Tissue tension

The population distribution elements of this model are described in Figure 3. Those distributions responding to a particular endpoint are plotted as a function of the inert gas tension in a characteristic tissue. This response would occur in an animal that had been exposed to a high pressure and then returned directly to 1 atm. Bubble formation begins when the tissue tension exceeds some lower limit and the population is... 

The pressure-based data were carried out by diving to increasing depths with a bottom time of 31 minutes. This time was determined from r8iow so that the tissue controlling the mortality incidence would be the slowest tissue (T8k)W) under all conditions. Figure 8 is a plot of the percent mortality vs. the inert gas tissue tension in the slowest tissue for these PB data. 

One may compute the inert gas tissue tension in the slow tissue at the end of the shorter bottom time dives in the TB series. These data points are plotted on Figure 9 where they are superimposed on the data from Figure 8. The dives corresponding to 2, 4, and 8 minutes fall significantly above the best fit curve based on the PB data. 

If we assume that all tissues have the same susceptibility to bubble formation, their inert gas tissue tension should be the same as the best experimental line for the PB data. By this method we can calculate back to determine what the time constant of these faster tissues would be in order to acquire this level of inert gas tension. When this is done, the tissue time constant is 6.3 minutes for the two-minute bottom time experiments. While this is significantly faster than the 25.5-minute constant measured for the slow tissues, it is still significantly greater than the slowest time constant measured in the nitrogen washout studies (Figure 12). Thus, it is assumed that the well-perfused tissues of the body would never be the sites of bubble formation for dives greater than two minutes. These data also confirm experimentally the generally held notion that there is a spectrum of response time for the body tissues. 

The oxygen consumption rate as a function of tissue tension is considered to have a Michaelis-Menten form. [It has been shown (8) that neuron activity increases to a much higher rate as tissue oxygen tension decreases (injury potential) and then it drops off to essentially zero. This would indicate that a true Michaelis-Menten form would not be followed.] A zero-order reaction is assumed for high tissue tension a first-order reaction is then imposed when the tension drops to a prescribed value, and then the consumption rate is set equal to zero at a second prescribed tissue tension (i.e., PT > 30 mm Hg, zero-order reaction, 20 < PT < 30 mm Hg, first-order reaction, and PT < 20, zero consumption). When the consumption rate goes to zero, the model restricts oxygen transport in the reverse direction (tissue to blood) even if the blood tension drops below the tissue tension. This assumption was included to achieve a flat plateau like the experimental results however, it is still open to speculation. Back diffusion can be considered in the model by simply removing a diode from the computer circuit. (This assumes a barrier to tissue washout.)... 

The experimental response curves demonstrate a constant tissue tension for as long as 60 sec after a drop in arteriole tension occurs (14). When tissue tension begins to drop, the recordings show that flow rate increases. This characteristic response has not been explained at this time however, it indicates that facilitated or active transport of oxygen in tissue might be present. Carefully planned experiments could elucidate this phenomenon. 

As reviewed in the section on endocardial lead extraction, the irregularity of a shocking coil may promote tissue ingrowth and will iuCTease risk of adhesion (53). In dual coil systems, the proximal coil has the potential to be placed with tissue tension along the SVC, a risk factor for adhesion. For this reason, the... 

As the immediate external environment of every Uving cell, fascia directly or indirectly influences the metaboUsm of these cells. Abnormal pressure or tension will alter the diffusion of nutrients and the eUmination of wastes, resulting in alterations in cell fimctioa A cell needs proper maintenance of osmotic pressure and tissue tension of the sunotmding interstitial fluid and ground substance for proper metabolism. 

Once the acute inflammation has subsided, some tissue tension will still remain. Range of motion will improve but may still be limited. The patient may now be treated with appropriate osteopathic manipulative techniques to the injured area or wherever somatic dysfunction is found. Muscle energy, counterstrain, lymphatic drainage techniques, cranial, and facilitated positional release techniques may be used judiciously. Thrusting techniques should not be used until the soft tissues are no longer boggy and warm. If necessary, they may be used to correct stubborn somatic dysfunctions with firm barriers to motion. 

