| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10927882 | Cryobiology | 2014 | 9 Pages |
Abstract
The present data shows that levosimendan ameliorates hypothermia-induced systolic dysfunction by elevating SV during rewarming from 15 °C. Inotropic treatment during rewarming from hypothermia in the present rat model is therefore better achieved through calcium sensitizing and PDE3 inhibition, than β-receptor stimulation.
Keywords
PVDFphosphodiesterase IIILVdP/dtmaxPDE3PDE3 inhibitorLVEDPPRSWcTnILVESVLVEDVLevosimendanpKacAMPCyclic adenosine monophosphatecTnCCardiac outputleft ventriclecardiac troponin CTroponin ILeft ventricular end-diastolic volumeleft ventricular end-systolic volumestroke volumeRewarmingCalcium sensitizerCardiovascular supportpolyvinylidene difluorideSarcoplasmic reticulumTPRcardiac indexmean arterial pressureleft ventricular end-diastolic pressurecardiac troponin Itotal peripheral resistancemapHypothermiaAccidental hypothermiaprotein kinase Apreload recruitable stroke workStroke work
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Authors
Erik Sveberg Dietrichs, Brage HÃ¥heim, Timofei Kondratiev, Gary C. Sieck, Torkjel Tveita,