Although hemoglobin is necessary for the transport of O2 to the tissues, it performs another function essential to life. This is its function as a “tissue oxygen buffer” system. That is, the hemoglobin in the blood is mainly responsible for stabilizing the PO2 in the tissues. This can be explained as follows.
Hemoglobin Helps Maintain Nearly Constant PO2 in the Tissues. Under basal conditions, the tissues require about 5 milliliters of O2 from each 100 milliliters of blood passing through the tissue capillaries. Referring to the O2-hemoglobin dissociation curve in Figure 1, one can see that for the normal 5 milliliters of O2 to be released per 100 milliliters of blood flow, the PO2 must fall to about 40 mm Hg. Therefore, the tissue PO2 normally cannot rise above this 40 mm Hg level because, if it did, the amount of O2 needed by the tissues would not be released from the hemoglobin. In this way, the hemoglobin normally sets an upper limit on the PO2 in the tissues at about 40 mm Hg.
Fig1. Effect of blood PO2 on the quantity of oxygen bound with hemoglobin in each 100 milliliters of blood.
Conversely, during heavy exercise, extra amounts of O2 (as much as 20 times normal) must be delivered from the hemoglobin to the tissues. However, this delivery of extra O2 can be achieved with little further decrease in tissue PO2 because of (1) the steep slope of the dissociation curve and (2) the increase in tissue blood flow caused by the decreased PO2; that is, a very small fall in PO2 causes large amounts of extra O2 to be released from the hemoglobin. Thus, the hemoglobin in the blood automatically delivers O2 to the tissues at a pressure that is held rather tightly between about 15 and 40 mm Hg.
When Atmospheric Oxygen Concentration Changes Markedly, the Buffer Effect of Hemoglobin Still Maintains Almost Constant Tissue PO2. The normal PO2 in the alveoli is about 104 mm Hg, but as one ascends a mountain or ascends in an airplane, the PO2 can easily fall to less than half this amount. Alternatively, when one enters areas of compressed air, such as deep in the sea or in pressurized chambers, the PO2 may rise to 10 times this level. Even so, the tissue PO2 changes little.
It can be seen from the oxygen-hemoglobin dis sociation curve in Figure 2 that when the alveolar PO2 is decreased to as low as 60 mm Hg, the arterial hemoglobin is still 89 percent saturated with O2—only 8 percent below the normal saturation of 97 percent. Further, the tissues still remove about 5 milliliters of O2 from each 100 milliliters of blood passing through the tissues; to remove this O2, the PO2 of the venous blood falls to 35 mm Hg—only 5 mm Hg below the normal value of 40 mm Hg. Thus, the tissue PO2 hardly changes, despite the marked fall in alveolar PO2 from 104 to 60 mm Hg.
Fig2. Oxygen-hemoglobin dissociation curve.
Conversely, when the alveolar PO2 rises as high as 500 mm Hg, the maximum O2 saturation of hemoglobin can never rise above 100 percent, which is only 3 percent above the normal level of 97 percent. Only a small amount of additional O2 dissolves in the fluid of the blood, as will be discussed subsequently. Then, when the blood passes through the tissue capillaries and loses several milliliters of O2 to the tissues, this reduces the PO2 of the capillary blood to a value only a few milliliters greater than the normal 40 mm Hg. Consequently, the level of alveolar O2 may vary greatly—from 60 to more than 500 mm Hg PO2—and still the PO2 in the peripheral tissues does not vary more than a few milliliters from normal, demonstrating beautifully the tissue “oxygen buffer” function of the blood hemoglobin system.
