O2-sensing by model airway chemoreceptors. Hypoxic inhibition of K+ channels in H146 cells.
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In a previous publication (Fowler et al., 1993), we reduced the classical cardiorespiratory control model of (Grodins et al., 1967) to a much simpler form, which we then used to study the phenomenon of periodic breathing. In particular, cardiac output was assumed constant, and a single (constant) delay representing arterial blood transport time between lung and brain was included in the model. In this paper we extend this earlier work, both by allowing for the variability in transport delays, due to the dependence of cardiac output on blood gas concentrations, and also by including further delays in the system. In addition, we extensively discuss the physiological implications of parameter variations in the model; several novel mechanisms for periodic breathing in clinical situations are proposed. The results are discussed in the light of recent observational studies.
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We studied nine "healthy" preterm infants (birthweight, 1,000 to 2,000 gm) 58 times during postnatal life to define the effects of gestational and postnatal age on the ventilatory response to carbon dioxide. The infants were given air and 2% and 4% carbon dioxide in air to breathe for five minutes each. We determined respiratory minute and tidal volumes, frequency,heart rate, and alveolar PCO2 and PO2. We measured ventilation with a nosepiece and a screen flowmeter, using a constant flow-through to eliminate valves and reduce diad space. Analysis were made during the fifth minute while the baby breathed the various gas mistures. The slope of the carbon dioxide response increased 42% from 32 to 37 weeks gestation (P smaller than .05) and 62% from 2 to 27 days of age (P smaller than. 025). However, the intercept at .3 liter/min/kg was the same at different gestational ages, but significantly greater at 2 compared with 27 days of age (P smaller than.05). We sugest that the unresposiveness primarily dependent on the mechanical abnormalities of the lung.
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The effects of N-methyl-D-aspartate (NMDA) glutamate receptor antagonist (+)-MK-801 hydrogen maleate (MR801) on plasticity of different sensory inputs of the L-RPl1 command neurons were studied in Helix lucorum snail during nociceptive sensitization. Application of sensitizing stimulation onto the snail head or foot in the control semi-intact preparation initiated depression of neural responses evoked by tactile or chemical sensory stimulation during the short-term period of sensitization and significant facilitation of neural responses during the long-period of sensitization. Sensitizing stimulation of snail head against the background of MK-801 application (10-30 microM) produced a pronounced depression of neural responses to chemical stimulation of the head both in the short- and long-term sensitization periods. At the same time, sensitizing stimulation of the foot or head during the MK-801 application produced the same changes in neural responses to chemical stimulation of the foot and tactile stimulation of the foot or head as in the control preparation. It can be suggested that NMDA-like glutamate receptors are selectively involved in the mechanisms of plasticity induction in the synaptic inputs of the command LPl1 and RPl1 neurons, which process the information resulting from chemical excitation of the snail head (a specific receptor skin site for these neurons in Helix lucorum).
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