Note tissue tension and vertebral positional rotation, as described for the conventional method. 

The brain itself is almost totally insensitive to pain. The scalp, arteries, muscles, mucous membranes of the sinuses, ear, and the teeth are all pain-sensitive structures. The crucial areas in the creation of headache are the suboccipital and upper cervical areas as well as the scalp. In the upper two cervical segments, the sensory fibers of the first three cervical segments are joined by the descending tracts of cranial nerves V, IX, and X. These three cranial nerves, along with the second cervical nerve, mediate the referral of excessive coimective tissue tension in the cervical area as pain in the cranial vault or cephalgia. 

Sutures are required to hold tissues together until the tissues can heal adequately to support the tensions exerted on the wound duting normal activity. Sutures can be used ia skin, muscle, fat, organs, and vessels. Nonabsorbable sutures are designed to remain ia the body for the life of the patient, and are iadicated where permanent wound support is required. Absorbable sutures are designed to lose strength gradually over time by chemical reactions such as hydrolysis. These sutures are ultimately converted to soluble components that are then metabolized and excreted ia urine or feces, or as carbon dioxide ia expired air. Absorbable sutures are iadicated only where temporary wound support is needed. 

At present there is only one commercially available tissue adhesive with approved on-label indications for skin closure. 2-Octyl-cyanoacrylate (Dermabond, Ethicon, Inc., Somerville, NJ) is presently indicated for skin closure in wounds which are not under extreme tension. This tissue adhesive is approved for topical skin application only. It is not indicated for internal use. The material is useful in closing traumatic skin lacerations [4,5] after wounds have been thoroughly cleaned as well as for minimally invasive surgical incisions and even larger surgical incisions in elective cases. The cyanoacrylate is applied while the skin... 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

The high active tension and/or high active strain that occurs in muscle during lengthening contractions is believed to cause mechanical disruption of muscle fibers and connective tissue (Armstrong, 1984 Lieber and Friden, 1993). Activa-... 

Tetanus occurs when Cl. tetani, ubiquitous in the soil and faeces, contaminates wounds, especially deep puncture-type lesions. These might be minor traumas such as a splinter, or major ones such as battle injury. At these sites, tissue necrosis and possibly microbial growth reduce the oxygen tension to allow this anaerobe to multiply. Its growth is accompanied by the production of a highly potent toxin which passes up peripheral nerves and diSuses locally within the central nervous system. It acts like strychnine by affecting normal function at the synapses. Since the motor nerves of the brain stem are the shortest, the cranial nerves are the first affected, with twitches of the eyes and spasms of the jaw (lockjaw). 

Phagocyte-derived ROMs have been implicated in the pathogenesis of a number of pulmonary diseases, including emphysema, acute respiratory distress syndrome, and various environmental diseases such as asbestos-related fibrosis and cancer (Mossman and Marsh, 1985). The relatively high oxygen tension in pulmonary tissue renders the lung prone to oxidative stress (Edwards and Lloyd, 1988). 

Muscle spasm. The pain induced by muscle spasm results partially from the direct effect of tissue distortion on mechanical nociceptors. Muscle spasm also causes tissue ischemia. The increased muscle tension compresses blood vessels and decreases blood flow. Furthermore, the increased rate of metabolism associated with the spasm exacerbates the ischemia. As discussed earlier, ischemia leads to stimulation of polymodal nociceptors. 

Pulmonary surfactant decreases surface tension of alveolar fluid. Reduced surface tension leads to a decrease in the collapsing pressure of the alveoli, an increase in pulmonary compliance (less elastic recoil), and a decrease in the work required to inflate the lungs with each breath. Also, pulmonary surfactant promotes the stability of the alveoli. Because the surface tension is reduced, the tendency for small alveoli to empty into larger ones is decreased (see Figure 17.2, panel b). Finally, surfactant inhibits the transudation cf fluid out of the pulmonary capillaries into the alveoli. Excessive surface tension would tend to reduce the hydrostatic pressure in the tissue outside the capillaries. As a result, capillary filtration would be promoted. The movement of water out of the capillaries may result in interstitial edema formation and excess fluid in the alveoli. 

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