![]() ![]() ![]() Carbon dioxide monotonically increases ventilation until the CO 2 exposure reaches approximately 8–10% thereafter, further increases in CO 2 inhibit ventilation ( Tepper et al., 1988). In terms of the assessment of altered ventilatory function during exposure to drugs, pollutants, or chemicals, CO 2 challenge has been used most frequently to improve detection of respiratory deficits. While elegant systems have been described for larger animals, only a limited number of publications have reported such exercise systems to aid in the enhancement of inhaled exposure and/or the detection of lung damage ( Kleinman and Mautz, 1991).įortunately, CO 2-induced hyperventilation, as an analogue of exercise, relies on similar mechanisms, and perhaps other factors related to cardiovascular and airway receptor responsiveness, to aid in the assessment of ventilatory capacity and improve the detection of functional lesions ( Tepper et al., 1988). Currently, however, there are few suitable methods for evaluating pulmonary function in small animals during exercise ( Mautz et al., 1985b, 1985a Harbison and Brain, 1983). Similarly, exercise could also be used to limit an experimental animal's ability to use functional reserves to evaluate disease status as well as to directly enhance deposition of inhaled chemicals. This approach affirms the notion that performance, or the lack thereof, is at the essence of respiratory disease assessments. For this reason, manipulations that involve exercise or other hyperventilatory stimulation have been utilized in an attempt to overcome this reserve and to demonstrate more subtle ventilatory deficits or disturbances ( Tepper et al., 1988 Mautz et al., 1985a, 1985b Wong et al., 1985).Įxercise techniques (e.g., treadmill) have been used in humans to stimulate ventilation and increase the time-constant heterogeneity of ventilatory units and have been useful in the evaluation of disease. Even dynamic compliance, which is influenced by both small airway function and parenchymal elasticity, may be insensitive to such lesions, due to the large ventilatory reserve of the lung ( Woolcock et al., 1969). Similarly, the composite nature of the distal ventilatory structure suggests that isolated lesions, within a limited group of ventilatory units, would likely have minimal, if any, impact on breathing patterns or total airway resistance, despite some misalignment of ventilation and perfusion. described the small airways (<2 mm in humans) as the “silent zone” of the lungs, since overall ventilatory function would likely remain within normal limits until airway obstruction of these airways is far advanced ( Woolcock et al., 1969). Costa, in Comparative Biology of the Normal Lung (Second Edition), 2015 Methods for Enhancing the Sensitivity of Ventilatory Tests ![]()
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