Physiological Parameter Values for Physiologically Based Pharmacokinetic Models

Hyperbaric oxygen — 100 percent oxygen at two to three times the atmospheric pressure at sea level — can result in arterial oxygen tension in excess of 2000 mm Hg1 and oxygen tension in tissue of almost 400 mm Hg.2,3 Such doses of oxygen have a number of beneficial biochemical, cellular, and physiologic effects, and today there are 259 hyperbaric facilities in the United States with 344 single-occupant (“monoplace”) hyperbaric-oxygen chambers.4 In this article, we review the mechanisms of action, evidence of clinical efficacy, and risks of therapy with hyperbaric oxygen. Physiologic Effects For hyperbaric oxygen, pressure is expressed . . .

Hyperbaric-Oxygen Therapy

Background Patients with acute carbon monoxide poisoning commonly have cognitive sequelae. We conducted a double-blind, randomized trial to evaluate the effect of hyperbaric-oxygen treatment on such cognitive sequelae. Methods We randomly assigned patients with symptomatic acute carbon monoxide poisoning in equal proportions to three chamber sessions within a 24-hour period, consisting of either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Oxygen treatments were administered from a high-flow reservoir through a face mask that prevented rebreathing or by endotracheal tube. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae six weeks after carbon monoxide poisoning. Results The trial was stopped after the third of four scheduled interim analyses, at which point there were 76 patients in ea...

Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning

Carbon monoxide intoxication continues to be one of the most common causes of morbidity due to poisoning in the United States.1,2 It may be intentional or accidental, and exposure may be lethal. Approximately 600 accidental deaths due to carbon monoxide poisoning are reported annually in the United States,3 and the number of intentional carbon monoxide–related deaths is 5 to 10 times higher.1 The rate of accidental death caused by carbon monoxide from motor vehicles is higher in the northern United States and peaks during the winter months.4 The intentional deaths occur year-round without significant peaks.1 The severe winter of . . .

Carbon Monoxide Poisoning

This minireview is an update of a 1997 review on erythropoietin (EPO) in this journal. EPO is a 30,400-dalton glycoprotein that regulates red cell production. In the human, EPO is produced by peritubular cells in the kidneys of the adult and in hepatocytes in the fetus. Small amounts of extra-renal EPO are produced by the liver in adult human subjects. EPO binds to an erythroid progenitor cell surface receptor that includes a p66 chain, and, when activated, the p66 protein becomes dimerized. EPO receptor activation induces a JAK2 tyrosine kinase, which leads to tyrosine phosphorylation of the EPO receptor and several proteins. EPO receptor binding leads to intracellular activation of the Ras/mitogen-activated kinase pathway, which is involved with cell proliferation, phosphatidylinositol 3-kinase, and STATS 1, 3, 5A, and 5B transcriptional factors. EPO acts primarily to rescue erythroid cells from apoptosis (programmed cell death) to increase their survival. EPO acts synergistically with several growth factors (SCF, GM-CSF, 1L-3, and IGF-1) to cause maturation and proliferation of erythroid progenitor cells (primarily colony-forming unit-E). Oxygen-dependent regulation of EPO gene expression is postulated to be controlled by a hypoxia-inducible transcription factor (HIF-1alpha). Hypoxia-inducible EPO production is controlled by a 50-bp hypoxia-inducible enhancer that is approximately 120 bp 3' to the polyadenylation site. Hypoxia signal transduction pathways involve kinases A and C, phospholipase A(2), and transcription factors ATF-1 and CREB-1. A model has been proposed for adenosine activation of EPO production that involves protein kinases A and C and the phospholipase A(2) pathway. Other effects of EPO include a hematocrit-independent, vasoconstriction-dependent hypertension, increased endothelin production, upregulation of tissue renin, change in vascular tissue prostaglandins production, stimulation of angiogenesis, and stimulation of endothelial and vascular smooth muscle cell proliferation. Recombinant human EPO (rHuEPO) is currently being used to treat patients with anemias associated with chronic renal failure, AIDS patients with anemia due to treatment with zidovudine, nonmyeloid malignancies in patients treated with chemotherapeutic agents, perioperative surgical patients, and autologous blood donation. A novel erythropoiesis-stimulating factor (NESP, darbepoetin) has been synthesized and when compared with rHuEPO, NESP has a higher carbohydrate content (52% vs 40%), a longer plasma half-life, the amino acid sequence differs from that of native human EPO at five positions, and has been reported to maintain hemoglobin levels just as effectively in patients with chronic renal failure as rHuEPO at less frequent dosing. The use of rHuEPO and darbepoetin to enhance athletic performance is officially banned by most sports-governing bodies because the excessive erythrocytosis can lead to increased thrombogenicity and can cause deep vein, coronary, and cerebral thromboses.

Erythropoietin: Physiology and pharmacology update

Calcium and magnesium binding properties of cell membrane materials

The increase in hypoxia tolerance of normal men accompanying the polycythemia induced by transfusion of erythrocytes

Body weight data, collected routinely from the US Air Force chimpanzee colony at Holloman AFB, was used for a longitudinal analysis of growth. Data were fitted to a model based on human growth patterns, which is described and compared to other treatments applied to growth data. Results are compared to other observations of chimpanzee and of human growth.

Weight growth of colony-reared chimpanzees.

Body and organ weights of sea level control rats were compared with those of rats (P) born at sea level and then exposed to 12,470 feet, and with those of rats (F2) of the second filial generation ...

Body and Organ Weights of Rats During Acclimatization to an Altitude of 12,470 Feet

The following formula was derived to describe the uptake of carbon monoxide by man: ..delta..% COHb = (parts CO (per 10,000) x minute vol. x exposure time)/(46.5 x blood volume). Thirty-two volunteers were tested at rest and after walking on a treadmill. The volunteers were exposed to 0.9 to 21.8 parts CO per 10,000 for 15 to 300 minutes. There was no control of smoking.

Formulation of the principal factors affecting the rate of uptake of carbon monoxide by man.

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