Electrical stimulation of arterial and central chemosensory afferents at different times in the respiratory cycle of the cat: I. Ventilatory responses

1985 ◽  
Vol 403 (4) ◽  
pp. 415-421 ◽  
Author(s):  
W. Marek ◽  
N. R. Prabhakar ◽  
H. H. Loeschcke
Keyword(s):  
Electrical Stimulation ◽  
Respiratory Cycle ◽  
Ventilatory Responses ◽  
Stimulation Of

Fictive cough in the cat

1991 ◽  
Vol 71 (6) ◽  
pp. 2325-2331 ◽  
Author(s):  
D. C. Bolser
Keyword(s):  
Electrical Stimulation ◽  
Mechanical Stimulation ◽  
Large Amplitude ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Afferent Feedback ◽  
Respiratory Cycle ◽  
Decerebrate Cats ◽  
Stimulation Of

Experiments were performed to determine whether cough could be elicited in paralyzed cats ventilated on a respiratory cycle-triggered pump. Midcollicular decerebrate cats were paralyzed and artificially ventilated on a phrenic-triggered pump. Phrenic and cranial iliohypogastric nerve efferent activities were recorded. Cough was elicited by electrical stimulation of the superior laryngeal nerve (SLN) or probing the intrathoracic trachea. Fictive coughs induced by electrical stimulation of the SLN or mechanical stimulation of the intrathoracic trachea consisted of large-amplitude bursts in phrenic discharge immediately followed by large bursts in cranial iliohypogastric discharge. During fictive cough, phrenic postinspiratory discharge was reduced relative to control cycles. Codeine (0.03–1 mg/kg iv) decreased both SLN- and probe-induced fictive cough. I conclude that fictive cough can be produced in paralyzed cats ventilated on a phrenic-triggered pump. Furthermore, fictive cough can be produced in the absence of afferent feedback associated with active expiration.

Time-dependent responses of expiration reflex in cats

1986 ◽  
Vol 61 (2) ◽  
pp. 430-435 ◽  
Author(s):  
T. Nishino ◽  
Y. Honda
Keyword(s):  
Electrical Stimulation ◽  
Mechanical Stimulation ◽  
Superior Laryngeal Nerve ◽  
Vocal Folds ◽  
Laryngeal Nerve ◽  
Time Dependent ◽  
Respiratory Cycle ◽  
Partial Pressures ◽  
Spontaneously Breathing ◽  
Stimulation Of

We investigated the effectiveness of the “expiration reflex” in 10 anesthetized spontaneously breathing cats. The expiration reflex was produced by mechanical stimulation of the vocal folds and electrical stimulation of the superior laryngeal nerve at different moments in the respiratory cycle and at various levels of respiratory chemical drive. The effectiveness of the expiration reflex was evaluated from sudden changes in expiratory flow immediately following the stimulation. Both mechanical and electrical stimulations given during early inspiration caused little or no expiratory efforts, whereas stimulations given during early expiration or hypocapnic apnea produced a typical expiration reflex. Changes in arterial CO2 and O2 partial pressures influenced neither the relationships between the stimulation and its effect on the expiration reflex nor the strength of the expiration reflex. These results indicate that the timing of stimulation with relation to the phase of the respiratory cycle is critical to its effect on the expiration reflex and that changes in respiratory chemical drive do not modify the expiration reflex characteristics.

Ventilatory Responses of Rats to Electrical Stimulation in CO2 Containing Atmospheres

1957 ◽  
Vol 191 (3) ◽  
pp. 423-427 ◽  
Author(s):  
William S. Yamamoto
Keyword(s):  
Carbon Dioxide ◽  
Electrical Stimulation ◽  
Steady State ◽  
Body Temperature ◽  
Gas Exchange ◽  
Wistar Rats ◽  
Ventilatory Responses ◽  
Constant State ◽  
Made In ◽  
Stimulation Of

Steady state measurements of metabolic gas exchange, ventilation and body temperature were made in anesthetized (urethane) Wistar rats breathing gas mixtures in compositions ranging from 20 to 30% oxygen, 0 to 10% carbon dioxide, and nitrogen. Metabolic rate was caused to vary by interrupted electrical stimulation of limb muscles. From 218 such determinations a regression was calculated, Vcoco2 = 0.00843 V (0.999Fe – Fi) – 0.091. It is concluded that the coco2 exchange of rats is similar to those reported in man and dog. Particular care was taken to assure a steady (constant) state at the time of measurement. Homeostatic defense against internally produced CO2 is good, whereas that against environmental CO2 changes is poor.

Medial vestibular nucleus mediates the cardiorespiratory responses to fastigial nuclear activation and hypercapnia

2004 ◽  
Vol 97 (3) ◽  
pp. 835-842 ◽  
Author(s):  
Joseph P. Hernandez ◽  
Fadi Xu ◽  
Donald T. Frazier
Keyword(s):  
Electrical Stimulation ◽  
Vestibular Nucleus ◽  
Ibotenic Acid ◽  
Medial Vestibular Nucleus ◽  
Ventilatory Responses ◽  
Cardiorespiratory Responses ◽  
Before And After ◽  
Bilateral Lesions ◽  
Spontaneously Breathing ◽  
Stimulation Of

Electrical stimulation of the cerebellar fastigial nucleus (FN) evokes hyperventilation and hypertension responses that are similar to those induced by stimulation of the medial region of the vestibular nucleus (VNM). Because there are mutual projections between these two nuclei morphologically, we hypothesized that the FN-mediated cardiorespiratory responses were related to the integrity of the VNM. Experiments were conducted on 21 anesthetized, tracheotomized, and spontaneously breathing rats. Electrical stimulation (∼10 s) of the FN was used to evoke cardiorespiratory responses, and the same stimulus was repeated 30–45 min after bilateral lesions of the VNM by local microinjection of ibotenic acid (100 mM, 100 nl). We found that FN stimulation-induced hyperventilation and hypertension were attenuated significantly by the lesions. The role of the VNM in the ventilatory responses to chemical challenges was subsequently defined. The animals were exposed to hypercapnia (10% CO2) and hypoxia (10% O2) for 1–2 min randomly before and after VNM lesions. The results showed that VNM lesions significantly attenuated the cardiorespiratory responses to hypercapnia but not to hypoxia, with little effect on baseline respiratory variables. These findings suggest that the VNM is required for full expression of the cardiorespiratory responses to electrical stimulation of the FN as well as to hypercapnia. However, neurons within the VNM do not appear to be critical for maintaining eupneic breathing and the cardiorespiratory responses to hypoxia.

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