Hypertrophied hearts: what of sevoflurane cardioprotection?

Autor: John Michael Hasenkam, Jens Rolighed Larsen, Morten Smerup, P. Torp, Kim Sivesgaard, Erik Sloth, S. D. Christensen
Rok vydání: 2009
Předmět:
Zdroj: Larsen, J K R, Smerup, M H, Hasenkam, J M, Christensen, S D, Sivesgaard, K, Torp, P & Sloth, E 2009, ' Hypertrophied hearts: what of sevoflurane cardioprotection? ', Acta Anaesthesiologica Scandinavica, vol. 53, no. 4, pp. 496-504 . https://doi.org/10.1111/j.1399-6576.2008.01889.x
ISSN: 1399-6576
DOI: 10.1111/j.1399-6576.2008.01889.x
Popis: Udgivelsesdato: 2009-Apr BACKGROUND: Recent studies have demonstrated that inhalation anaesthetics, like sevoflurane, confer cardioprotection both experimentally and clinically. However, coexisting cardiac disease might diminish anaesthetic cardioprotection and could partly explain why the clinical results of cardioprotection with anaesthetics remain controversial--in contrast to solid experimental evidence. Concomitant left ventricular hypertrophy is found in some cardiac surgery patients and could change cardioprotection efficacy. Hypertrophy could potentially render the heart less susceptible to sevoflurane cardioprotection and more susceptible to ischaemic injury. We investigated whether hypertrophy blocks sevoflurane cardioprotection, and whether tolerance to ischaemia is altered by left ventricular hypertrophy, in an established experimental animal model of ischaemia-reperfusion. METHODS: Anaesthetized juvenile pigs (n=7-12/group) were subjected to 45 min distal coronary artery balloon occlusion, followed by 120 min of reperfusion. Controls were given pentobarbital, while sevoflurane cardioprotection was achieved by 3.2% inhalation throughout the experiment. Chronic banding of the ascending aorta resulted in left ventricular hypertrophy development in two further groups and these animals underwent identical ischaemia-reperfusion protocols, with or without sevoflurane cardioprotection. Myocardial infarct sizes were compared post-mortem. RESULTS: The mean myocardial infarct size (% of area-at-risk) was reduced from mean 55.0 (13.6%) (+/-SD) in controls to 17.5 (13.2%) by sevoflurane (P=0.001). Sevoflurane reduced the infarct size in hypertrophied hearts to 14.6 (10.4%) (P=0.001); however, in hypertrophic controls, infarcts were reduced to 34.2 (10.2%) (P=0.001). CONCLUSION: Sevoflurane abrogated ischaemic injury to similar levels in both normal and left ventricular hypertrophied hearts.
Databáze: OpenAIRE