We have previously shown that large inspired volumes can be achieved in phrenicotomized animals by intercostal/accessory muscle activation via spinal cord stimulation. In the present study, we evaluated the utility of this technique to provide complete ventilatory support for prolonged time periods (6 to 8 h, selected arbitrarily). In 10 deeply anesthetized dogs, a single electrode was introduced onto the epidural surface of the spinal cord and positioned at the T2-T3 spinal level. Bilateral phrenicotomy was performed in all animals to prevent possible diaphragm activation. The spinal cord was rhythmically stimulated approximately 13 times/min with trains of 15- to 20-Hz impulses of sufficient amplitude to achieve inspired volumes of 13 to 15 ml/kg and pressure-time index (product of duty cycle and delta P/Pmax) of less than 0.15 with each contraction. Level of alveolar ventilation was monitored by end-tidal PCO2 and intermittent arterial blood gas measurements. Mean inspired volume and minute ventilation were 236 +/- 7.84 (SE) ml and 3.12 +/- 0.13 (SE) L/min, respectively, and not significantly different between the first and sixth hours of continuous stimulation. Mean duty cycle (Ti/Ttot) was 0.26 +/- 0.01. Mean airway pressure (delta P) during prolonged electrical stimulation under conditions of airway occlusion was 8.05 +/- 0.61 (SE) cm H2O. Mean ratio of delta P/Pmax was 0.47 +/- 0.03 (SE) cm H2O; mean pressure-time index was 0.12 +/- 0.01 (SE). There was no evidence of system fatigue, as evidenced by the lack of any significant shift in the pressure frequency curve over a 6-h time period.(ABSTRACT TRUNCATED AT 250 WORDS)
Unilateral focal cold blocks (20 degrees C) in structures located ventrolaterally in rostral medulla consistently caused apnoea or deep depression of inspiratory motor output. The inhibitory effect could be correlated with the cooling temperature. Apnoeic response occurred either with complete absence of any inspiratory activity or combined with low level tonic inspiratory motor activity ('tonic apnoea'). The appearance of apnoea was CO2-independent, whereas the tonic component of the latter increased with increasing levels of PCO2. The results suggest that the structures in the deep, ventro-lateral aspect of rostral medulla, from which apnoea can be induced, correspond partly to the nucleus paragigantocellularis lateralis (nPGL) and the nucleus preolivaris. These structures appear to be relevant for the drive inputs necessary for respiratory rhythmogenesis. Unilateral focal cooling in the rostral medulla, including the 'Bötzinger Complex', caused increments in respiratory rate both in vagotomized and non-vagotomized animals. The increase in respiratory rate in response to cooling in the region of the 'Bötzinger Complex' was combined with either an enhancement or some depression of respiratory motor output. This area in the rostral part of the ventral respiratory group (VRG) seems not to be crucial for respiratory rhythmogenesis, but to play a role in determining both the intensity and timing of the respiratory activity. All effects of unilateral cold block were bilaterally symmetrical.
The mechanical interaction of the inspiratory muscles in the generation of changes in airway pressure is unclear. Using upper thoracic spinal cord stimulation to activate the intercostal muscles (IC) and bilateral supramaximal phrenic nerve stimulation to activate the diaphragm (D), we measured the changes in airway pressure produced by separate and combined IC and D activation over a wide range of lung volumes. Changes in parasternal IC and D length were assessed by sonomicrometry. With increasing lung volume, activation of the IC and D resulted in progressive decrements in generated airway pressure. Combined IC and D contraction produced greater negative swings in airway pressure than the arithmetic sum of separate IC and D contraction alone, indicating a synergistic effect. Moreover, synergism increased progressively with increasing lung volume. During combined muscle contraction, both the IC and D shortened less than during contraction of either muscle group alone. The tendency for the parasternal muscle to lengthen for a given change in airway pressure during D contraction alone increased with increasing lung volume, suggesting that the tendency for the rib cage to recoil inward increased progressively with increasing lung volume. Likewise, the tendency of the D to lengthen for a given change in airway pressure during IC contraction alone also increased progressively with increasing lung volume, suggesting that the tendency for the abdomen-D compartment to recoil inward also increased with increasing lung volume. We conclude that the IC and D interact synergistically to produce changes in airway pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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