Behavioral and respiratory characteristics during sleep in neonatal DBA/2J and A/J mice.

The ventilatory response to hypoxia depends on the carotid body function and sleep-wake states. Therefore, the response must be measured in a consistent sleep-wake state. In mice, EMG with behavioral indices (coordinated movements, CMs; myoclonic twitches, MTs) has been used to assess sleep-wake states. However, in neonatal mice EMG instrumentation could induce stress, altering their behavior and ventilation. Accordingly, we examined: (1) if EMG can be eliminated for assessing sleep-wake states; and (2) behavioral characteristics and carotid body-mediated respiratory control during sleep with EMG (EMG+) or without EMG (EMG-). Seven-day-old DBA/2J and A/J mice were divided into EMG+ and EMG- groups. In both strains, CMs occurred when EMG was high; MTs were present during silent/low EMG activity. The durations of high EMG activity and of CMs were statistically indifferent. Thus, CMs can be used to indicate wake state without EMG. The stress caused by EMG instrumentation may be distinctively manifested based on genetic background. Prolonged agitation was observed in some EMG+ DBA/2J (5 of 13), but not in A/J mice. The sleep time and MT counts were indifferent between the groups in DBA/2J mice. The EMG+ A/J group showed longer sleep time and less MT counts than the EMG- A/J group. Mean respiratory variables (baseline, hyperoxic/hypoxic responses) were not severely influenced by EMG+ in either strain. Individual values were more variable in EMG+ mice. Carotid body-mediated respiratory responses (decreased ventilation upon hyperoxia and increased ventilation upon mild hypoxia) during sleep were clearly observed in these neonatal mice with or without EMG instrumentation.

Analysis of lung parenchyma as a parametric porous medium.

The dynamic behavior of the lung in health and disease depends on its viscoelastic properties. To better understand these properties, several mathematical models have been utilized by many investigators. In the present work, we present a new approach that characterizes the dynamics of gas flow into a viscoelastic porous medium that models the lung structure. This problem is considered in terms of the lung input impedance on a macro level and parenchymal tissue impedance on the level of an alveolar wall. We start from a basic theoretical analysis in which macroscopic tissue deformations are represented in accordance with the linearized Navier-Stokes equations. This approach has strong theoretical underpinnings in other situations but has not been applied to analyze the impedance of the inflated lung. Our analysis provides a theoretical basis for analyzing the interaction between flow into the lungs as a biophysical diffusion process and parenchymal viscoelasticity described phenomenologically, within the frameworks of standard viscoelasticity and structural damping. This lung impedance incorporates parameters of porosity, permeability, and viscoelasticity on micro and macro levels of parenchymal tissue. The analysis shows the theoretical basis of the transformation from the impedance of alveolar walls or isolated tissue strips to that of the intact parenchyma. We also show how the loading impedance at the lung boundary may have a significant impact on the dynamic behavior of whole lung viscoelasticity. Our analysis may be useful in directing specific tests of different models and for analyzing experimental measurements of viscoelastic parameters of lung material under normal and pathological conditions.

Patch clamp study of mouse glomus cells using a whole carotid body.

Some electrophysiological characteristics of mouse glomus cells (DBA/2J strain) were investigated using an undissociated carotid body. The carotid body with major carotid arteries was placed in a recording chamber, and glomus cells were visualized with a water immersion lens combined with an infrared differential interference video camera. Patch clamp experiments revealed that voltage-gated outward current, but not inward current, was easily observed in glomus cells. Pharmacological experiments and the kinetics of the current suggest that outward current is via delayed rectifier, A type, and large conductance calcium-activated K channels. Furthermore, K current was reversibly attenuated by mild hypoxia. The results suggest electrophysiological similarities of glomus cells among the cat, the rat, and the DBA/2J mouse. The method appears useful for physiological experiments.