Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature measuring sites are completely non-invasive and easy to use — especially in patients not having general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients having general anesthesia exceeding 30 minutes in duration, and in patients having major operations under neuraxial anesthesia.

Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature triggering cold defenses including arterio-venous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, and the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extant than general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.

/pdf/temperature-monitoring-and-perioperative-thermoregulation-cj55n8uy0l.pdf

Temperature monitoring and perioperative thermoregulation.

Biosynthesis of dicarboxylic acids by carbon dioxide fixation; isolation and properties of an enzyme from pigeon liver catalyzing the reversible oxidative decarboxylation of 1-malic acid.

Rats were exposed to 98.5% oxygen at 765 torr for 6–72 hr. The pulmonary changes were investigated by electron microscopy and by morphometric methods. A progressive thickening of the air-blood barrier, from the normal 1.5 to 3 µ after 3 days, was due primarily to enlargement of the interstitial space by accumulation of edema which was replaced secondarily by cells and fibrin. This was accompanied by destruction of about 50% of the capillaries. Morphometric data allowed an estimate of the degree of impairment of lung function. The primary cellular damage was located in endothelial cells which underwent cytoplasmic changes and, finally, fragmentation. In contrast, the damage to the epithelial lining of alveoli was relatively scarce compared to the extensive endothelial changes. This pertained even to severely damaged lungs with 65% of the alveoli obliterated by a heterogeneous exudate. Possible causes for this apparently different reaction of epithelium (the first target cell) and endothelium to toxic oxygen effects are discussed.

/pdf/development-of-fine-structural-damage-to-alveolar-and-2lip08tk48.pdf

Development of fine structural damage to alveolar and capillary lining cells in oxygen-poisoned rat lungs.

IN two instances, the distribution of isotopic carbon in the product of a metabolic process has been used to infer that a symmetrical intermediate compound is not involved. Wood et al.1 showed that isotopic carbon, introduced as carbon dioxide together with pyruvate, led to the formation of ketoglutarate which contained isotopic carbon only in the carboxy group next to the keto group; on these grounds, they excluded citrate as an intermediate. Sbemin2 found that when glycine is formed from serine, containing isotopic nitrogen and isotopic carbon in its carboxy group, the relative abundance of nitrogen-15 and carbon-13 in the glycine was the same as in the serine; he argued that amino-malonic acid is therefore not an intermediate in this process.

/pdf/interpretation-of-experiments-on-metabolic-processes-using-2uyfralmmt.pdf

Interpretation of experiments on metabolic processes, using isotopic tracer elements.

Considerations for the measurement of core, skin and mean body temperatures.

Fixation of carbon dioxide by pigeon liver in the dissimilation of pyruvic acid

http://www.jbc.org/content/139/1/365.full.pdf

Allan Hemingway

Papers

Fixation of carbon dioxide by pigeon liver in the dissimilation of pyruvic acid

Heavy carbon as a tracer in heterotrophic carbon dioxide assimilation

The position of carbon dioxide carbon in succinic acid synthesized by heterotrophic bacteria

Mechanism of fixation of carbon dioxide in the krebs cycle

The autonomic nervous system and regulation of body temperature.