Hypoxic pulmonary vasoconstrictor response

Halothane (Fluothane) Mechanism unclear. Induces rapid, comfortable anesthesia and skeletal muscle relaxation. i cardiac output, mild T of systemic vascular resistance, typically no effect on heart rate, 1 right atrial pressure, moderate depression of myocardial function, most likely to sensitize myocardium to catecholamines and i baroreceptor reflex. t ventilation control (T tidal volume, >1 rate of breathing, i response to CCfe and hypoxia), bronchodilation (mostpotent), No effect on hypoxic pulmonary vasoconstrictor response, depression of ciliary function and mucous clearance. 

Isoflurane (Forane) Least likely to T right atrial pressure, depress myocardial function, or sensitize myocardium to catecholamines. Greatly i systemic vascular resistance. Marked T heart rate Least potent suppressor of ventilation control and bronchodilation. Marked suppression of hypoxic pulmonary vasoconstrictor response, little effect on secretions. 

The carotid body is the primary sensor of hypoxemia across many species. When stimulated by a decrease in Pa02 or hypoxic perfusates, it promotes many cardiopulmonary responses. Ventilation, static lung volumes, airway resistance, and airway secretions increase. The hypoxic pulmonary vasoconstrictor response and the systemic vascular vasodilator responses are attenuated bronchial vascular resistance decreases (for review see Ref 1). A current question is How does the carotid body transduce a low Pa02 stimulus into increased neural output traveling to the nucleus tractus sohtarii Here the increased neural traffic is processed and distributed to various other nuclei responsible for the increased breathing and the autonomicaUy regulated changes in the cardiopulmonary system. 

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