January 14, 2009Respiration
Adrenergic Mechanisms and the Pulmonary Vascular Response to Respiratory Acidosis
Key result
Adrenergic mechanisms do not mediate respiratory acidosis-induced PVR increases, though beta-blockade enhances vasoconstriction.
Why the study?
The role of sympathetic mechanisms in mediating the pulmonary vasoconstrictor response to respiratory acidosis was unclear.
Does alpha- or beta-adrenergic blockade alter the pulmonary vascular response to respiratory acidosis in intact dogs?
Population
Intact dogs
Comparison
Breathing 5% CO2 with alpha-adrenergic blockade vs beta-adrenergic blockade vs control
Design
Preclinical experimental study
Follow-up
10 minutes
Authors
Discussion
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Member takes
Implication
Beta-blockade may worsen acidosis-induced pulmonary vasoconstriction; leaves open non-adrenergic mediators and needs clinical validation.
Structured PICO
Does alpha- or beta-adrenergic blockade alter the pulmonary vascular response to respiratory acidosis in intact dogs?
P
Population
Intact dogs subjected to respiratory acidosis via 5% CO2 breathing for 10 minutes to study pulmonary vascular responses.
I
Intervention
Breathing 5% CO2 for 10 min during constant level of alpha-adrenergic blockade (phenoxybenzamine) or beta-adrenergic blockade (propranolol)
C
Comparator
Control values (resting levels without blockade)
O
Outcome
Pulmonary vascular resistance (PVR) and pulmonary perfusion pressuresurrogate
Adrenergic mechanisms do not mediate the pulmonary vasoconstrictor response to respiratory acidosis, though beta-blockade enhances it, suggesting unmasking of alpha-receptors.
Cite This Study
Malik et al. (2009) studied Respiratory acidosis. Alpha- and beta-adrenergic blockade (phenoxybenzamine and propranolol) vs. Control values (no blockade) was evaluated on Pulmonary vascular resistance (PVR) and pulmonary perfusion pressure. Adrenergic mechanisms do not mediate the rise in pulmonary vascular resistance induced by respiratory acidosis, though beta-blockade with propranolol enhanced the vasoconstrictor response.