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The present study compared the responses of rib cage and abdominal expiratory muscles to chemical and mechanical stimuli. In pentobarbital-anesthetized spontaneously breathing dogs, electromyograms (EMG) were recorded from the triangularis sterni (TS) and transverse abdominis (TA) muscles using bipolar intramuscular wire electrodes. During resting oxygen breathing, both muscles were electrically active during expiration. Progressive hyperoxic hypercapnia significantly augmented the expiratory activity of both the TA and the TS. However, the mean percent increases in electrical activity in response to CO2 were substantially greater for the TA than for the TS at all PCO2 levels greater than 50 Torr (P less than 0.01). Occlusion of the airway at end inspiration significantly delayed the onset of TS EMG (from 0.35 +/- 0.07 to 3.35 +/- 0.67 sec; P less than 0.002) and decreased TS EMG rate of rise (P less than 0.002), but did not significantly alter these parameters for the TA. Esophageal distension increased TS EMG in all dogs (by mean of 220 +/- 64%; P less than 0.01), but in contrast decreased TA EMG in all dogs (by a mean of 63 +/- 12%; P less than 0.001). The response to esophageal distention occurred in a graded manner and appeared to be mediated predominantly via vagal afferents. We concluded that expiratory muscles of the rib cage and abdomen manifest substantial differences in their electrical responses to chemoreceptor, pulmonary stretch receptor, and esophageal mechanoreceptor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   
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To assess the role of structures located superficially near the ventrolateral surface of the medulla on the reflex constriction of tracheal smooth muscle that occurs when airway and pulmonary receptors are stimulated mechanically or chemically, experiments were conducted in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated cats. Pressure changes within a bypassed segment of the trachea were used as an index of alterations smooth muscle tone. The effects of focal cooling of the intermediate areas or topically applied lidocaine on the ventral surface of the medulla on the response of the trachea to mechanical and chemical stimulation of airway receptors were examined. Atropine abolished tracheal constriction induced by mechanical stimulation of the carina or aerosolized histamine, showing that the responses were mediated over vagal pathways. Moderate cooling of the intermediate area (20 degrees C) or local application of lidocaine significantly decreased the tracheal constrictive response to mechanical activation of airway receptors. Furthermore, when the trachea was constricted by histamine, cooling of the intermediate area significantly diminished the increased tracheal tone, whereas rewarming restored tracheal tone to the previous level. These findings suggest that under the conditions of the experiments the ventral surface of the medulla plays an important role in constriction of the trachea by inputs from intrapulmonary receptors and in the modulation of parasympathetic outflow to airway smooth muscle.  相似文献   
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Complex relationships exist among electromyograms (EMGs) of the upper airway muscles, respective changes in muscle length, and upper airway volume. To test the effects of preventing lung inflation on these relationships, recordings were made of EMGs and length changes of the geniohyoid (GH) and sternohyoid (SH) muscles as well as of tidal changes in upper airway volume in eight anesthetized cats. During resting breathing, tracheal airway occlusion tended to increase the inspiratory lengthening of GH and SH. In response to progressive hypercapnia, the GH eventually shortened during inspiration in all animals; the extent of muscle shortening was minimally augmented by airway occlusion despite substantial increases in EMGs. SH lengthened during inspiration in six of eight animals under hypercapnic conditions, and in these cats lengthening was greater during airway occlusion even though EMGs increased. Despite the above effects on SH and GH length, upper airway tidal volume was increased significantly by tracheal occlusion under hypercapnic conditions. These data suggest that the thoracic and upper airway muscle reflex effects of preventing lung inflation during inspiration act antagonistically on hyoid muscle length, but, because of the mechanical arrangement of the hyoid muscles relative to the airway and thorax, they act agonistically to augment tidal changes in upper airway volume. The augmentation of upper airway tidal volume may occur in part as a result of the effects of thoracic movements being passively transmitted through the hyoid muscles.  相似文献   
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We studied the central effects of N-methyl-D-aspartate (NMDA) on respiration in 18 artificially ventilated cats anesthetized with alpha-chloralose. Unilateral topical application of NMDA (1 x 10(-8) mol) to the intermediate region of the ventrolateral medulla exaggerates the phrenic response to CO2 at end-tidal PCO2 levels of less than 50.0 Torr. At higher end-tidal PCO2 levels, however, such differences disappear. Unilateral NMDA application increases the activity of the right and left phrenic nerves equally. Furthermore, the magnitude of the phrenic response after unilateral application of NMDA was not different from that after bilateral application. NMDA also had a vasopressor action when applied to the ventrolateral medullary surface. In contrast to respiratory responses, bilateral application of NMDA caused a significant increase in blood pressure compared with unilateral application of NMDA. Application of the NMDA antagonist 2-amino-5-phosphonovaleric acid abolished both the blood pressure and respiratory effects of NMDA. These results suggest that CO2 and NMDA may act on a common respiratory premotoneuron to produce stimulation of breathing. Because blood pressure responses, unlike respiratory responses, were greater after bilateral application than after unilateral application of NMDA, it is suggested that the neural substrates for the two effects of NMDA seem to be different.  相似文献   
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The effects of diaphragm paralysis on respiratory activity were assessed in 13 anesthetized, spontaneously breathing dogs studied in the supine position. Transient diaphragmatic paralysis was induced by bilateral phrenic nerve cooling. Respiratory activity was assessed from measurements of ventilation and from the moving time averages of electrical activity recorded from the intercostal muscles and the central end of the fifth cervical root of the phrenic nerve. The degree of diaphragm paralysis was evaluated from changes in transdiaphragmatic pressure and reflected in rib cage and abdominal displacements. Animals were studied both before and after vagotomy breathing O2, 3.5% CO2 in O2, or 7% CO2 in O2. In dogs with intact vagi, both peak and rate of rise of phrenic and inspiratory intercostal electrical activity increased progressively as transdiaphragmatic pressure fell. Tidal volume decreased and breathing frequency increased as a result of a shortening in expiratory time. Inspiratory time and ventilation were unchanged by diaphragm paralysis. These findings were the same whether O2 or CO2 in O2 was breathed. After vagotomy, no significant change in phrenic or inspiratory intercostal activity occurred with diaphragm paralysis in spite of increased arterial CO2 partial pressure. Ventilation and tidal volume decreased significantly, and respiratory timing was unchanged. These results suggest that mechanisms mediated by the vagus nerves account for the compensatory increase in respiratory electrical activity during transient diaphragm paralysis. That inspiratory time is unchanged by diaphragm paralysis whereas the rate or rise of phrenic nerve activity increases suggest that reflexes other than the Hering-Breuer reflex contribute to the increased respiratory response.  相似文献   
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Periodic breathing in dogs   总被引:4,自引:0,他引:4  
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