Relaxin‐3 receptor (RXFP3) mediated modulation of central respiratory activity

Exposure to hyperbaric pressure causes a constellation of motor disturbances and ventilatory difficulties in animals and humans. The present experiments were designed to examine the effects of hyperbaric pressure on the rhythmic activity of the respiratory center in the absence of peripheral sensory afferents by using the isolated brain stem-spinal cord preparation from newborn rats. In addition, we examined the effect of pressure on the response of the respiratory center to sensory input from the trigeminal and vagus cranial nerves. Hyperbaric pressure significantly depressed the mean inspiratory drive (frequency X time integral of single electrical bursts) in C5 but not in C1 ventral roots. Pressure also reduced the amount of inhibition on the respiratory activity normally exerted by trigeminal and vagal nerve stimulation and in some cases reversed it to excitation. It is concluded that in the absence of sensory input, exposure to hyperbaric pressure depresses central respiratory activity. However, in an intact system, it may alter the balance between excitation and inhibition and render the system hyperexcitable to the same sensory input.

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The Combined Effects of Sevoflurane and Remifentanil on Central Respiratory Activity and Nociceptive Cardiovascular Responses in Anesthetized Rabbits

Anesthesia & Analgesia ◽

10.1097/00000539-199908000-00039 ◽

1999 ◽

Vol 89 (2) ◽

pp. 453-461 ◽

Cited By ~ 1

Author(s):

Daqing Ma ◽

Mihir K. Chakrabarti ◽

James G. Whitwam

Keyword(s):

Respiratory Activity ◽

Cardiovascular Responses ◽

Combined Effects ◽

Central Respiratory Activity

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Regulation of fetal breathing

Reproduction Fertility and Development ◽

10.1071/rd9960023 ◽

1996 ◽

Vol 8 (1) ◽

pp. 23 ◽

Cited By ~ 7

Author(s):

H Rigatto

Keyword(s):

Molecular Mass ◽

Umbilical Cord ◽

Neuronal Network ◽

Respiratory Activity ◽

In Utero ◽

Cold Stimulation ◽

The Past ◽

Fetal Breathing ◽

Central Respiratory Activity ◽

Made In

Traditionally, the idea of transient asphyxia plus some degree of cold stimulation has been used to explain the establishment of continuous breathing at birth. This idea was nurtured by observations made in the acute fetal preparation at a time when fetal breathing was considered absent. Experimental observations made in the past two decades have challenged this traditional view. First, complete peripheral chemodenervation, essential to the hypoxic stimulus theory, did not affect fetal breathing or the establishment of continuous breathing at birth. Second, occlusion of the umbilical cord in utero, as long as some oxygenation is provided to the fetus in order to avoid fetal hypoxaemia, establishes continuous breathing in utero, in the absence of all sensorial input thought to be important for the establishment of continuous breathing. These observations led us to hypothesize the presence of a placental factor responsible for the inhibition of breathing in utero. This placental factor appears to be a peptide with a molecular mass between 3.5 and 10 kDa. This review will also explore some new observations regarding the generation of central respiratory activity in the fetus, and suggests that the rhythm generator is a neuronal network in which the unit is a pacemaker-like cell uniquely responsive to CO2.

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