Pulmonary vascular resistance (PVR)

PVR is the resistance to flow that must be overcome to push blood through the lungs.

Any change in the viscosity of blood (such as due to a change in hematocrit) would also affect the measured vascular resistance. There are many factors that alter the vascular resistance. Many of the platelet-derived substances, including serotonin, are vasodilatory when the endothelium is intact and are vasoconstrictive when the endothelium is damaged.

Cholinergic stimulation causes release of endothelium-derived relaxing factor (EDRF) (later it was discovered that EDRF was nitric oxide) from intact endothelium, causing vasodilation. If the endothelium is damaged, cholinergic stimulation causes vasoconstriction.

The major determinant of vascular resistance is small arteriolar (known as resistance arterioles) tone. These vessels are from 450 μm down to 100 μm in diameter (as a comparison, the diameter of a capillary is about 5 to 10 μm). Another determinant of vascular resistance is the pre-capillary arterioles. These arterioles are less than 100 μm in diameter. They are sometimes known as autoregulatory vessels since they can dynamically change in diameter to increase or reduce blood flow

Any change in the viscosity of blood (such as due to a change in hematocrit) would also affect the measured vascular resistance.

Pulmonary vascular resistance (PVR) also depends on the lung volume, and PVR is lowest at the functional residual capacity (FRC). The highly compliant nature of the pulmonary circulation means that the degree of lung distention has a large effect on PVR. This results primarily due to effects on the alveolar and extra-alveolar vessels. During inspiration, increased lung volumes cause alveolar expansion and lengthwise stretching of the interstitial alveolar vessels. This increases their length and reduces their diameter, thus increasing alveolar vessel resistance. On the other hand, decreased lung volumes during expiration cause the extra-alveolar arteries and veins to become narrower due to decreased radial traction from adjacent tissues. This leads to an increase in extra-alveolar vessel resistance. PVR is calculated as a sum of the alveolar and extra-alveolar resistances as these vessels lie in series with each other. Because the alveolar and extra-alveolar resistances are increased at high and low lung volumes respectively, the total PVR takes the shape of a U curve. The point at which PVR is the lowest is near the FRC.

References:

https://www.sciencedirect.com/topics/medicine-and-dentistry/lung-vascular-resistance#:~:text=Pulmonary%20vascular%20resistance%20is%20the,s%2Fcm%E2%88%92%205).

http://en.wikipedia.org/wiki/Vascular_resistance