Experimental data show that nervous tissue is sensitive to heat. Animal data indicate that the maximum tolerated heat dose after local hyperthermia of the central nervous system (CNS) lies in the range of 40-60 min at 42-42 x 5 degrees C or 10-30 min at 43 degrees C. No conclusions concerning the heat sensitivity of nervous tissue can be derived from clinical studies using localized hyperthermia. The choice whether or not to exceed the critical heat dose, as derived from laboratory studies, in clinical practice is very much dependent on the clinical situation such as the anatomical site and volume of the tissue involved, and prior therapy. Data on clinical application of whole body hyperthermia (WBH) show that nervous tissue can withstand a slightly higher heat dose than after localized heating, which might be the result of developing thermal resistance during treatment. Expression of thermotolerance was observed in the spinal cord of laboratory animals. After WBH in man at a maximum between 40 and 43 degrees C for 6 h-30 min CNS complications were reported, but other complications seemed to be more life-threatening. Most studies indicate that impairment of the CNS after WBH was not due to direct heat injury to the brain or spinal cord, but was secondary as a result of physiological changes. Heat, at least if applied shortly after X-rays, enhances the response of nervous tissue to radiation. Neurotoxicity of chemotherapeutic drugs does not seem to be a limiting complication in hyperthermia if combined with chemotherapy, but only few data are available. The limited clinical experience shows that safe hyperthermic treatment of CNS malignancies or tumours located close to the CNS seems feasible under appropriate technical conditions with adequate thermometry and taking the sensitivity of the surrounding normal nervous tissue into account.

Radiation-induced heart disease (RIHD), characterized by accelerated atherosclerosis and adverse tissue remodeling, is a serious sequelae after radiotherapy of thoracic and chest wall tumors. Adverse cardiac remodeling in RIHD and other cardiac disorders is frequently accompanied by mast cell hyperplasia, suggesting that mast cells may affect the development of cardiac fibrosis. This study used a mast celldeficient rat model to define the role of mast cells in RIHD. Mast cell-deficient rats (Ws/Ws) and mast cell-competent littermate controls (+/ /+ + +) were exposed to 18 Gy localized single-dose irradiation of the heart. Six months after irradiation, cardiac function was examined by echocardiography and Langendorff-perfused isolated heart preparation, whereas structural changes were assessed using quantitative histology and immunohistochemical analysis. Mast celldeficient rats exhibited more severe postradiation changes than mast cell-competent littermates. Hence, mast celldeficient rats exhibited a greater upward/ /leftward shift in the left ventricular (LV) diastolic pressure-volume relationship (P = 0.001), a greater reduction in in vivo LV diastolic area ( from 0.50 F F 0.024 cm in age-matched controls to 0.24 F F 0.032 cm after irradiation; P = 0.006), and a greater increase in LV posterior wall thickness ( from 0.13 F F 0.003 cm in agematched controls to 0.15 F F 0.003 cm after irradiation; P = 0.04). Structural analysis revealed more pronounced postradiation accumulation of interstitial collagen III but less myocardial degeneration in hearts from mast cell-deficient rats. These data show that the absence of mast cells accelerates the development of functional changes in the irradiated heart, particularly diastolic dysfunction, and suggest that, in contrast to what has been the prevailing assumption, the role of mast cells in RIHD is predominantly protective. (Cancer Res 2005; 65(8): 3100-7)

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: Background and Objectives : Anesthesiologists are reluctant to consider higher levels for spinal anesthesia, largely due to direct threats to the spinal cord. The goal of this study is to investigate, with magnetic resonance imaging (MRI), the distances between the relevant structures of the spinal canal (spinal cord, thecal tissue, etc.) to determine modal anatomical positions for neuraxial anesthesia. Method : A group of 19 patients were imaged with an MRI scanner in supine position. Medial sagittal slices of the thoracic and lumbar spine were measured for the relative distances between anatomical structures, including epidural space, dura, and spinal cord. Results : The posterior dura -spinal cord distance is significantly greater in the middle thoracic region than at upper and lower thoracic levels (e.g. T6 9.5 ± 1.8 mm, T12 3.7 ± 1.2 mm, p < 0.001, T1 4.7 ± 1.7 mm, p < 0.001). There is variation in modal distances between the structures important for neuraxial anesthesia, at different levels of the spinal canal. Conclusions :The spinal cord tends to follow the straightest line through the imposed geometry of the spine. Considering the necessary angle of entry of the needle at mid-thoracic levels, there is relatively (more than at upper thoracic and lumbar levels) substantial separation of cord and surrounding thecal tissue. Anesthesiologists perform spinal blockades up to the L2-L3 interspace, but avoid higher levels for fear of neurological damage. The information that there is substantially more space in the dorsal subarachnoid space at thoracic level, might lead to potential applications in regional anesthesia. In contrast, the cauda equina sits more dorsally in the lumbar region.