Wholebody hyperthermia

The critical temperature of 42.2 °C for cellular heat injury in living animals and man has been established only recently as a direct result of the application of whole-body hyperthermia in the treatment of cancer. Patients have withstood up to 4 h exposure to internal temperatures of 41.8 °C, monitored by esophageal probes, without harmful effects. Cellular injury is irreversible at 45 °C and varies directly with the duration of exposure and exponentially with the temperature elevation. Cellular injury from secondary and tertiary protein denaturation occurs in 50 min at 42.2 °C, 20 min at 43 °C, and 10 min at 45 °C ( SMnla,:eL&L 1.99.4).

Metabolism increases rapidly with increasing temperature until 42.2 °C is reached. At about this temperature, the cell's capacity to balance anabolism and catabolism is altered, phosphorylation is uncoupled, cell membranes become disrupted, the sodium pump fails, and cellular proteins are denatured. This involves all enzymes in living plants and animals, effectively halting cellular respiration and possibly being responsible for the more extensive injury and higher fatality seen with exertional heatstroke. Heat shock proteins, which are also found in sepsis, are manufactured by normal cells with sublethal heat exposure (40-45 °C) and account for the cardiovascular collapse.

Cases of heatstroke survivors with rectal temperatures of 47 °C are unexplained ( KhogaliJ994). At this temperature all living plant and animal cells (eukaryocytes) and most bacteria and algae (prokaryocytes) are rapidly destroyed, except for a special class of bacteria and fungi called thermophiles. Thermophiles belong to a new superkingdom, and are normally present in soil and feces; they may be responsible for the tolerance to high temperatures (47 °C) that would otherwise be incompatible with life.

Hypoxia has been suggested as one cause of cardiovascular collapse, although direct evidence is lacking. The lack of cellular enzymatic function associated with high temperatures is associated with normal tissue oxygen, high venous oxygen saturation, and low accumulation of lactate levels ( Ash.,§nd,K§sh.m§e.ry,199.5), suggesting, as discussed above, that oxygen is being delivered but not utilized.

Rebound temperature elevation has frequently been reported following aggressive external cooling. This is similar to the delayed elevation of temperature following prolonged whole-body hyperthermia. It is possible that this 'rebound' is not the result of inadequate cooling but is an expected response to the cellular injury which has occurred.

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