PubMed · 13103430
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J SEUSING. 1953. [Causes of decrease of pulse frequency under air pressure].. https://pubmed.ncbi.nlm.nih.gov/13103430/
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Animal models have been used to study the pathophysiology of the obstructive sleep apnea/hypopnea syndrome (SAHS). Nevertheless, in none of the models described to date have the animals been subjected to the different patterns of upper airway obstructive events (apneas, hypopneas, and inspiratory flow limitation) characterizing SAHS. Our aim was to devise and test a computer-controlled collapsible upper airway segment applicable to rats and able to realistically mimic obstructive SAHS events. The collapsible segment (total volume <2 cm(3) and a dead space of approximately 0.25 cm(3)) consisted of a Starling resistor based on a latex membrane subjected to an external pressure applied by a computer-controlled pressure source. The collapsible segment was tested in eight anaesthetized and tracheostomized rats. The upper airway segment allowed us to induce obstructive apneas and hypopneas with flow and inspiratory effort waveforms similar to the ones observed in patients with SAHS. This collapsible upper airway segment may be a useful tool to implement a rat model of SAHS.
High pressure (>1.5 MPa) induces a series of disturbances of the nervous system that are generically termed high-pressure nervous syndrome (HPNS). HPNS is characterized by motor and cognitive impairments. The neocortex and the hippocampus are presumably involved in this last disorder. The medial perforant path (MPP) synapse onto the granule cells of the dentate gyrus is the main connection between these structures. We have studied high-pressure (HP) effects on single and frequency response of this synapse. Since effects of HP on various synapses were mimicked by reducing [Ca2+]o, results under these conditions were compared. Medial perforant path-evoked field excitatory postsynaptic potentials (fEPSPs) were recorded from granule cells in rat brain slices. Slices were exposed to high pressure of helium (0.1-10.1 MPa) at 30 degrees C. HP depressed single fEPSPs by 35 and 55% at 5.1 and 10.1 MPa, respectively, and increased paired-pulse facilitation (PPF) at 10- to 40-ms inter-stimulus intervals. Frequency-dependent depression (FDD) was enhanced by HP during trains of stimuli at 50 but not at 25 Hz. Depression of single fEPSPs by reduction of [Ca2+]o from 2 mM control to 1 mM at normal pressure was equivalent to the effect of 10.1 MPa at control [Ca2+]o. However, this low [Ca2+]o induced greater enhancement of PPF, and in contrast, turned FDD at 25-50 Hz into frequency-dependent potentiation. These results suggest that HP depresses single synaptic release by reducing Ca2+ entry, whereas slowing of synaptic frequency response is independent of Ca2+. These findings increase our understanding of HPNS experienced by deep divers.
Ventilator-induced lung injury has been proposed as being caused by overdistention and closure and reopening of small airways and alveoli. Here we investigate the possibility that heterogeneous constriction increases airflow-related shear stress to a dangerously high level that may be sufficient to cause injury to the epithelial cells during mechanical ventilation. We employed an anatomically consistent model of the respiratory system, based on Horsfield morphometric data, and solved for the time evolution of pressure and flow along the airway tree during mechanical ventilation. We simulated constant-flow ventilation with passive expiration in two different conditions: baseline and highly heterogeneous constriction. The constriction was applied with two strategies: establishing a simple diameter reduction or adding also a length shortening. The shear stress distribution on airway walls was analyzed for airways ranging from the trachea to the acini. Our results indicate that 1). heterogeneous constriction can amplify the maximal values of shear stress up to 50-fold, with peak values higher than 0.6 cmH2O; 2). the highest shear stress is found in pathways constricted by 60-80%; 3). simultaneous diameter reduction and shortening amplifies the shear stresses by three- to fourfold, with shear stresses reaching 2 cmH2O; and 4). there is a range of airways (diameters from 0.6 to 0.3 mm at baseline) that appear to be at risk of very high stresses. We conclude that elevated airflow-related shear stress on the epithelial cell layer can occur during heterogeneous constriction and conjecture that this may constitute a mechanism contributing to ventilator-induced lung injury.