Acute Effects of Burn Injury on Tissue Gas Tensions in the Rabbit

Abstract

Early effects of 10% full-thickness skin burn on subcutaneous tissue PO2 and PCO2 levels were studied in anesthetized rabbits. Tissue gas tensions were determined by means of implanted Silastic tonometers in two different areas in each animal--the burn site itself, and an area remote from the injured tissue. Thermal injury resulted in a rapid, progressive decrease of the tissue PO2 in both locations, with the greatest decrease at the burn site. The minimum PO2 levels were achieved 3-6 hours post burn. The POC2 values increased markedly both in the burn areas and in the distant tissues immediately after the trauma and reached their maximum within 1-3 hours post burn. The greatest accumulation of carbon dioxide occured at the burn site. Six hours after burn the tissue PCO2 levels had been normalized. During the 6-hour observation period the mean arterial PO2 of the burned animals increased gradually from 73 to 95 mmHg, while the mean arterial PCO2 decreased by more than 50% of the original level. The latter effect was probably caused by hyperventilation. Intra-arterial injection of 5 ml of arterial blood from a burned rabbit into a control animal 3 hours post burn induced a significant decrease in cardiac output as well as decline in arterial, intraperitoneal, and tissue PO2 levels in the control rabbit, probably due to a circulatory depressant factor(s) present in the burn blood. When the same test was carried out one hour post burn or with normal blood, no decrease in oxygen tension occurred.

Oxygen concentration in milk of healthy and mastitic cows and implications of low oxygen tension for the killing ofStaphylococcus aureusby bovine neutrophils

“…The O 2 tension in normal milk of cows was in the same range as that reported in the mammary gland tissue of the rabbit (Cross & Silver, 1961) and in other tissues such as subcutaneous tissue (Niemimen et al 1977) and muscle (Jussila et al 1978). However, direct comparison of PO 2 is difficult because proximity to the blood supply and other factors affecting diffusion of O 2 can profoundly affect the result (Norton & Rand, 1974;Nunn, 1977).…”

“…Inflammation of the mammary gland results in a dramatic reduction in the O 2 concentration of milk to a level < 10% of that in normal milk. A reduction of PO 2 associated with inflammation has been reported in other situations such as abscesses (Silver, 1977;Hays & Mandell, 1974), maxillary sinusitis (Carnfelt & Lundberg, 1977) and burns (Niemimen et al 1977). This fall in O 2 concentration is probably caused by an increased demand for O 2 in the udder owing to O 2 utilization by the large numbers of neutrophils migrating to the inflamed area as inflammation associated with bacterial infections results in larger falls in PO 2 than those associated with sterile inflammatory responses and is correlated with the accumulation of neutrophils (Silver, 1977).…”