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BACKGROUND: Xenon induces early myocardial preconditioning of the rat heart in vivo, but whether xenon induces late cardioprotection is not known. Cyclooxygenase-2 (COX-2) has been shown to be an important mediator in the signal transduction of myocardial ischemic late preconditioning (i-LPC). We investigated whether xenon induces late preconditioning (Xe-LPC) and whether COX-2 activity and/or expression are involved in mediating this effect.

METHODS: Anesthetized male Wistar rats were instrumented with a coronary artery occluder. After 7 d of recovery, animals were randomized to 1 of 5 groups each containing 8 animals. The i-LPC group underwent 5 min of coronary occlusion to induce i-LPC. Xe-LPC was achieved by administration of xenon (70 volume%) for 15 min. Additional rats were pretreated with the COX-2 inhibitor NS-398 (5 mg kg^–1 body weight i.p.) with and without Xe-LPC. A group of sham operated animals not undergoing i-LPC or Xe-LPC served as controls (Con). After 24 h, all animals were anesthetized and underwent 25 min of myocardial ischemia induced by tightening of the coronary artery occluder followed by 2 h of reperfusion. Myocardial infarct size was assessed by triphenyltetrazolium chloride staining. In additional experiments, hearts were excised at different time points after preconditioning to investigate COX-2 mRNA and protein expression by polymerase chain reaction and infrared Western blot, respectively.

RESULTS: Both i-LPC and Xe-LPC reduced myocardial infarct size (% of the area at risk) compared with Con (i-LPC: 29 ± 7%; Xe-LPC 31 ± 8%, both P < 0.05 vs Con 64 ± 6%). NS-398 abolished the cardioprotective effect of Xe-LPC (61 ± 6%, P < 0.05 vs Xe-LPC). COX-2 mRNA and protein expression was only increased in the i-LPC group, but not in the Xe-LPC group.

CONCLUSION: Xenon induces late myocardial preconditioning that is abolished by functional blockade of COX-2 activity. In contrast to i-LPC, Xe-LPC did not lead to an increased expression of COX-2 mRNA and protein. These data suggest differences in COX-2 regulation in i-LPC and Xe-LPC.

The Origin of Species
Written by Charles Darwin

Perhaps the most readable and accessible of the great works of scientific imagination, The Origin of Species sold out on the day it was published in 1859. Theologians quickly labeled Charles Darwin the most dangerous man in England, and, as the Saturday Review noted, the uproar over the book quickly "passed beyond the bounds of the study and lecture-room into the drawing-room and the public street." Yet, after reading it, Darwin's friend and colleague T. H. Huxley had a different reaction: "How extremely stupid not to have thought of that."
Based largely on Darwin's experience as a naturalist while on a five-year voyage aboard H.M.S. Beagle, The Origin of Species set forth a theory of evolution and natural selection that challenged contemporary beliefs about divine providence and the immutability of species. A landmark contribution to philosophical and scientific thought, this edition also includes an introductory historical sketch and a glossary Darwin later added to the original text.

Charles Darwin grew up considered, by his own account, "a very ordinary boy, rather below the common standard of intellect." A quirk of fate kept him from the career his father had deemed appropriate--that of a country parson--when a botanist recommended Darwin for an appointment as a naturalist aboard H.M.S. Beagle from 1831 to 1836. Darwin is also the author of the five-volume work Zoology of the Voyage of the Beagle (1839) and The Descent of Man (1871).


From the Trade Paperback edition.