Figure 2 shows two mechanisms by which mechanical stresses develop in the capillary wall. The first is the hoop or circumferential stress that results from the difference of pressure between the inside and outside of the capillary (transmural pressure) acting across the curved capillary wall according to the Laplace relationship. We can think of the capillary as part of a thin-walled cylindrical tube, and in such a structure the wall stress S is given by Pr/t, where P is the transmural pressure, r is the radius of curvature, and t is the thickness of the load-bearing structure.
It is informative to make an approximate calculation of this hoop or circumferential stress. First, how high can the transmural pressure in human capillaries rise during exercise? Pulmonary arterial wedge pressures (a measure of pulmonary venous pressure) as high as 21mmHg have been recorded. Consistent with this, mean pulmonary artery pressures have been shown to be as high as 37.2 mmHg during exercise. Micropuncture studies of the pressures in small pulmonary blood vessels in anesthetized cats have shown that mean capillary pressure is about halfway between arterial and venous pressures, but that much of the fall in pressure occurs in the capillary bed. Therefore a conservative estimate for capillary pressure at midlung during maximal exercise is about 29 mmHg, although the pressures seen by capillary segments in the upstream regions of the bed will be higher. If we add the hydrostatic gradient for capillaries at the bottom of the upright human lung, this gives a capillary pressure there of about 36mmHg .
There are no good data on the radius of human pulmonary capillaries at high capillary pressures, but in rabbit and dogs the value is about 3.5 mm . The most elusive number is the thickness of the load-bearing structure, but if we assume that this is the thin band of type IV collagen in the center of the extracellular matrix of the thin side of the blood-gas barrier, the value is of the order of 50 nm. Inserting these numbers into the Laplace relationship gives a tensile stress in the layer of type IV collagen of about 3 x 105 Nm-2, which is approaching the ultimate tensile strength of type IV collagen as discussed earlier. The upshot of all this is that the normal lung does not appear to have a great deal of reserve in terms of the strength of the capillary wall, and this is consistent with evidence for changes in the structure of the wall that we have seen in elite athletes at high levels of exercise as discussed later.
The second mechanism for increasing mechanical stresses in the capillary wall is increased tension in the alveolar wall as a result of inflating the lung to high volumes. We can think of the alveolar wall as a string of capillaries with part of the longitudinal tension of the wall being transmitted to the capillary walls. As we shall see later, there is strong evidence that when the lung is inflated to high volumes, for example as a result of high levels of positive end-expiratory pressure, the capillary wall is damaged.
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