The Effect of Sympathetic Nerve Stimulation on Ventilation and Upper Airway Resistance in the Anaesthetized Rat

Author(s):  
K. D. O’Halloran ◽  
A. K. Curran ◽  
A. Bradford
1974 ◽  
Vol 52 (3) ◽  
pp. 699-705 ◽  
Author(s):  
Stanley Greenberg ◽  
Linda Howard ◽  
William R. Wilson

Prostaglandin B2 (PGB2) may be formed from PGA2in vivo. The following study compares the effects of equivalent concentrations of PGA2 and PGB2 on systemic pressure, heart rate, airway resistance, cutaneous vascular resistance, and responses to sympathetic nerve stimulation and to norepinephrine and tyramine in the acutely denervated canine hind paw perfused with autologous blood at constant flow. Intra-arterial (i.a.) PGB2 (1 and 10 μg/min) produced concentration-dependent vasoconstriction. Fifteen minutes after PGB2 administration the pressor responses of the paw to sympathetic nerve stimulation were enhanced, whereas the pressor responses to norepinephrine and tyramine were unchanged. In contrast, low concentrations of PGA2 produced systemic and transient cutaneous dilation whereas the higher concentration (10 μg/min i.a.) produced systemic dilation and constriction of the acutely denervated paw. The pressor responses of the perfused paw to sympathetic nerve stimulation were enhanced with the higher infusion rate of PGA2. However, the pressor responses to norepinephrine and tyramine were unchanged during PGA2. In addition, PGB2, but not PGA2, increased airway resistance. These results suggest that: (1) PGB2 and PGA2 have different effects on systemic pressure and airway resistance but have similar effects on the cutaneous vascular bed; (2) both PGB2 and PGA2 selectively enhance neurotransmitter release from the catecholamine pool susceptible to activation by the nerve action potential; and (3) PGB2 is more potent in its ability to enhance neurotransmitter release than PGA2. The vasoconstriction and facilitation of sympathetic neurotransmission by PGA2 may be related to formation of PGB2 within the paw.


2018 ◽  
Vol 125 (3) ◽  
pp. 763-769 ◽  
Author(s):  
Matthew Schiefer ◽  
Jenniffer Gamble ◽  
Kingman P. Strohl

Obstructive sleep apnea (OSA) is a disorder characterized by collapse of the velopharynx and/or oropharynx during sleep when drive to the upper airway is reduced. Here, we explore an indirect approach for activation of upper airway muscles that might affect airway dynamics, namely, unilateral electrical stimulation of the afferent fibers of the sciatic nerve, in an anesthetized rabbit model. A nerve cuff electrode was placed around the sciatic and hypoglossal nerves to deliver stimulus while airflow, air pressure, and alae nasi electromyogram (EMG) were monitored both before and after sciatic transection. Sciatic nerve stimulation increased respiratory effort, rate, and alae nasi EMG, which persisted for seconds after stimulation; however, upper airway resistance was unchanged. Hypoglossal stimulation reduced resistance without altering drive. Although sciatic nerve stimulation is not ideal for treating OSA, it remains a target for altering respiratory drive. NEW & NOTEWORTHY Previously, sciatic nerve stimulation has been shown to activate upper airway and chest wall muscles. The supposition that resistance through the upper airway would be reduced with this afferent reflex was disproven. Findings were in contrast with the effect of hypoglossal nerve stimulation, which was shown to decrease resistance without changing muscle activation or ventilatory drive.


1992 ◽  
Vol 33 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Katsusuke YANO ◽  
Masanobu HIRATA ◽  
Takao MITSUOKA ◽  
Yoriaki MATSUMOTO ◽  
Tetsuya HIRATA ◽  
...  

1985 ◽  
Vol 58 (5) ◽  
pp. 1489-1495 ◽  
Author(s):  
J. P. Farber

The suckling opossum exhibits an expiration-phased discharge in abdominal muscles during positive-pressure breathing (PPB); the response becomes apparent, however, only after the 3rd-5th wk of postnatal life. The purpose of this study was to determine whether the early lack of activation represented a deficiency of segmental outflow to abdominal muscles or whether comparable effects were observed in cranial outflows to muscles of the upper airways due to immaturity of afferent and/or supraspinal pathways. Anesthetized suckling opossums between 15 and 50 days of age were exposed to PPB; electromyogram (EMG) responses in diaphragm and abdominal muscles were measured, along with EMG of larynx dilator muscles and/or upper airway resistance. In animals older than approximately 30 days of age, the onset of PPB was associated with a prolonged expiration-phased EMG activation of larynx dilator muscles and/or decreased upper airway resistance, along with expiratory recruitment of the abdominal muscle EMG. These effects persisted as long as the load was maintained. Younger animals showed only those responses related to the upper airway; in fact, activation of upper airway muscles during PPB could be associated with suppression of the abdominal motor outflow. After unilateral vagotomy, abdominal and upper airway motor responses to PPB were reduced. The balance between PPB-induced excitatory and inhibitory or disfacilitory influences from the supraspinal level on abdominal motoneurons and/or spinal processing of information from higher centers may shift toward net excitation as the opossum matures.


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