Tissue temperature

When administered intraperitoneaHy, sulfolane is excreted both unchanged and as 3-hydroxysulfolane [13031 -76-0] (24). Sulfolane injected intraperitoneaHy in mice and rats at 200—800 mg/kg at ambient temperatures of 15 and 25°C caused a dose-related inhibition of the metaboHc rate and hypoactivity, accompanied by hypothermia 60 min after injection. Despite their hypothermic condition these animals did not select a warm ambient temperature. Because sulfolane toxicity appears to be greater upon increased tissue temperature, the behavior of these animals seeking lower environmental temperature appears to enhance their chance of survival (25—28). 

Each of these chemical changes promotes vasodilation of arterioles. In addition, the increase in tissue temperature associated with increased metabolism further contributes to metabolic vasodilation. The resulting increase in local blood flow restores these substances to their resting values. More oxygen is delivered and excess carbon dioxide, hydrogen and potassium ions, and adenosine are removed. 

We have considered the Einolf and Carstensen model as a basis for those bioeffects in which it appears that thermal noise at normal tissue temperature is substantially larger than the tissue components of imposed electric fields (23, 30). The Boltzmann equation may be written in terms that model the cell surface in the region of the counterion layer as a low-pass filter ... 

No processes should raise tissue temperature to higher than 60 °C, as this will cause severe loss of antigenicity that may not... 

If we ignore transpiration and assume uniform tissue temperatures, the time constant for temperature changes equals... 

E Assume that 30% of the incident shortwave is absorbed by the stem surface for the cactus with spines. What is the net energy balance averaged over the stem surface What is the hourly change in mean tissue temperature Assume that the volumetric heat capacity is 80% of that of water, and ignore transpiration. 

Okuyama R, Marshall S. UDP-N-acetylglucosaminyl transferase (OGT) in brain tissue temperature sensitivity and subcellular distribution of cytosolic and nuclear enzyme. J. Neurochem. 2003 86 1271-1280. 

Unlike photochemical injury, thermal injury does not exhibit reciprocity between intensity and length of exposure. Injury only occurs if the light intensity is sufficient to raise tissue temperature above 45°C. In the case of less intense light and longer exposure, normal heat transfer mechanisms within the body serve to cool the exposed tissue. 

C. H. Barlow et al., Tissue Temperature by Near-Infrared Spectroscopy, in Optical Tomography, Photon Migration, and Spectroscopy of Tissue and Model Media (B. Chance and R. R. Alfano, eds.), SPIE, 2389, 818 (1995). 

Here, T is the tissue temperature, C is the tissue heat capacity, p is the tissue density, k is the tissue thermal conductivity, Qm is the rate of metabolic heat generation, and Qb is the rate of heat exchange with blood. Qm is generally small and is calculated from the oxygen consumption of the tissue (Jain, 1984). The estimation of Qb is discussed next. 

Implicit in this equation is the assumption that because of a large vascular surface area, the blood temperature equilibrates with the tissue temperature. The concept of effective thermal conductivity has been used by several investigators in thermal physiology (Shitzer and Eberhart, 1985). Jain and Wei (1977) also used this concept to describe the drug distribution in tumors. 

It is assumed that there is perfect heat transfer between tissue and blood in the capillaries and the temperature of blood leaving the capillaries is equal to the local tissue temperature. This is not strictly correct, but it seems to be a reasonable approximation. Recently Keller (30) has pointed out that blood flowing through small vessels may serve as an effective heat transfer medium which, in effect, increases the apparent thermal conductivity of tissue. 

Lowering the brain tissue temperature during the preparation is effective in reducing file sensitivity of neurons to ischemia. 

The safety limit for cranial use is 30 mW of power, and the snrronnding tissue temperature should be raised by no more than 1°C otherwise cells will be killed (Patel, 2009). 

When the active electrode touches the tissue and the current flows directly from the electrode into the tissue without forming an arc, the rise in tissue temperature follows the bioheat equation... 

Sandsund, M., et al., 2012. Effect of ambient temperature on endurance performance while wearing cross-country skiing clothing. Eur. J. Appl. Physiol. 112 (12), 3939 3947. Thomley, L.J., Maxwell, N.S., Cheung, S.S., 2003. Local tissue temperature effects on peak torque and muscular endmance during isometric knee extension. Eur. J. Appl. Physiol. 

For the above reasons, even if the heat transfer function of the vascular system has been appreciated since the mid-nineteenth century, only in the past 2 decades, has there been a revolution in our understanding of how temperature is controlled at the local level, both in how local microvascular blood flow controls the local temperature field and how the local tissue temperature regulates local blood flow. 

The effects of blood flow on heat transfer in living tissue have been examined for more than a century, dating back to the experimental studies of Bernard in 1876. Since then, mathematical modeling of the complex thermal interaction between the vasculature and tissue has been a topic of interest for numerous physiologists, physicians, and engineers. A major problem for theoretical prediction of temperature distribution in tissue is the assessment of the effect of blood circulation, which is the dominant mode of heat removal and an important cause of tissue temperature inhomogeneity. 

Pennes Bioheat Transfer Model. It is known that one of the primary functions of blood flow in a biological system is its ability to heat or cool the tissue, depending on the relative local tissue temperature. The existence of a temperature difference between the blood and tissue is taken as evidence of its function to remove or release heat. On the basis of this speculation, Pennes [Pennes, 1948] proposed his famous bioheat transfer model, which is called Pennes bioheat equation. Pennes suggested that the effect of blood flow in the tissue be modeled as as heat source or sink term added to the traditional heat conduction equation. The Pennes bioheat equation is given by... 

This is a partial differential equation for the tissue temperature. As long as an appropriate initial condition and boundary conditions are prescribed, the transient and steady-state temperature field in the tissue can be determined. 

The limitations of the Pennes equation come from the basic assumptions introduced in this model. First it is assumed that the temperature of the arterial blood does not change when it travels from the heart to the capillary bed. As shown in Sec. 2.2, small temperature variations occur only in blood vessels with a diameter larger than 300 jum. Another assumption is that the venous blood temperature is approximated by the local tissue temperature. This is valid only for blood vessels with a diameter smaller than 50 ju.m. Thus, without considering the thermal equilibration in the artery and vein in different vessel generations, the Pennes source term obviously overestimates the effect of blood perfusion. To accurately model the effect of blood perfusion, the temperature variation along the artery and the heat recaptured by the countercurrent vein must be taken into consideration. 

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