Fig. 3. (  A ) Composite left pulmonary vascular pressure–flow (LPQ) plots in six dogs during normoxia in the conscious state, during normoxia under ketamine anesthesia, and during hypoxia with systemic arterial PO2of 60 mmHg and 50 mmHg during ketamine anesthesia. Compared with normoxia in the conscious state, there was no change in the LPQ relationship during ketamine anesthesia. During ketamine anesthesia, hypoxia resulted in pulmonary vasoconstriction (*  P < 0.01), which increased (†  P < 0.01) as systemic arterial PO2decreased from 60 mmHg to 50 mmHg. (  B ) Composite hypoxic pulmonary vasoconstriction (HPV) response at systemic arterial PO2of 50 mmHg as a function of left pulmonary flow in the conscious state and during ketamine anesthesia. During ketamine anesthesia, the HPV response was preserved compared with that measured in the conscious state. 

Fig. 3. (  A ) Composite left pulmonary vascular pressure–flow (LPQ) plots in six dogs during normoxia in the conscious state, during normoxia under ketamine anesthesia, and during hypoxia with systemic arterial PO2of 60 mmHg and 50 mmHg during ketamine anesthesia. Compared with normoxia in the conscious state, there was no change in the LPQ relationship during ketamine anesthesia. During ketamine anesthesia, hypoxia resulted in pulmonary vasoconstriction (*  P < 0.01), which increased (†  P < 0.01) as systemic arterial PO2decreased from 60 mmHg to 50 mmHg. (  B ) Composite hypoxic pulmonary vasoconstriction (HPV) response at systemic arterial PO2of 50 mmHg as a function of left pulmonary flow in the conscious state and during ketamine anesthesia. During ketamine anesthesia, the HPV response was preserved compared with that measured in the conscious state. 

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