Gastrointestinal lavage reduces total body water

BACKGROUND: The aim of this study was to measure changes in total body water (TBW) in surgical patients after gastrointestinal lavage. METHODS: In a prospective, controlled study we used bioelectrical impedance to calculate the change in TBW in two groups of general surgical patients in the pre-operative period: the colonic lavage group consisted of patients fasted overnight who received 3 L of gastrointestinal lavage solution (GLS; n = 30), and the control group consisted of patients fasted overnight only (n = 30). Total body water was measured before and after either lavage and fasting (lavage group) or fasting alone (control group). RESULTS: The lavage group had a mean TBW loss of 729 mL +/- s.e. 217 and the control group a mean loss of 84 mL +/- s.e. 93 (P < 0.01 unpaired t-test). CONCLUSIONS: The results suggest that GLS results in a net loss of TBW. Although this fluid loss is modest, it may be important in surgical patients who have minimal cardiovascular reserve.     

Evidence for McKusick''s hypothesis of deficient collagen cross-linking in patients with homocystinuria

Fractionation of the venom of the spider Phoneutria nigriventer revealed that it was a mixture of several neurotoxic peptides. The peptides so far characterized either inhibited or induced neurotransmitter release. These effects were mediated by Ca2+ channels or increasing Na+ permeability through voltage sensitive Na(+)-channels, respectively. The pooled toxic components (fraction P4) showed stimulatory effects on acetylcholine release from brain cortical slices. In addition, a component of the observed effects resembling that of alpha-latrotoxin was identified, which was characterized by the ability to provoke release of acetylcholine (ACh) at low temperature and in a manner independent of extracellular Ca2+ and of voltage sensitive Na(+)-channels.     

N-Methyl-D-aspartate attenuates opioid receptor-mediated G protein activation and this process involves protein kinase C

The effects of N-methyl-D-aspartate (NMDA) on opioid receptor-mediated G protein activation were explored in neuroblastoma X glioma hybrid (NG108-15) cells. Treatment of the cells with NMDA resulted in a remarkable attenuation of [35S]guanosine-5'-O-(3-thio)triphosphate binding stimulated by [D-Pen2,D-Pen5]-enkephalin (DPDPE), a delta-opioid receptor agonist. The effects of NMDA were dose and time dependent with an IC50 value of 5 nM and could be blocked by NMDA receptor antagonists. After NMDA treatment, the DPDPE dose-response curve shifted to the right (EC50 value increased approximately 7-fold, from 6 to 40 nM), and the maximal response induced by DPDPE was reduced by approximately 60%. The effects of NMDA were reversible, and the DPDPE response could recover within 60 min. The functional responses of delta-, mu-, and kappa-opioid receptors in primarily cultured neurons also were attenuated significantly by NMDA treatment. The inhibitory effects of NMDA on opioid receptor-mediated G protein activation could be blocked by coadministration of the protein kinase C (PKC) inhibitors or by elimination of the extracellular Ca2+. Correspondingly, NMDA treatment of NG108 cells significantly elevated cellular PKC activity and stimulated Gialpha2 phosphorylation. Transient transfection into NG108-15 cells of the wild-type Gialpha2 and a mutated Gialpha2 (Ser144Ala) resulted in a 2-fold increase in DPDPE-stimulated G protein activation. The DPDPE responses were greatly inhibited by NMDA treatment in the wild-type Gialpha2-transfected cells but much less affected in the mutant Gialpha2-transfected cells. In summary, NMDA attenuates opioid receptor/G protein coupling, and this process requires activation of PKC.