ABSTRACT
The purpose of this review is to, first, determine the static factors that affect the length of the human trachea across different populations and, second, to investigate whether or not there are dynamic factors that cause the length of the human trachea to vary within the same individual. We also investigated whether these changes in tracheal length within the same individual are significant enough to increase the risk of endobronchial intubation or accidental extubation. A PubMed/MEDLINE and a Web of Science database English-language literature search was conducted in May 2016 with relevant keywords and MeSH terms when available. We found that gender, extremes of age, patient height, postsurgical changes and co-existing disease are static patient factors that affect the length of the human trachea. Dynamic clinical changes that occur under anaesthesia, including Trendelenburg position, head and neck flexion and extension, paralysis of the diaphragm and pneumoperitoneum, cause the trachea to act as an accordion, decreasing and increasing its length. The length of the human trachea in both awake and anaesthetised and paralysed patients is a critical consideration in preventing both endobronchial intubation and tracheal extubation. It is clear from the literature that tracheal length varies widely across populations and, additionally, with the dynamic clinical changes that occur under anaesthesia, the trachea acts as an accordion decreasing and increasing its length within the same individual. Knowledge of the magnitude of the change in tracheal dimensions in response to these factors is an important clinical consideration.
Subject(s)
Intubation, Intratracheal/methods , Trachea/anatomy & histology , Adult , Age Factors , Aged , Aged, 80 and over , Body Height , Female , Head-Down Tilt , Humans , Intubation, Intratracheal/adverse effects , Male , Middle AgedABSTRACT
AMP-activated protein kinase (AMPK) has been identified as a regulator of gene transcription, increasing mitochondrial proteins of oxidative metabolism as well as hexokinase expression in skeletal muscle. In mice, muscle-specific knockout of LKB1, a component of the upstream kinase of AMPK, prevents contraction- and 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR)-induced activation of AMPK in skeletal muscle, and the increase in hexokinase II protein that is normally observed with chronic AICAR activation of AMPK. Since previous reports show a cAMP response element in the promoter region of the hexokinase II gene, we hypothesized that the cAMP-response element (CRE) binding protein (CREB) family of transcription factors could be targets of AMPK. Using radioisotopic kinase assays, we found that recombinant and rat liver and muscle AMPK phosphorylated CREB1 at the same site as cAMP-dependent protein kinase (PKA). AMPK was also found to phosphorylate activating transcription factor 1 (ATF1), CRE modulator (CREM), and CREB-like 2 (CREBL2), but not ATF2. Treatment of HEK-293 cells stably transfected with a CREB-driven luciferase reporter with AICAR increased luciferase activity approximately threefold over a 24-h time course. This increase was blocked with compound C, an AMPK inhibitor. In addition, AICAR-induced activation of AMPK in incubated rat epitrochlearis muscles resulted in an increase in both phospho-acetyl-CoA carboxylase and phospho-CREB. We conclude that CREB and related proteins are direct downstream targets for AMPK and are therefore likely involved in mediating some effects of AMPK on expression of genes having a CRE in their promoters.
