Measurements conducted on microvessels show that the O2 saturation at the entrance of capillaries typically drops to around 80% due to the diffusion of O2 from arterioles and small arteries. Additionally, the loading of CO2 and resulting shifts in the oxyhemoglobin dissociation curve occur in the precapillary vessels. As a result, not only does gas exchange take place at the capillaries, but O2 and CO2 can also pass directly between adjacent arterioles and venules, and possibly between arteries and veins (countercurrent exchange). This countercurrent exchange leads to a diffusion-based diversion of gas away from the capillaries, potentially limiting the supply of O2 to the tissue when blood flow rates are low.

Capillary filtration occurs in regions where the permeability of the capillary endothelial membrane is not uniform. For instance, liver capillaries exhibit higher permeability, allowing albumin to escape at a rate several times greater than in less permeable muscle capillaries. Moreover, permeability varies along the length of the capillary, with greater permeability observed at the venous ends compared to the arterial ends. The venules possess the highest permeability due to a larger number of pores in these regions.

Filtration primarily occurs through the apertures (pores) present in the endothelial walls of the capillaries. Skeletal and cardiac muscle capillaries contain pores with diameters of approximately 4 nm. Clefts also exist between adjacent endothelial cells in cardiac muscle, with the narrowest point measuring around 4 nm. However, these clefts (pores) are sparse and only constitute approximately 0.02% of the capillary surface area. Cerebral capillaries lack pores due to the presence of the blood-brain barrier, which prevents the entry of many small molecules.

In addition to clefts, certain capillaries with higher porosity (e.g., those in the kidneys and intestines) feature fenestrations ranging from 20 to 100 nm in width. On the other hand, capillaries in the liver possess a discontinuous endothelium. These fenestrations and discontinuous endothelia allow the passage of molecules that are too large to traverse the intercellular clefts of the endothelium.

The movement of water across the capillary wall depends on the algebraic sum of the hydrostatic and osmotic pressure differentials. An increase in intracapillary hydrostatic pressure encourages fluid movement from the vessel interior to the interstitial space, while an increase in the concentration of osmotically active particles within vessels facilitates fluid movement into the vessels from the interstitial space.

Hydrostatic pressure within capillaries, also known as blood pressure, is not constant and is influenced by arterial and venous pressure, as well as precapillary resistance in the arterioles and postcapillary resistance in the venules and small veins. Higher arterial or venous pressure elevates capillary hydrostatic pressure, while a decrease in arterial or venous pressure has the opposite effect. An increase in arteriolar resistance or arterial closure leads to a reduction in capillary pressure, while greater resistance to flow in venules and veins raises capillary pressure.

Hydrostatic pressure serves as the primary driving force for capillary filtration. Changes in venous pressure have a greater impact on capillary hydrostatic pressure compared to equivalent changes in arterial pressure. Approximately 80% of an increase in venous pressure is transmitted back to the capillaries.

Capillary hydrostatic pressure (Pc) varies across different tissues. On average, direct measurements in human skin show values of approximately 32 mm Hg at the arterial end of capillaries and around 15 mm Hg at the venous end of capillaries at the level of the heart.
Measurements of the partial pressure of O2 (PO2) and O2 saturation of blood in microvessels indicate that in many tissues, O2 saturation at the entrance of capillaries has decreased to approximately 80% as a result of diffusion of O2 from arterioles and small arteries. Moreover, CO2 loading and the resulting intravascular shifts in the oxyhemoglobin dissociation curve occur in the precapillary vessels. Hence, in addition to gas exchange at the capillaries, O2 and CO2 pass directly between adjacent arterioles and venules and possibly between arteries and veins (countercurrent exchange). The countercurrent exchange represents a diffusional shunting of gas away from the capillaries; this shunting may limit the supply of O2 to the tissue at low blood flow rates.
Capillary Filtration. The permeability of the capillary endothelial membrane is not uniform. For example, liver capillaries are quite permeable, and albumin escapes from them at a rate several times greater than that from the less permeable muscle capillaries. Furthermore, permeability is not uniform along the length of the capillary. The venous ends are more permeable than the arterial ends, and permeability is greatest in the venules, a property attributed to the greater number of pores in these regions.
Where does filtration occur? Some water passes through the capillary endothelial cell membranes, but most flows through apertures (pores) in the endothelial walls of the capillaries (
Figs. 17.26 17.27 ). The pores in skeletal and cardiac muscle capillaries have diameters of approximately 4 nm. There are clefts between adjacent endothelial cells in cardiac muscle, and the gap at the narrowest point is approximately 4 nm. The clefts (pores) are sparse and represent only approximately 0.02% of the capillary surface area. Pores are absent in cerebral capillaries, where the blood-brain barrier blocks the entry of many small molecules.
In addition to clefts, some of the more porous capillaries (e.g., those in the kidneys and intestines) contain fenestrations 20 to 100 nm wide, whereas other capillaries (e.g., those in the liver) have a discontinuous endothelium (see
Fig. 17.27 ). Fenestrations and discontinuous endothelia allow the passage of molecules that are too large to pass through the intercellular clefts of the endothelium.
The direction and magnitude of water movement across the capillary wall can be estimated as the algebraic sum of the hydrostatic and osmotic pressure that exists across the wall. An increase in intracapillary hydrostatic pressure favors movement of fluid from the vessel interior to the interstitial space, whereas an increase in the concentration
CHAPTER 17 Properties of the Vasculature of osmotically active particles within vessels favors movement of fluid into the vessels from the interstitial space (
Fig. 17.28
Hydrostatic Forces. Hydrostatic pressure (blood pressure) within capillaries is not constant. Instead, it depends on arterial and venous pressure and on precapillary resistance (in the arterioles) and postcapillary resistance (in the venules and small veins). An increase in arterial or venous pressure elevates capillary hydrostatic pressure, whereas a reduction in arterial or venous pressure has the opposite effect. An increase in arteriolar resistance or closure of arteries reduces capillary pressure, whereas a greater resistance to flow in venules and veins increases capillary pressure.
Hydrostatic pressure is the principal force in capillary filtration. A given change in Pv produces a greater effect on capillary hydrostatic pressure than does the same change in Pa. Approximately 80% of an increase in Pv is transmitted back to the capillaries.
Capillary hydrostatic pressure (Pc) varies from tissue to tissue. Average values, obtained from direct measurements in human skin, are approximately 32 mm Hg at the arterial end of capillaries and approximately 15 mm Hg at the venous end of capillaries at the level of the heart (see