Blood flow and intravascular volume of mammary adenocarcinoma 13726A and normal tissues of rat during and following hyperthermia.

The effects of hyperthermia on blood flow and intravascular volume were studied in mammary adenocarcinoma 13762A growing subcutaneously in the leg of Fischer F344 rats. The blood flow was determined using microspheres labelled with 125I, and the blood volume was determined using red blood cells labelled with 51Cr. At the end of heating with water bath at 43.5 degrees C for 1 hour, there was a marked elevation of 51Cr in tumor. The 125I content in tumor also was mildly elevated. Histologically there was a greater number of patent blood vessels per unit area, and they were dilated and hyperemic. In addition, widespread and diffuse hemorrhage could be seen. It appeared, therefore, that the increased 51Cr and 125I label in the tumors immediately after heating was, at least in part, a result of leakage of the labels to extravascular space in addition to possible vasodilation and increased blood flow. At 1 and 5 hours after heating, tumor blood flow was considerably reduced, and at 16 hours both tumor blood flow and blood volume were considerably reduced. Histological examination demonstrated that the tumor blood vessels remained dilated and hyperemic after heating. The effect of heat on blood flow and blood volume in the skin and muscle adjacent to the tumors was also investigated. Blood flow and blood volume in the surrounding normal tissues were significantly elevated at the end of heating. Blood flow was relatively unchanged at 1, 5, and 16 hours after heating, but blood volume was reduced to about one half. These findings indicate that hyperthermia may induce greater damage to vasculature of tumors than normal tissues, and that vascular damage in tumors may take some time to express itself following moderate hyperthermia.

Uptake of carbon monoxide by C3H mice following X irradiation of lung only or total-body irradiation with 60Co.

Carbon monoxide uptake (Vco) and ventilation rate (VR) of C3H mice were determined at 14 weeks following either X irradiation of lungs only or total-body irradiation with 60Co at different dose rates. Following localized X irradiation of lung at 97 cGy/min there was a reduction in Vco, which was inversely related to radiation dose, with a small reduction below control levels being detected at 7 Gy, the lowest dose tested. An increase in VR could be detected only at doses of 11 Gy, or more. Another group of animals received 11.5 Gy total-body irradiation at either 26.2 or 4.85 cGy/min followed by transplantation with syngeneic bone marrow. Following total-body irradiation, Vco was significantly reduced by about 37% at the higher dose rate and 23% at the lower dose rate. In contrast, a trend toward elevated VR was detected only at the higher dose rate. The results indicate that Vco is a sensitive indicator of radiation-induced lung injury and that under the experimental conditions used Vco is a more sensitive indicator of radiation-induced lung injury in C3H mice than VR.