Background: Erythrocytes are transfused to improve oxygen delivery and prevent or treat inadequate oxygenation of tissues. Acute isovolemic anemia subtly slows human data processing and degrades memory, increases heart rate, and decreases self-assessed energy level. Erythrocyte transfusion is efficacious in reversing these effects of acute anemia. We tested the hypothesis that increasing arterial oxygen pressure (Pao2) to 350 mmHg or greater would supply sufficient oxygen to be equivalent to augmenting hemoglobin concentration by 2-3 g/dl and thus reverse the effects of acute anemia.
Methods: Thirty-one healthy volunteers, aged 28 +/- 4 yr (mean +/- SD), were tested with verbal memory and standard, computerized neuropsychologic tests before and twice after acute isovolemic reduction of their hemoglobin concentration to 5.7 +/- 0.3 g/dl. Two sets of tests were performed in randomized order at the lower hemoglobin concentration: with the volunteer breathing room air or oxygen. The subject and those administering the tests and recording the results were unaware which gas was administered. As an additional control for duration of the experiment, 10 of these volunteers also completed the same tests on a separate day, without alteration of hemoglobin concentration, at times of the day similar to those on the experimental day. Heart rate, mean arterial blood pressure, and self-assessed sense of energy were recorded at the time of each test.
Results: Reaction time for digit-symbol substitution test increased, delayed memory was degraded, mean arterial pressure and energy level decreased, and heart rate increased at a hemoglobin concentration of 5.7 g/dl (all P < 0.05). Increasing Pao2 to 406 +/- 47 mmHg reversed the digit-symbol substitution test result and the delayed memory changes to values not different from those at the baseline hemoglobin concentration of 12.7 +/- 1.0 g/dl, and decreased heart rate (P < 0.05). However, mean arterial pressure and energy level changes were not altered with increased Pao2 during acute anemia. 相似文献
Gene amplification occurs frequently in tumour tissues yet is,in general, non-inheritable. To study the molecular mechanismsconferring this restraint, we created transgenic mice carryinga human butyrylcholinesterase (BCHE) coding sequence, previouslyfound to be amplified in a father and son. Blot hybridizationof tail DNA samples revealed somatic transgene amplificationswith variable restriction patterns and intensities, suggestingthe occurrence of independent amplification events, in 31% (11/35)of mice from the FII generation but in only 3.5% (2/58) of theFII and FIV generations. In contrast, >10-fold amplificationsof the BCHE transgene and the endogenous acetylcholinesteraseand c-raf genes appeared in both testis and epididymis DNA from>80% of FIII mice. Drastic, selective reductions in testisBCHEmRNA but not in actin mRNA were detected by the PCR amplificationof testis cDNA from the transgenic mice, and apparently resultedin the limited transmission of amplified genes. The testicularamplification of the BCHE transgene may potentially representa general phenomenon with clinical implications in human infertility. 相似文献
Air embolism produced by vaginal insufflation is an unusual but potentially lethal consequence of sexual activity, especially in the pregnant patient. Reported here is the case of a young pregnant woman who presented to the ED in full cardiac arrest, with little history to explain her condition. Despite aggressive resuscitative measures, the patient died, but her infant son was delivered via perimortem cesarean section and survived. A high level of suspicion for air embolism should be maintained for young women who unexpectedly develop cardiac arrest, particularly during sexual activity. Air embolism patients may require vigorous medical resuscitation, hyperbaric oxygen therapy, or surgical intervention to survive. The emergency physician should be familiar with the indications for perimortem cesarean delivery in the third-trimester patient presenting to the ED with cardiac arrest. 相似文献
ABA-1 is an approximately 14,000 molecular weight (MW) allergen which is among the most abundant proteins synthesized by the nematode parasite Ascaris. IgG and IgE responses to it are major histocompatibility complex (MHC)-restricted in rodents and have only been found to occur in rats of the RT1u haplotype and mice of the H-2s haplotype. Humans infected with the parasite vary substantially in their immune response to the allergen, but the genetic basis for this unknown. H-2 recombinant mice were used to identify the region within the MHC controlling antibody responses to the allergen. IgG antibody to immunoaffinity purified ABA-1 was assayed by radio-immunoassay and IgE by passive cutaneous anaphylaxis. This showed that the restriction element is the I-A molecule and that there was some evidence for I-E modulation of the level of response. 相似文献