT in CF p<.005.↓%FVC and/or ↑HbAIc merits investigation for IGT. Full significance of IGT in CF remains to be established.

Blood was drawn from 10 fasted, healthy volunteers and stored under standard blood bank conditions in citrate-phosphate-dextrose-adenine (CPDA-1). Blood was sampled before storage (Day 0) and on Days 5, 12, 19, 26, and 35. Laboratory testing for glucose, HbAla + b, HbAlc, pyruvic acid, lactic acid, adenosine triphosphate (ATP), 2, 3-diphosphoglycerate (2,3DPG), plasma free hemoglobin (Hb) and pH (blood gases) were performed. In addition, P50 was also serially measured in two of the individuals and in their stored blood. Significant elevations of HbAla + b and HbAlc (fast hemoglobins) were found on Days 12 and 19 of storage (p less than 0.05). These elevations of fast hemoglobins are due to hypoxia, acidosis, and hyperglycemia. Following the initial elevation of the fast hemoglobins (Hbs), there was a decline in their concentration, from Day 12, which could partly be explained by cell death.

Stressors, such as hypoxia and asphyxia induce CA secretion by the newborn's adrenal medulla. The effect of cold-stress upon adrenal CA content in the neonatal rat was assessed by exposing day old fed rat pups to either control temperature (25°C) or cold-stress (4°C) for 5 mins. The pups were dispatched and adrenal glands were immediately processed for measurement of norepinephrine (NE), epinephrine (EPI) and dopamine (DA) using high performance liquid chromatography and electrochemical detection.There was a significant depletion of both NE and EPI with a significant increase in DA(p<0.05). The cold-stress used produces neither hypoxia nor respiratory acidosis (Barlow & Santulli, Surgery 77: 687-690,1975). The decreased adrenal CA content is then a direct response of the animal to the cold-stress. In conclusion, cold-stress,like hypoxia and/or asphyxia, depletes adrenal EPI and NE in the day old fed pup. The elevated DA suggests a compensatory CA synthesis in response to cold-stress. Full characterization of the CA response needs to be established.

The tocolytic agent R is used to prevent premature labor by direct effects (β-agonist) upon uterine smooth muscle. The pharmacology of R is much like the CA epinephrine(EPI)in its metabolic effects. Since R is EPI-like,the effects on pup adrenal CA content was investigated by delivering to the Dam pharmacologic R (13.8 mg/M2/hr),by subcutaneous osmotic mini-pump on days 15-21 gestation. Control Dams were identical to R treated except pumps contained saline. On day 21 pups were taken by C-section and adrenals were immediately processed for CA analysis by high perform ance liquid chromatography with electrochemical detection. The EPI was significantly reduced (↓28%) in the R treated group; no effects were seen in dopamine(DA)or norepinephrine(NE)content.The decreased adrenal EPI content is most likely due to either displacement of EPI by R and/or an inhibition of EPI synthesis. The mechanism and ramifications of R's effect on pup adrenal EPI content remain to be established.