Do We Need a Fluid Bolus? The Necessary Refinement of Pediatric Propofol Sedation - a Quality Improvement Project.

Background: Propofol is commonly used for pediatric MRIs to minimize patient movement. At our institution, intensivists typically administer a prophylactic 20 ml/kg saline bolus to maintain blood pressure (BP) during propofol sedation. This quality improvement project assessed whether a 10 ml/kg and a completely eliminated saline bolus are as effective as the standard 20 ml/kg bolus in completing pediatric propofol sedation and maintaining Mean Arterial Pressure (MAP).

Prescription drug misuse among U.S. active duty military personnel: a secondary analysis of the 2008 DoD survey of health related behaviors.

Objectives: This study identifies predictors of prescription drug misuse among U.S. active duty service members (ADSM).

The involvement of hypothalamic sleep pathways in general anesthesia: testing the hypothesis using the GABAA receptor beta3N265M knock-in mouse.

The GABA(A) receptor has been identified as the single most important target for the intravenous anesthetic propofol. How effects at this receptor are then translated into a loss of consciousness, however, remains a mystery. One possibility is that anesthetics act on natural sleep pathways.

Role of endogenous sleep-wake and analgesic systems in anesthesia.

Classical anesthetics of the gamma-aminobutyric acid type A receptor (GABA(A))-enhancing class (e.g., pentobarbital, chloral hydrate, muscimol, and ethanol) produce analgesia and unconsciousness (sedation).

Gastroenteropancreatic hormones and metabolism in fish.

Metabolism of vertebrates integrates a vast array of systems and processes, including the pursuit and capture of food, feeding and digestion of ingested food, absorption and transport of nutrients, assimilation, partitioning and utilization of energy, and the processing and elimination of wastes. Fish, which are the most diverse group of vertebrates and occupy a wide range of habitats and display numerous life history patterns, have proven to be important models for the study of the structure, biosynthesis, evolution, and function of gastroenteropancreatic (GEP) hormones. Food intake is promoted by galanin, neuropeptide Y, and pancreatic polypeptide (PP), while cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) inhibit food intake.

Insulin and growth hormone stimulate somatostatin receptor (SSTR) expression by inducing transcription of SSTR mRNAs and by upregulating cell surface SSTRs.

This study examined the effects of insulin (INS) and growth hormone (GH) on mRNA and functional expression of somatostatin receptors (SSTRs). Rainbow trout liver was used as a model system to evaluate the direct effects of INS and GH on mRNA expression of three SSTR subtypes characterized previously from this species: SSTR1A, SSTR1B, and SSTR2. INS and GH directly stimulated steady-state levels of all SSTR mRNAs in a concentration- and time-dependent manner; however, the pattern of expression was hormone and SSTR subtype specific.

Regulation of somatostatins and their receptors in fish.

The multifunctional nature of the somatostatin (SS) family of peptides results from a multifaceted signaling system consisting of many forms of SS peptides that bind to a variety of receptor (SSTR) subtypes. Research in fish has contributed important information about the components, function, evolution, and regulation of this system. Somatostatins or mRNAs encoding SSs have been isolated from over 20 species of fish.

The alpha2-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects.

Background: The authors investigated whether the sedative, or hypnotic, action of the general anesthetic dexmedetomidine (a selective alpha -adrenoceptor agonist) activates endogenous nonrapid eye movement (NREM) sleep-promoting pathways.

Methods: c-Fos expression in sleep-promoting brain nuclei was assessed in rats using immunohistochemistry and hybridization. Next, the authors perturbed these pathways using (1) discrete lesions induced by ibotenic acid, (2) local and systemic administration of gamma-aminobutyric acid receptor type A (GABA ) receptor antagonist gabazine, or (3) alpha2-adrenoceptor antagonist atipamezole in rats, and (4) genetic mutation of the alpha -adrenoceptor in mice.

Evidence for the involvement of spinal cord alpha1 adrenoceptors in nitrous oxide-induced antinociceptive effects in Fischer rats.

Background: In a previous study, the authors found that nitrous oxide (N2O) exposure induces c-Fos (an immunohistochemical marker of neuronal activation) in spinal cord gamma-aminobutyric acid-mediated (GABAergic) neurons in Fischer rats. In this study, the authors sought evidence for the involvement of alpha1 adrenoceptors in the antinociceptive effect of N2O and in activation of GABAergic neurons in the spinal cord.

Methods: Adult male Fischer rats were injected intraperitoneally with alpha1 adrenoceptor antagonist, alpha2 adrenoceptor antagonist, opioid receptor antagonist, or serotonin receptor antagonist and, 15 min later, were exposed to either air (control) or 75% N2O.

Nitrous oxide exerts age-dependent antinociceptive effects in Fischer rats.

Nitrous oxide (N(2)O) is an inhalational anesthetic/analgesic gas that has been used for clinical practice for more than a century. While its anesthetic mechanisms remain largely unknown, the underlying analgesic mechanisms are now being unraveled. It has been proposed that N(2)O induces opioid peptide release in the midbrain, leading to the activation of descending noradrenergic inhibitory neurons, which modulates pain processing within the spinal cord.