Tissue hypoxia during acute hemorrhage
© BioMed Central Ltd 2013
Published: 28 March 2013
Calzia and colleagues argue  that tissue hypoxia in a rat model of hemorrhage that led to an oxygen deficit of 120 ml/kg with hyperlactacidemia  may be modest, and may not affect hydrogen sulfide oxidation since '... the arterial oxygen partial pressure was still normal ...' . This contention requires clarification.
This tells us very little about the level of tissue hypoxia.
In all of the models used to study an acute hemorrhage, the baseline oxygen delivery rate is three to four times higher than , despite a large discrepancy in per kilogram between a 500 g rat, a 20 kg pig or a human being: cardiac output, DO2 and do share a similar allometric function with body weight, so that the blood oxygen content is the same in most species. drops dramatically during hemorrhage, reducing DO2. The level of DO2 decreases up to 10 times while drops by four times regardless of the size of animal chosen [3, 4] so that both DO2 and reach one-third of the baseline metabolic rate at the end of a severe hemorrhage! This should certainly lead to one of the most severe forms of tissue hypoxia - with normal arterial blood oxygen partial pressure - unless a decrease in oxygen demand contributes significantly to the reduction in induced by the decline in DO2. Indeed, although the relationship between DO2 and is similar across species, the meaning of a reduction in can greatly differ among animal models according to their ability to decrease the oxygen demand [3, 5] - a phenomenon present during hemorrhage in small mammals . It is eventually this ability to modify oxygen demand during a hemorrhage, in keeping with DO2, which controls the level of tissue hypoxia, and not the absolute levels of PaO2, DO2 or .
concentration (content) of oxygen in the arterial gas
rate of oxygen delivery
partial pressure of oxygen in the alveolar gas
partial pressure of oxygen in the inspired gas
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