TY - JOUR
T1 - Hypocapnia-dependent facilitation of augmented breaths
T2 - Observations in awake vs. anesthetized rats
AU - Moore, J.
AU - Haouzi, P.
AU - Van de Louw, A.
AU - Bell, H. J.
N1 - Funding Information:
We thank Maeve Philmon for providing excellent technical assistance in the completion of these experiments. This study received internal financial support in the form of laboratory start-up funds from the Department of Medicine, Penn State University College of Medicine . J.M. was supported in part through the SURIP program, Department of Cellular and Molecular Physiology, Penn State University.
PY - 2012/1/15
Y1 - 2012/1/15
N2 - We investigated whether commonly used injectable laboratory anesthetics alter the regulation of augmented breaths (ABs) in different respiratory backgrounds. Male rats were studied on three separate experimental days, receiving one of three injections in randomized order: ethyl carbamate ('urethane'; 1.2mgkg -1), ketamine/xylazine (ket/xyl; 80/10mgkg -1), or normal saline. Following each of the three interventions, breathing was monitored during 15min exposures to normoxia (room air), hypoxia (10% O 2) and hypoxia+CO 2 (10% O 2, 5% CO 2). Urethane anesthesia completely eliminated ABs from the breathing rhythm in room air conditions (p<0.001), and decreased the hypocapnia-dependent component of this response (p<0.001). ket/xyl left the normal incidence of ABs in room air breathing intact but significantly suppressed the hypoxia-induced facilitation of ABs (p=0.0015). These results provide the first clear evidence that laboratory anesthesia can profoundly alter the regulation of ABs including the hypocapnia-dependent component of their facilitation.
AB - We investigated whether commonly used injectable laboratory anesthetics alter the regulation of augmented breaths (ABs) in different respiratory backgrounds. Male rats were studied on three separate experimental days, receiving one of three injections in randomized order: ethyl carbamate ('urethane'; 1.2mgkg -1), ketamine/xylazine (ket/xyl; 80/10mgkg -1), or normal saline. Following each of the three interventions, breathing was monitored during 15min exposures to normoxia (room air), hypoxia (10% O 2) and hypoxia+CO 2 (10% O 2, 5% CO 2). Urethane anesthesia completely eliminated ABs from the breathing rhythm in room air conditions (p<0.001), and decreased the hypocapnia-dependent component of this response (p<0.001). ket/xyl left the normal incidence of ABs in room air breathing intact but significantly suppressed the hypoxia-induced facilitation of ABs (p=0.0015). These results provide the first clear evidence that laboratory anesthesia can profoundly alter the regulation of ABs including the hypocapnia-dependent component of their facilitation.
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U2 - 10.1016/j.resp.2011.10.016
DO - 10.1016/j.resp.2011.10.016
M3 - Article
C2 - 22063924
AN - SCOPUS:83555179114
SN - 1569-9048
VL - 180
SP - 105
EP - 111
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
IS - 1
ER -