No abstract

Total parenteral nutrition has been extensively used to feed patients with a variety of gastrointestinal diseases, but little attention has focused on the nutritional requirements of the gut. To investigate intestinal consumption of intravenously administered nutrients, uptake of three principal fuels determined from in vitro studies was quantitated in seven awake, unrestrained dogs. Portal blood flow was measured by a dye dilution technique and, simultaneously, substrate samples were obtained from chronic indwelling arterial and portal venous catheters. Studies were performed during a postabsorptive basal period and during separate infusions of glutamine (0.10 mmol/kg X min), glucose (0.10 mmol/kg X min), and beta-hydroxybutyrate, (0.40 mmol/kg X min). During the basal period there was a significant arterial-portal vein gradient for glucose (144 +/- 26 mumol/liter) and glutamine (49 +/- 11 mumol/liter). These substances were taken up by the gut at rates of 4.11 +/- 1.23 and 1.43 +/- 0.19 mumol/kg X min, respectively. No significant uptake of beta-hydroxybutyrate was determined in the basal studies (0.27 +/- 0.10 mumol/kg X min). During substrate infusion, gut glucose uptake was unchanged (2.68 +/- 1.67 mumol/kg X min, NS), but consumption of glutamine (4.60 +/- 0.66 mumol/kg X min, p less than 0.001) and beta-hydroxybutyrate (4.33 +/- 0.71 mumol/kg X min, p less than 0.001) increased significantly. During parenteral feedings in patients with gastrointestinal disorders, circulating levels of beta-hydroxybutyrate and glutamine are often low, and glutamine is absent from standard amino acid solutions. Current parenteral formulation may not provide appropriate fuels for the gastrointestinal tract.

A new calcium channel blocker, nicardipine, was studied for treatment of Raynaud's phenomenon in a double-blind, placebo-controlled, crossover trial during the winter months. Clinical response was assessed by a patient-kept diary of symptoms and finger systolic pressure that was measured at room temperature and during cold challenge. In vivo platelet activation was determined by measuring plasma levels of the plateletspecific proteins, beta-thromboglobulin and platelet factor 4. When treatment with placebo was compared with treatment with nicardipine, no significant differences were found in the namber of Raynaud's attacks per day, the severity of attacks, change in character in Raynaud's phenomenon, use of hands in winter months, patient assessment of medication or objective measurements of finger systolic pressure, and critical closing temperature. There was a reduction of plasma levels of beta-thromboglobulin and platelet factor 4 in the overall study group while taking nicardipine compared with that during the placebo period (mean change 5.0 f 2.4 ng/ml, P = 0.054, and 1.4 f 0.6 ng/ml, P < 0.01, respectively). These results demonstrate that while nicardipine was not effective in reducing the episodes of Raynaud's phenomenon, it did inhibit in vivo platelet activation. These findings suggest that platelet activation