Key result
Brachiocephalic artery occlusion produced no evidence of active pulmonary vasomotion in awake dogs or at any tested halothane concentration.
Brachiocephalic artery occlusion does not induce active pulmonary vasomotion in dogs, regardless of whether they are awake or under halothane anesthesia.
The pulmonary haemodynamic response to brachiocephalic artery occlusion (BCO) was studied in nine dogs. The animals were chronically instrumented for the measurement of pulmonary artery pressure and flow together with left atrial pressure. Measurements were performed in the awake state and also at end-tidal halothane levels averaging 0.74 +/- 0.02 (H1), 0.92 +/- 0.02 (H2) and 1.13 +/- 0.03 (H3) %, with and without nitrous oxide. Halothane at any of the above concentrations, with or without nitrous oxide, had no effect on pulmonary vascular resistance compared to awake values. Most importantly, we found no evidence for active pulmonary vasomotion in response to BCO in the awake animal, or at any anaesthetic concentration.
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Bagshaw et al. (1983) studied this question. Brachiocephalic artery occlusion (BCO) and halothane anaesthesia vs. Awake state was evaluated on Pulmonary haemodynamic response (pulmonary vascular resistance and active pulmonary vasomotion). Brachiocephalic artery occlusion produced no evidence of active pulmonary vasomotion in awake dogs or at any tested halothane concentration.
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