Background: Hypoxic pulmonary vasoconstriction (HPV) is one cause of mountain sickness such as lung edema. However, few studies have examined the effects of increased pulmonary blood flow and viscosity on HPV.
Objectives: We postulated that increasing blood flow and viscosity inhibit HPV during exercise. We therefore measured pulmonary arterial pressure with stepwise changes of perfusate flow and viscosity under conditions of normoxia (20% O
2) and hypoxia (0% O
2) in isolated perfused rat arteries. We used a pharmacological inhibitor (L-NAME) to assess whether nitric oxide synthase contributes to flow- and viscosity-induced inhibition of HPV. Methods: Isolated pulmonary arteries were attached to the blood vessel perfusion system and pulmonary arterial pressure was recorded. The perfusate was physiological salt solution (PSS) without or with 5% Dextran (PSSD). The flow rate of the perfusate was increased from 0.03 to 0.0902 mL/g/min in stepwise increments of 0.02 mL/g/min over 5 min during exposure to normoxia and hypoxia.
Results: The increase in flow and viscosity of both perfusates did not affect HPV. However, increasing flow and viscosity of each perfusate increased HPV after L-NAME administration. Conclusion: We found that HPV might be inhibited by NO release induced by shear stress such as pulmonary blood flow and viscosity, in rat isolated pulmonary arteries.
View full abstract