Anaemia and Anaesthesia I. D. S. Gillies

Gillies, Iain

doi:10.1093/bja/46.8.589

Cited by 102 publications

(101 citation statements)

References 76 publications

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“…Although not very frequently, intragenic regulatory elements have been described for the glucocorticoid responsive element (Moore et al, 1985) and the thyroid hormone responsive element (Sap et al, 1990) in the human growth hormone gene and the serum responsive element in the ,B-actin gene (Kawamoto et al, 1988). Tissue-specific enhancers have also been ascribed intragenic locations in the human thymidine kinase gene (Merrill et al, 1984) and the murine genes for the heavy (Gillies et al, 1983) and light chains of immunoglobulins (Queen and Baltimore, 1983). However, in such cases, regulatory elements are restricted to non-coding exons or introns.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the hormone responsive element involved in the regulation of the progesterone receptor gene.

et al. 1991

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The transcription of the progesterone receptor gene is induced by estrogens and decreased by progestins. Studies were performed to define the regions of the gene and the molecular mechanisms involved. No hormonal regulation could be observed using 5′ flanking regions of the gene up to −2762 in front of a heterologous gene. Estrogen and progestin regulation could be observed only when using fragments of the gene extending down to +788. Progressive deletions from the 5′ and 3′ ends, site‐directed mutagenesis and DNase protection experiments with purified estrogen receptor suggested that the biologically active estrogen responsive element (ERE) is present at +698/+723, overlapping the initiation of translation. An oligonucleotide was synthesized bearing this ERE and shown to impart estrogen inducibility to a heterologous gene. Its regulation by anti‐estrogens corresponded to that of the in situ progesterone receptor gene since tamoxifen was a partial agonist whereas ICI 164384 was a full antagonist. This ERE also mediated down‐regulation by progestins in the presence of the progesterone receptor, even though it has no progesterone receptor binding ability. DNase footprinting showed that this effect was not due to a decrease of estrogen receptor affinity for the ERE in the presence of progesterone receptor. Finally, use of deletion mutants of the progesterone receptor showed that the steroid binding and the DNA binding domains were necessary for down‐regulation whereas deletions of various parts of the N‐terminal domain were without effect.

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Section: Discussionmentioning

confidence: 99%

Characterization of the hormone responsive element involved in the regulation of the progesterone receptor gene.

et al. 1991

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“…Oxygen consumption (V0 2 ) was calculated according to the for mula [16]: V02 -Cl x 10 x [(Hb x l.39x ASO>/l00) + (0.003l x APo. )], where 10 = factor to convert arteriovenous O2 content difference from ml O2/IOO ml to ml O2/I liter blood: 1.39 = oxygen-hemoglobin equivalent (amount of O2 capable of combining with 1 g of hemo globin); ASO2 = difference in O2 saturation of arterial and mixed venous blood; AP02 = difference in Po> of arterial and mixed venous blood.…”

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confidence: 99%

“…The expression 10 x (Hb x 1.39 XASO2/100)+ (0.0031 x APo>) has been termed 'Aa-v O2 content' [16], Standard procedures were used for statistical analysis. For com parison of pre-and postdialysis values the paired t test was applied.…”

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confidence: 99%

Oxygen Consumption during Maintenance Hemodialysis

Blumberg¹,

Keller²

1979

Nephron

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The influence of hemodialysis on oxygen consumption was studied in 15 patients on maintenance dialysis. Red cell 2,3-DPG, P₅₀, an inverse measure of oxygen affinity of hemoglobin, arterial and central venous blood gases and cardiac index were measured. 2,3-DPG remained unchanged, whereas in vivo P₅₀ fell significantly during dialysis due to a rise of pH (Bohr effect). Arterial PO₂ was lower after than before dialysis, but arterial and central venous oxygen saturations did not change significantly. Cardiac index increased from 3.66 to 4.05 liter/min/m². Oxygen consumption rose from 120.5 to 131.7 ml/min/m² (p < 0.05), the rise being accounted for by an increase in cardiac index and by a slight post-dialysis hemoconcentration. However, even correcting for these parameters did not reveal a decrease in oxygen consumption. It is concluded that, contrary to previous assumptions, the hemodialysis-induced rise in pH with its consequent increase of oxygen hemoglobin affinity did not impair oxygen delivery in this group of patients on maintenance dialysis.

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“…This conclusion could reasonably be applied to all elective surgical procedures performed under general anaesthesia, especially in patients with anaemia. 6 …”

Section: Discussionmentioning

confidence: 99%