PubMed · 15310651
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Tiberiu Ezri, Marian Weissenberg, Ofer Yanai, Michael Sullam-Muggia, Zion Houri, Peter Szmuk. Internal or external diameter?. https://doi.org/10.1007/bf03018441
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We investigated the effect of surfactant deficiency on airway patency and the effectiveness of surfactant replacement as either an instilled liquid bolus, a non-hygroscopic aerosol or a hygroscopic aerosol. Small airway patency was assessed in isolated piglet lungs by passing a continuous flow of gas though a cannulated airway. Occlusion was assessed by measuring increases in pressure in the cannula that resulted from airway obstruction. In surfactant-deficient conditions the amount of airway closure increased approximately three-fold. However, administration of exogenous surfactant as an instilled liquid bolus, non-hygroscopic aerosol or a hygroscopic aerosol decreased airway closure such that it was statistically similar to that recorded prior to induction of surfactant deficiency, although the instilled and hygroscopic aerosol surfactant both appeared superior to the non-hygroscopic aerosol. These experiments showed that pulmonary surfactant does have a role in maintaining airway patency and that airway closure induced by surfactant deficiency could be reduced by administration of surfactant in any of the aforementioned forms.
Estimation of mechanical properties of the respiratory system may be disturbed by instrumentation and physical set-up. The effects of lowpass filtering, filter mismatch and inter-channel delay in the digital converter are assessed on numerically simulated signals from a nonlinear model of the respiratory system. Large biases in model parameter estimates (up to about -300% for some parameters) were caused by these instrumental interferences and were reduced by including an inertance in the retrieved model. The results reinforce the importance of a careful evaluation of the instrumental set-up used in physiological measurements.
This review summarizes the recent neuroanatomical and physiological studies that form the neural basis for the state-dependent changes in airway resistance. Here, we review only the interactions between the brain regions generating quiet (non-rapid eye movement, NREM) and active (rapid eye movement, REM) sleep stages and CNS pathways controlling cholinergic outflow to the airways. During NREM and REM sleep, bronchoconstrictive responses are heightened and conductivity of the airways is lower as compared to the waking state. The decrease in conductivity of the lower airways parallels the sleep-induced decline in the discharge of brainstem monoaminergic cell groups and GABAergic neurons of the ventrolateral periaqueductal midbrain region, all of which provide inhibitory inputs to airway-related vagal preganglionic neurons (AVPNs). Withdrawal of central inhibitory influences to AVPNs results in a shift from inhibitory to excitatory transmission that leads to an increase in airway responsiveness, cholinergic outflow to the lower airways and consequently, bronchoconstriction. In healthy subjects, these changes are clinically unnoticed. However, in patients with bronchial asthma, sleep-related alterations in lung functions are troublesome, causing intensified bronchopulmonary symptoms (nocturnal asthma), frequent arousals, decreased quality of life, and increased mortality. Unquestionably, the studies revealing neural mechanisms that underlie sleep-related alterations of airway function will provide new directions in the treatment and prevention of sleep-induced worsening of airway diseases.