Effect of hyperthermia and Pa CO2 on the slowly adapting pulmonary stretch receptor

1972 ◽  
Vol 222 (1) ◽  
pp. 68-72 ◽  
Author(s):  
EP Schoener ◽  
HM Frankel
Author(s):  
Edward J. Zuperku ◽  
Francis A. Hopp ◽  
Eckehard A.E. Stuth ◽  
Astrid G. Stucke

Neonatology ◽  
2004 ◽  
Vol 86 (2) ◽  
pp. 73-80 ◽  
Author(s):  
Esther Rieger-Fackeldey ◽  
Richard Sindelar ◽  
Anders Jonzon ◽  
Andreas Schulze ◽  
Gunnar Sedin

1989 ◽  
Vol 75 (1) ◽  
pp. 75-88 ◽  
Author(s):  
Heather A. McLean ◽  
Gordon S. Mitchell ◽  
William K. Milsom

1993 ◽  
Vol 43 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Shigeji Matsumoto ◽  
Takahiro Kanno ◽  
Masao Yamasaki ◽  
Tadanori Nagayama ◽  
Masatoshi Tanno ◽  
...  

1978 ◽  
Vol 56 (2) ◽  
pp. 191-198 ◽  
Author(s):  
Urs Gerber ◽  
Canio Polosa

The response of 47 sympathetic preganglionic neurons (SPNs) of the cervical nerve to activation of pulmonary stretch receptors has been studied in Nembutal-anaesthetized. paralyzed, thoracotomized, artificially ventilated cats. The discharge of 62% of the SPNs was depressed by lung inflation or by electrical stimulation of the lowest threshold afferent fibers in the vagus nerve. The SPNs which were most sensitive to these manoeuvers were those whose discharge had an inspiration-synchronous component. All the SPNs of this type tested were depressed. Their response paralleled that of phrenic motoneurons. The SPNs which were least sensitive to these manoeuvers were those whose firing pattern showed no respiratory modulation. Only 12% of the SPNs of this type tested were depressed. In some SPNs, selective suppression of inspiration-synchronous activity by hypocapnia revealed a residual firing which could not be altered by pulmonary stretch receptor afferent activation. For comparison, the reflex response of the same sample of SPNs to the systemic arterial pressure increase caused by intravenous injection of noradrenaline (5 μg/kg) was studied. The discharge of 85% of the SPNs was depressed during the pressor effect of noradrenaline. The frequency of occurrence of depressant effects was similar in respiratory-modulated and nonmodulated SPNs. Also depressed was the residual discharge in hypocapnia of respiratory-modulated SPNs. Thus, the distribution in the SPN pool of the depression evoked by a systemic arterial pressure rise contrasts with that caused by activation of pulmonary stretch receptor afferents. These results provide a direct demonstration of the depressant action of pulmonary stretch receptor afferents on SPNs, an action that had previously been hypothesized on the basis of indirect evidence. The observation that activation of these afferents depresses mainly the inspiration-synchronous component of SPN firing suggests that the effect is predominantly relayed to the SPN pool via the respiratory center.


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