Zero Stress State is not Permanent

When the blood pressure in a blood vessel is reduced to zero (i.e., when the pressures inside and outside the vessel are the same), the vessel is unloaded. But the vessel may still have a longitudinal residual stress. When the longitudinal stress is released with a cross cut, the vessel shortens. Now if you cut the isolated vessel radially, you will see that it opens up into a sector as shown in Figure 4A. Further cuts will cause only unmeasurable insignificant changes. We may say that as a shell, the cut specimen is at a zero-stress state. The zero-stress state is measured by its opening angle, which is shown in Figure 4A, and defined as the angle between two radii, with origin at the midpoint of the endothelium and tips at the end of the cut endothelium. The opening angle characterizes the zero-stress state of the blood vessel. Further dissection of the vessel wall into an intima-media layer and an adventitia layer shows that these two layers may have different opening angles. So, in the undissected arterial wall, some minor residual stress remains.

The interesting thing about the opening angle is that it changes with tissue remodeling. In the case of a pulmonary artery subjected to hypoxic hypertension, the opening angle changes with time as shown in Figure 4B. We find large opening angles in most curved cylindrical organs. In veins, airways, and intestines, opening angles are large. In round organs such as heart, the description of the zero-stress state is more complex.

We must conclude that living organs at the in vivo state have residual stress and residual strain, and the zero-stress state changes as the tissue remodels.

No-Load State

Normalized Opening Angle

0 s 10 is 111 35 30 Time, days

Figure 4. A: Definition of opening angle a, see text. B: Action of gene PIX #7122 (pleckstrin 2 homolog gene), vs. the change of opening angle (¿¡OA) of the pulmonary arterial trunk vessel. Gene action equals to (mean of gene expression in 4 rats at a specific day/mean of gene expression in 4 rats at day 0)-l. The gene name and its identification number (PIX no.) are listed in the software GENEPIX PRO 3.0 (Axon Instruments), Symbols: small circle, o, normalized change of opening angle, e one SGM flag up; ♦ , normalized gene action, e one SEM flag down (Modified from Ref. 21).

8.2. Morphology as a Motion Picture

The history of the changes of the thickness of the media layer from that at normal condition is described by a solid curve in Figure 5A (21). Before time zero, the animal was in a normal stable equilibrium condition. The existence of such a condition in vivo is an axiom of biology. Thus, the change of media thickness is zero for tsO. At t>0, the media thickness increases with time. The corresponding change of the thickness of the adventitia layer of the pulmonary artery is shown in Figure 5B (21). The sum ofthe thickness ofthe intima, media, and adventitia layer is the thickness of the arterial wall. It is obvious that the thickness ofthe arterial wall changes with time in hypertension. The diameter of the artery also changes with time in hypertension.

8.3. Mechanical Properties Remodel

We measured the mechanical properties of the blood vessel material. We found that if we fit the experimental results with a stress-strain law, the material

No-Load State

Normalized Opening Angle

0 s 10 is 111 35 30 Time, days

Figure 4. A: Definition of opening angle a, see text. B: Action of gene PIX #7122 (pleckstrin 2 homolog gene), vs. the change of opening angle (¿¡OA) of the pulmonary arterial trunk vessel. Gene action equals to (mean of gene expression in 4 rats at a specific day/mean of gene expression in 4 rats at day 0)-l. The gene name and its identification number (PIX no.) are listed in the software GENEPIX PRO 3.0 (Axon Instruments), Symbols: small circle, o, normalized change of opening angle, e one SGM flag up; ♦ , normalized gene action, e one SEM flag down (Modified from Ref. 21).

constants a„ a2, and b„ b2, b4will vary with time. An example is shown in Figure 5C (21), which shows the variation of the circumferential Young's modulus of elasticity with time after the onset of hypertension.

Figure 5. A: Action of gene PIX #8713 (inorganic pyrophosphatase gene), vs. the change of media thickness (Hmd) of pulmonary arterial trunk. B: Action of gene PIX #3759 (osteoblast-specific factor 2, fasciclin I-like gene) vs. the change of adventitia thickness (HJ) of pulmonary arterial trunk. C: Action of gene PIX #44 (dynein, cytoplasmic light polypeptide gene), vs. the change of Young's modulus of elasticity of the pulmonary artery, Ym relating circumferential stress and strain. Symbols: small circle, o, normalized physiological changes, e 1 SEM flag up; ♦ , normalized gene action, e 1 SEM flag down (reprinted from Ref. 21).

Figure 5. A: Action of gene PIX #8713 (inorganic pyrophosphatase gene), vs. the change of media thickness (Hmd) of pulmonary arterial trunk. B: Action of gene PIX #3759 (osteoblast-specific factor 2, fasciclin I-like gene) vs. the change of adventitia thickness (HJ) of pulmonary arterial trunk. C: Action of gene PIX #44 (dynein, cytoplasmic light polypeptide gene), vs. the change of Young's modulus of elasticity of the pulmonary artery, Ym relating circumferential stress and strain. Symbols: small circle, o, normalized physiological changes, e 1 SEM flag up; ♦ , normalized gene action, e 1 SEM flag down (reprinted from Ref. 21).

8.4. Physiological Changes

These examples show that tissue remodeling is a set of continuing processes. For medical reasons, we wish to know how reversible the processes are, how superposable the processes are, how linear the processes are, how nonlinearity can be described, and how important are these nonlinearities. For scientific reasons, we wish to know how these processes can be explained. Can they be explained quantitatively in toto (including histories of all aspects of physiology) by the distribution of ions and functions of ion channels? What other factors must be brought in?

There exists almost a limitless list ofthings to be learned, of ideas to be tried, and of theories to be checked. Yet experimental physiology is empiricism. Mechanics and physics provide a unifying theme for theoretical understanding. How can we go beyond the empiricism and current physics and mechanics, and advance to the next level of understanding and development? We think the next level lies in the study of genes. Someday in the future, we should be able to deduce all the features of tissue formation and remodeling theoretically from the molecular mechanics of the genes. To initiate this research, we shall first show that the physiological changes in tissue remodeling and the actions of the genes are related.

Reducing Blood Pressure Naturally

Reducing Blood Pressure Naturally

Do You Suffer From High Blood Pressure? Do You Feel Like This Silent Killer Might Be Stalking You? Have you been diagnosed or pre-hypertension and hypertension? Then JOIN THE CROWD Nearly 1 in 3 adults in the United States suffer from High Blood Pressure and only 1 in 3 adults are actually aware that they have it.

Get My Free Ebook


Post a comment